Talk:Alzheimer's disease/Archive 2

Aluminum

 * Research ?

Years ago while studying a water option to get rid of a spring fed water supply in favor of a lake water source and alot of filtration it was noted that in Canada and the USA, they use Aluminum Sulfate to filter water. Problem is this adds to the Aluminum in the water, from .02 mg to .32 mg/litre.

No problem in Canada no standards for Aluminum in drinking water; why ?

Have the lobby groups manipulated government ?

Months later I found this scientest on the Internet, a Dr. Squitti doing research on Alzheimers and Copper...well she told me that Aluminum was always suspected of contributing to Alzheimers.

Well in Canada we got rid of glass pop bottles in favor of aluminum cans, and today Alcan Aluminum collects cans for Alzheimers Research; imagine that.

Remember the cigarette companies and how scientests preseted evidence to some grand jury that cigarettes did not cause cancer; well they lied.

--Son of Maryann Rosso and Arthur Natale Squitti 04:36, 20 August 2006 (UTC)

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On the other hand, they're the most politically active age group -- they've more leisure time. There's a reason politicians in the US and elsewhere don't dare touch pensions, for example.

-

The article incorrectly stated that Alzheimer first identified the symptoms of the disease and therefore (citing the authoritative reference from the historian of the institute where they worked) I took the liberty of making this correction: The symptoms of the disease as a distinct nosologic entity were first identified by Emil Kraepelin, and the characteristic neuropathology was first observed by Alois Alzheimer in 1906. In this sense, the disease was co-discovered by Kraepelin and Alzheimer, who worked in Kraepelin's laboratory. Because of the overwhelming importance Kraepelin attached to finding the neuropathological basis of psychiatric disorders, Kraepelin made the generous decision that the disease would bear the name of Alzheimer (J. Psychiat. Res, 1997, Vol 31, No. 6, pp. 635-643).

Stem Cells
I was informed about stem-cell therapy related to AD. Does anyone have information about it, or any name I could contact about this new research?


 * No, this concerns Parkinson's, not Alzheimer's. There is no proof that stem ells would work in AD. JFW | T@lk  03:33, 23 Jan 2005 (UTC)


 * I recently read something (a heading, yes, no time to read the article) on Google News that would disagree. It's recent, within a day or two, and says something about Brain Stemcells being used to combat Alzheimer's. --24.76.141.132 05:15, 23 Mar 2005 (UTC)


 * That's experimental, like most unproven theories mentioned in this article. Shall we concentrate on the present management? Stem cells are only used in bone marrow disorders, and the rest is all daydreaming out of therapeutic embarassment. JFW | T@lk  07:49, 23 Mar 2005 (UTC)

Rewrite for those who need this article -- families, policy makers
There is a danger in starting a rewrite from the medical profession's literature, because of the prevasive effect of drug company studies combined with the medical model's focus primarily on perscription drugs, and primarily after diagnosis. The result is a subtle and pervasive bias in the medical journals' point of view, and adopting it uncritically would threaten to obscure the most useful information that a Wikipedia article can provide.

The audience that Wikipedia's Alzheimer's Disease article serves may include a few merely curious souls who want to know the basics, but far more often information on Alzheimer's is sought by family members struggling with the news of diagnosis of a loved one, or concerned about their own fate in old age, and directly or indirectly perhaps by policy makers.

There is a subtly slanted point of view pervasive in the medical literature, including the article on which it is suggested that this article be patterned. Neurological literature is driven by publication of new research studies. And the overwhelming majority of research studies are financed by drug companies hoping to promote costly proprietary treatments for Alzheimer's. Lost in this torrent of publications is the fact that efforts to find a cure have so far proven to provide very modest value at best.

Meanwhile, the large gains available in the way of prevention have so far been demonstrated in only a few studies, those for which financing was found with non-company money. Impressive results have been observed with certain NSAIDs, vitamins C and E in combination, and exercise, among others. But these important results have drowned in the flood of publications reported in the journals most consulted by neurologists, which discuss drug company studies of (largely ineffective post-diagnosis) drugs. In reporting these studies, the medical journals adopt a pervasive POV focused on present and possible future profitable medicines. This focus has effectively buried the story about prevention, which is the actual headline. To the extent that medical doctors see their role as providing prescription rather than non-prescription remedies, and as acting only after diagnosis, rather than before, their POV conincides with that of the drug companies. If information isn't about cure after diagnosis, it receives short schrift in the medical journals and in medical practices alike.

But for families and individuals who need information on Alzheimer's, prevention and care are the information of greatest value. Prevention and nursing care are salient for families (news they can use) and useful in framing public policy. Information about the present, largely-ineffective proprietary treatements will be provided by almost any health-care professional consulted, and often adopted because not taking the (admittedly near-useless) patent medicines is presented as "doing nothing."

Wikipedia should not allow the POV that focuses exclusively on these low-value / high-cost treatments to crowd out useful, practical NPOV information that patients and their families desperately need on diagnosis, prognosis, nursing care (whether family provided or otherwise), and especially prevention.

Information about the gains in prevention is urgently needed in the debates by public policy makers. As some recent comments point out, most people currently get Alzheimer's if they live long enough. Most are cared for by female relatives, as one inestimable social cost. The remaining nursing-care costs threaten to swamp the social safety net in developed countries, which all have aging populations. Though few, the available studies show that cost-effective prevention works. The information in these studies is more valuable and more important than the many re-hashing drug treatments that have but little effect.


 * The review I suggested is quite impartial, and does not "rehash drug company studies". Of course the social context should be firmly embedded in the article. You may be shouting at a strawman. JFW |  T@lk  22:22, 26 Mar 2005 (UTC)

Pathology photo
The gross image of the "Alzheimer's Brain" appears to be one of frontotemporal dementia, not Alzheimer's. It is of course possible that this is Alzheimer's degeneration, but it would be an atypical case. I would like to suggest replacing this image with one showing the more typical parietal and medial temporal atrophy pattern associated with Alzheimer's disease. sallison 02:53, 6 January 2006 (UTC)
 * You're totally correct. I've fixed this accordingly. Semiconscious ( talk  ·  home) 07:30, 6 January 2006 (UTC)
 * I'm glad you caught my mistake, by the way. Thank you. :) Semiconscious ( talk  ·  home) 07:30, 6 January 2006 (UTC)

What is it like? I want to know what it is like to live with someone with Alzheimers. Most of the articles I've read say that it kind of a drag but it doesn't have actual people with relatives that have Alzheimers. Someone that care for a person with Alzheimers should write their own version of what is like it live with them, we can't take doctors words as if its stone. Perhaps their relatives dont consider it boring and a drag.

Question
I have been reading a lot of material about nCJD being misdiagnosed as Alzheimers - supposedly indicating why cases of Alztheimers are doubling/tripling (?) recently. Can anyone provide points of view on either side of this aurgument ? Thanks


 * nCJD has a rather typical presentation of rapidly progressive diffuse mental deterioration and specific motor symptoms (such as myoclonic jerks). I think the increase in Alzheimer's is a result of people getting older in general and surviving other previously mortal diseases in particular. I think it would be immensely speculative to attribute this increase to CJD. JFW | T@lk  16:02, 16 February 2006 (UTC)

Bold textMy mother had Alzheimer's and my best friend's mother has it in very advanced stages today. My mother was a version of Betty White off the Golden Girls, always dressed perfectly, every hair in place(done every Friday for 50 years). At first, no one could tell unless you talked with her more than 45min, when she then began to repeat herself. Even though she would be polite to people, you could see the fear in her eyes of not remembering who these people were. It was very dramatice for her to the point she stopped going to Church for fear someone would speak to her and she not know who they were. During this disease, there can be "cute-funny" parts of it, like blue skies and white puffy clouds or those are the prettiest red Christmas lights I've ever seen....and it's a see of red car taillights at 5:00 traffic.It is stressful for the caregiver....they do their best to help and frustrated to see their loved one digress. It's like taking care of a 2yr old. The patient gets very frustrated...they know they have something to say but cant remember how to talk...so they bang on the counter in anger and frustration. Same thing with using a bathroom...they forget where it is or how to use it...so they urinate on the floor....they look in your eyes knowing you are a safe person to them but seeing the confusion of who you are...this tears your heart to pieces. The ultimate is when they forget how to chew and swallow. These are pictures one never forgets no matter how much you focus on the funny and good times in your life with this person. The fact you are helpless in helping someone who is helpless is a horrible feeling. To me, this is the worst disease out there...it has no cure and it humiliates and degrade the person who has it.Making sure they live a full and happy life til the end is very important and NEVER take anything they may say or do personally....they are living in total confusiion and it is not you, the caregiver.Never speak to them like they are a child....always treat them the way you want to me treated...never yelled at, spoken to softly and kindly....keep them safe from themselves and outside influences. Take locks off bedroom and bathroom doors so they don't lock themselves in there. Dont let them watch vioent tv show/movies.....they cant tell the difference between real and not. It's a 24/7 job being a caretaker but it is the most rewarding job one can accomplish. To know you made a difference for someone special is very important for them and for you. I could write page after page on this subject....both my mother and my friend's have passes away. Patience, guidance, love and caring are required at all times and the rewards are ten times fold.Wenboop 16:18, 23 April 2006 (UTC)

Language simplification...
This article is probably quite accurate, but at the expense of accessibility. Can't some of the jargon be taken out of the article, particularly the introduction? --Robert Merkel 22:37, 19 March 2006 (UTC)
 * I've looked at the language in the intro and while bits of it are quite technical most of the terms are explained or a link is offered that explains the term. This article has become rather untidy and could do with a complete review.  The introduction as it is now does present a number of advanced notions that perhaps could be discussed later on in the article.  I'll try to have a go at tidying it up, perhaps with the help of some of my colleagues.  I know JFW wanted to have a go at it, maybe we’ll do it soon. JASFonseca 20:37, 22 March 2006 (UTC)
 * Good idea, I'll help out if I can. I agree with simplifying the language where it makes sense. -Ravedave 04:01, 23 March 2006 (UTC)

I changed the "unbiased clinicians" part- we should not imply that every pharmaceutical company is biased.

CAVEAT LECTOR (Let the Reader Beware)
This article has fallen prey to individuals pushing fringe theories with respect to the pathogenesis and treatment of the disease, such as the sections on heavy metal administration to rabbits and therapeutic use of Indian spices (turmeric), which have now mercifully been deleted. I would request that other neurologists and neuroscientists specializing in Alzheimer's disease join me in providing surveillance of this page so that the lay public can find a concise presentation of well-substantiated and valid information on the subject. There is already far too much quackery and chicanery concerning Alzheimer's disease available on the internet, which does a huge disservice to family members searching for information that possibly could help their loved one(s). The clinical and research communities should work together to make Wikipedia a sound and reliable source on medical subjects for patients and family members. -- Ve ri tas 22 April 2006


 * You are welcome to participate. I agree that only very popular and notable remedies should be mentioned; this information is notoriously hard to verify. JFW | T@lk  10:50, 23 April 2006 (UTC)

What Considers As Famous?
So who are these people?


 * You see, they were randomly inserted because people thought it would be interesting to know that their favourite historical personality had Alzheimer's. I think only the very most famous people should be listed here (Ronald Reagan comes to mind), and the rest either removed or forked to a different page. JFW | T@lk  20:28, 1 May 2006 (UTC)

Drinking more than 2 cups of green tea a day could help prevent Alzheimer's
Do we really need an entire section with this title? I'll bet there are dozons of studies being done on nutritional aspects of Alzheimer's. Could we just merge a summary of this into 'treatment'? DJ Clayworth 14:27, 7 June 2006 (UTC)

Alzheimer's Blogs
I know a great site that provides a ton of Alzheimer's general info, but more importantly it has expert patient blogs, hospital and doctor recomendations, and message boards that promote communication between patrients, caregivers, and doctors. I tried to add this site to the external links section but was not able to. Does anyone know who I can get permission from to do this?

Alzheimer's Vaccine Shows Promise
Just wanted to link this before I forgot. I'll try and add it if not someone else can... Alzheimer's Vaccine Shows Promise -Ravedave 15:22, 13 June 2006 (UTC)

Statistical indications
In the Epidemiology section, there is mention that smoking and drinking reduce the risk. What is the basis for this kind of conclusion? Was it part of the same report from Duijin and Hofman?

I could probably show that a healthy dose of radioactive uranium will keep people from getting Alzheimer's. The people in the test will all be dead well before they could ever see the symptoms of Alzheimer's.  But something tells me that people would not be lining up at the airport with plane tickets to Chernobyl. Before people read this article and start new smoking and drinking habits to prevent Alzheimer's, someone please show the scientific validity of such a conclusion. jordan 19:05, 16 June 2006 (UTC)

List of Alzheimer's articles
There seem to be new Alzheimer's articles every week, so I am just going to start listing any I find here. Please feel free to add to the list.
 * Alzheimer's Vaccine Shows Promise
 * Chinese Moss Extract Tested as Alzheimer's Drug
 * Green tea could protect against Alzheimer's, (catechins).
 * Antioxidant in Green tea may fight Alzheimer's, (EGCG).
 * Alzheimer's Association International Conference 2006 overview.
 * A new drug, called PBT2, shows promise


 * There are new Alzheimer's articles every week, which shouldn't come as a surprise. But please don't list them here, as that would be an entirely unacceptable use of a talk page. If you'd like to summarize these alternative therapies, pointing to peer-reviewed studies, noting the rampant pseudoscience and quackery, then by all means, feel free. But do not clutter this talk page with a mere list of links to news articles when only a vanishingly small subset of their authors have bothered to read and understand the study in the first place. --David Iberri (talk) 23:08, 6 July 2006 (UTC)


 * Its a talk page I'll do what I want. Alzheimer's Association International Conference overview -Ravedave 00:16, 18 July 2006 (UTC)
 * That type of response is not in the spirit of Wikipedia's collaborative nature and is generally unhelpful. You will find that other editors are far more likely to work productively with you if you'd lose the pouty, "I'll do what I want" attitude. That said, my point remains: Talk pages are for discussing how to improve articles, not for linkspamming. Please do not add more links to this talk page unless you plan on discussing the merits of referencing them in the article. --David Iberri (talk) 03:13, 18 July 2006 (UTC)
 * I'll change my attitude if you drop the holier than thou "You have to spend 50 hours finding peer review articles and weaving them into the article to contribute" attitude. I don't have the desire to search academic papers, but I do want to improve the article. Did you read the links? They are from Forbes and WebMD, reputable organizations. I am not an MD, I do not have the knowledge to decide if these are worth including on the article page HENCE THE LINKS. If someone with the knowledge can actually review them then the article improves. I am tryign to collaborate as much as I can in an area I don't understand. Also before I added those links the possible cures section was totally unreferenced. So please before you jump in and accuse someone of adding linkspam and quakery take a second and wonder why they are on the TALK page and not the article.  -Ravedave 04:02, 18 July 2006 (UTC)
 * I appreciate the effort it takes to contribute to a WP article on a topic in which you are not an expert. I do it all the time. :-) By no means did I mean to insinuate that your contributions amount to quackery. I just wanted to suggest that if you were to add a section on alternative AD therapies, then you'd prominently mention the quackery involved in many of them. And the reason I suggested peer-reviewed studies is that they are generally preferred over news articles in medical topics. The reason I called it linkspam is that you originally said you'd be adding any articles you found to the talk page, which IMO amounts to spamming. I hope you can see that I wasn't trying to be condescending. Cheers, David Iberri (talk) 04:35, 18 July 2006 (UTC)

Proposed major revision
I'm proposing a major revision of the later sections of this article which have become unwieldy at best. As per the comments of Veritas and JFW above, data has been added non-selectively, described in excess detail and used to support overly broad clinical assertions.

I'd suggest the following components for a revision:
 * Break off the list of "famous" disease sufferers to its own page, and include a sentence like this one somewhere in the article: "Famous Alzheimer's disease sufferers have included President Ronald Reagan, Ralph Waldo Emerson, and Rita Hayworth."
 * Convert the prevention section to bullet point format, including only popular and/or validated treatments. Where popular therapies have been called into question, include this information
 * Limit external links to a few of the many available highly reliable sites. If we're going to offer links, they should be neither redundent nor POV nor self-promotional.
 * Choose a consistent citation format for scientific and other articles (footnote or inline or PMID reference with or without full reference at the article's end). I propose the new new Cite.php footnote format with full references.

Towards this end, I've combined the epidemiology and prevention sections and converted it to an annotated bullet point format. I've based the information on prevention recommendations in Up-To-Date and the Cochrane databases. It should be notable that I've removed references to such things as green tea and caloric restriction. I've used the Cite.php format converted the only other two complete references as well. (The molecular pathway "reference" moved to external links since it wasn't really a reference.)

Depending on feedback, I'll complete additional parts of this revision in the next few days.

—The preceding unsigned comment was added by Ipeltan (talk • contribs).
 * Sounds good! -Ravedave 15:11, 17 June 2006 (UTC)
 * Bravo! Much needed. Ve ri tas 17:28, 18 June 2006 (UTC)

Role of glycoprotein Reelin in the disease
Hi. I'm writing a page on reelin and stumbled upon this article about Reelin's role in Alzheimer's. I've included these facts in the reelin page. I thought you may be interested in this. --CopperKettle 15:25, 21 June 2006 (UTC)\ P.S. A quote from the article: "the involvement of the Reelin signaling pathway in neurodegeneration has also been proposed (1, 6, 9, 15–17). First, Reelin binds to apolipoprotein E (ApoE) receptors, and some ApoE gene polymorphisms are considered risk factors for Alzheimer’s disease (AD). Moreover, the lack of Reelin is associated with increased phosphorylation of Tau (1, 2, 18), whose hyperphosphorylation leads to intracellular tangles and neuronal degeneration (19). Disabled-1 binds to -amyloid precursor protein (20, 21) family members, whose proteolytic processing leads to the A-peptide-forming amyloid plaques. Recent data also indicate that Reelin is present in -amyloid plaques in a transgenic mouse model of AD (22). "--CopperKettle 15:50, 21 June 2006 (UTC)

Standards for external links
There was a question as to why the link to the Wash U. Alzheimer's site was deleted. First, the page states at it's top that is a copy of material from the government's Alzheimer.org site. The link should therefore go to that site and not the Wash U. site. Second, and more importantly, the same statement dates the material to 2000, which is extremely outdated in the world of Alzheimers. Much of the information at that site is therefore likely outdated. Third (and least important), the link is not formatted in the style now being used in this article.

Other standards for external links include relevance and non-commercial/non-promotional. --Ipeltan 17:36, 26 June 2006 (UTC)

Standarts for external links -- Question
I 100% agree with what you say. The reason I provided a link to this page is that it includes numerous information related to the Alzheimer's which is not mentioned. So, if it is possible, can you read that report through and incorparatre it to the wikipedia's article on AD ??

Also please check the following link: http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=104300. It contains a very extensive description of all aspects of the AD. And I would recommend strongly to provide a link to it in the main page. Please let me know what you think ??

--Igor V. June 28


 * If the WUSTL information is relevant to an encyclopedia article and should be included, please feel free to work it in. You could also link to sites that provide it, as long as they're up to date (i.e. not from 2000).  I meant to add the OMIM link before, thanks for reminding me. --Ipeltan 13:13, 3 July 2006 (UTC)


 * I think the following information, which can be supported by WUSTL, will be a good contribution to the article, since it gives the reader an important prospective on simular neurodegenerative diseases, which makes main article more informative for the reader. Before adding it to the main article I want to find out here if it is a relevant inquiry ?


 * the title can be: "Simularities to Other Neurodegenerative Diseases", or "Parallels between AD and Other Progressive Neurodegenerative Disorers, or "Overlapping Characteristics betweein AD and Other Neurodegenerative Diseases."
 * A common thread in neurodegenerative disorders is the abnormal aggregation of the proteins in the brain. Examples of these proteins include amyloid in AD; synuclein in Parkinson's disease; prions in prion diseases; huntington in Huntington's disease; BRI in familial British dementia; and tau in taupathies, such as frontotemporal dementia with Parkinson's disease, progressive palsy, and Pick's disease. Most reaserchers believe the the protein aggregates formed are toxic and give rise to the multiple brain changes that characterize the different neurodegenerative diseases. If one relationship between these diseases really is abnormal protein aggregation, then discovering ways to prevent aggregation, or the processes set in motion by the aggregation, may halt the disease process.
 * -- Igoruha 12:12, 4 July 2006 (UTC)


 * Added your text into section on pathogenesis --Ipeltan 09:01, 7 July 2006 (UTC)


 * In my opinion, the section on Potential Treatments is one of the weakest elements in the main article. It should look to the future, and therefore should give a reader a full prospective on what is or will be studied in the current research (which, of course, would need to be constantly undated ). Here are some suggestions.
 * I would start as follows:
 * It has been hypothesized that an approach to preventing AD is to block the production of amyloid in the brain, though there is as yet no formal proof that this would prevent the development of the clinical symptoms of AD. An important focus of scientific focus research, therefore, if finding out how to block the formation of beta-amyloid. Another is finding ways to inhibit amyloid’s deposition into insoluble plaques. Here is the list of some potential treatments that are being explored in current research:
 * - pursuing an anti-amyloid vaccine.
 * - removing amyloid ( like, brain microglia, which may destroy amyloid naturally)
 * - preventing beta-amyloid from forming (for example, estrogen might reduce the risk of developing AD by lowering beta-amyloid secretion)
 * - breaking down beat-amyloid (which believed to be accomplished by “insulin degrading enzyme”)
 * - presenilins
 * - programmed cell death (apoptosis) (for example, telomerase, an enzyme that maintains chromosome structure, under certain circumstances can block specific apoptotic pathways and in tissue culture can decrease vulnerability to cell death induced by beta-amyloid)


 * As you see this is just a backbone (or a part of it, since I talk only about amyloid) of what can become, in my opinion, a great addition/revision to the main article. As so, I would like to fully develop this “backbone” here before posting it. Please, offer your suggestions.
 * --Igoruha 9:10, 7 July 2006 (UTC)


 * The most reliable and extensive information about current state on Alzheimer’s Disease may be found in the current progress report on AD (from NIA website), here is the link,
 * http://www.nia.nih.gov/NR/rdonlyres/E601F872-FE6D-4930-9724-9D826DA37208/0/Progress_Report_on_Alzheimers_Disease_20042005small.pdf
 * I think we should provide a direct link to this report, due to it extensive discussion of AD, and because it is really hard to find this report on the NIA website, that we provide a link to on the main page.
 * --Igoruha 11:06, 8 July 2006 (UTC)

Definitive diagnosis must await microscopic examination of brain tissue?
Question. Diagnosis section of article says "...a definitive diagnosis of Alzheimer's disease must await microscopic examination of brain tissue,generally at autopsy." I'm looking at some pictures from www.alz.org/brain/overview.asp. Will a qualified doctor please look at pictures 8 and 9? They seem to show a very obvious, visibile-to-the-naked-eye deterioration of the brain. I was a bit shocked when I saw these because I had no idea that an Alzheimer's-afflicted brain looked so markedly different from a healthy brain--I thought the difference would be indiscernable to a layman. According to these pictures, the brain of a person with advanced Alzheimer's actually looks shrunken and shriveled--macroscopically. So, would the micronanalysis of brain tissue really be necessary other than to confirm the obvious? Or, are the pictures exaggerated to make it more intuitively clear to the lay-viewer. Does the Alzheimer's brain not really look this bad? Seems to me it actually shrinks to a substantial degree. Surely the tissue analysis is just to make it "official?" Thanks in advance. Colin.65.102.39.98 00:13, 27 June 2006 (UTC)

At the recent International Congress on Alzheimer's Disease in Madrid, post-mortem evidence was required to give a definitive diagnosis of Alzheimer's Disease. Several of the presentations on imaging were asked about post-mortems and that was the ONLY way to give a definitive diagnosis. Some of the imaging methods get to 90% sensitivity and 90% specificity, but they still need the post-mortem. Chris |Chrispounds

This is a Good Article
After review, I'm promoting this article to GA status, based on the qualifications. I think it is well written, and seems fairly up-to-date. However, I do have some suggestions for further improvement.


 * The article needs more references. In fact, the references section is borderline. If I had chosen to fail the article, it would have been due to references. Things like statistics and the claims of the various theories of the disease pathophysiology really need references, so people can evaluate how up-to-date and valid the information is. I'd recommend sticking with the cite.php format, which is already in use for most of the references. Remember that external links can be cited in the same way, particularly if they are stable online documents, and not just a 'general site about the topic'. For FA status, people like to see at least one reference per paragraph, typically. Keep this in mind as a goal while improving.
 * Continued expansion in the prevention and treatment sections would be nice. This is the part of the disease that is likely the most important to people, and should be very complete. It is good now, but would be a good place for more information.
 * Some images would be good. It's not as critical for articles of this type, but a few images can do a lot of good. Do any universities release medical images under a free license? If not, are there some particularly illustrative ones that we could use under a good fair-use rationale?

Thanks for your hard work everyone. Keep working on the article, and keep your standards high. If you would like any clarification on my reasons for promoting this article, please leave me a message on my talk page. Phidauex 18:50, 3 July 2006 (UTC)


 * Thanks Phidauex. Just added a couple of images from the Wikimedia commons, but we could really use some amyloid plaque and tangle images. Are any researchers/doctors have their own pathology or research images they could upload? --Ipeltan 09:01, 7 July 2006 (UTC)

Why not add the 4 articles to External links?
As of July 6, 2006, there are 4 Alzheimer's articles. Why not add these four to the "External Links" section on the main page? Not everyone reads the discussion page, there are only 4 articles, and I think they contain information a person should know about and can use; such as drinking Green tea, or taking Chinese Moss Extract better known as Huperzine A, which is sold at health food/vitamin stores.204.80.61.10 18:22, 6 July 2006 (UTC)Bennett Turk


 * About Green Tea and Moss Extract – just a pseudoscience. We are trying to post whatever is generally accepted by the scientific community, not some medical quackery. Therefore, it would make the main article look unprofessional.
 * -- Igoruha 10:49, 6 July 2006 (UTC)

The four links have strong medical backing; (1) the Alzheimer's Vaccine is listed at the online edition of "The Proceedings of the National Academy of Sciences". (2) The Chinese Moss extract is undergoing testing directed by Georgetown University. (3) The Green tea, (catechins), study is published in "The American Journal of Clinical Nutrition". (4) The Green tea, (EGCG), study is found in "The Journal of Neuroscience". Those are four reliable medical sources. In addition, according to the Wikipedia link to Huperzine A; the National Institute on Aging is conducting a Phase II clinical trial as far as it's safety and efficiency in treating Alzheimer's.24.195.241.149 00:39, 8 July 2006 (UTC)Bennett Turk

Aluminum
Aluminum is not a heavy metal, but I don't know if they're talking real heavy metals (thallium, lead, mercury) or aluminum. I've heard the aluminum theory (deoderant and soda cans) but I don't have a reference, so i'm not changing it. Edit: Oh wait, according to [heavy metals] "In medical usage, the definition is considerably looser, and "heavy metal poisoning" can include excessive amounts of iron, manganese, aluminium, or beryllium (the second-lightest metal) as well as the true heavy metals."

That's retarded.

tobycallahan | T@lk  9:49am, 23 July 2006

More about amyloid plaques
I'd like to point out that the deposition of amyloid-beta into plaques is itself is not abnormal. Most people develop some plaques in their brain tissue as they age. However, the AD brain has many more plaques in certain brain regions. |Igoruha 8:38, 24 July 2006 (UTC)

the new AAGP guidelines Medscape Summary point out that amyloid deposition is thought to accellerate AD progression. |Chrispounds

Potential treatments section policy
Given the consistent addition to the potential treatments section of compounds/therapies backed only by early-stage laboratory/animal evidence, I've tried to incorporate a way to include such material in the article while (1) making clear that these compounds are far from clinical use and (2) not using up extensive space in an Alzheimer's article on far-fetched therapies. Due to the abysmal relationship of effects on surrogate markers to effects on clinical disease course with this disease in particular, I think that these compounds should not be in the article, but the consensus seems to be against me on this.

Proposed policy: The way I propose to handle these compounds is as another list. Failure to follow the following standards should result in deltion of the listing with a reference to the talk page. Standards for inclusion:
 * A correctly-formatted and complete reference to a reputable source. Although a news report can supplement the reference to provide for a lay-language explanation of the scientific data, the primary scientific reference must be cited.
 * A wikilink should be part of the listing. If the compound/treatment is significant enough to merit a listing in an encyclopedia, it should exist in the wikipedia in some form.  If it doesn't have it's own entry, a sentence or two describing the research data should be included in some relevant target entry.  (This assumes the editors of that article find it merits inclusion.  Of course, if they don't, it probably doesn't belong in the AD article either.)

I'm aware that the PBT2 entry does not currently meet these standards, but I'll look to the editor who added it to bring it up to code. --Ipeltan 01:37, 8 August 2006 (UTC)
 * Why don't we discuss this policy before deciding on its use. I personally do not believe each treatment needs a wikilink, a link to a good source should be enough. -Ravedave
 * I would agree that having late-stage compounds be described would be the best strategy. Alzforum has a brief review 53 compounds in trials or that have been in trials.    Would we want to refer folks to that for further details on potential treatments?  Also the AAGP guidelines summarized here  discount the ginko, NSAID, and estrogen paths as viable treatments.  --Chrispounds 14:47, 8 August 2006 (UTC)
 * I agree that this would be ideal, and better for article than what will quickly become a long list of potential therapies. What about the possibility of breaking this material off into a separate article?
 * The info from the AAGP guidelines is very good and merits significant revision of the article. Because of the significant and serious consideration that treatments like ginko, NSAIDs etc previously received and still receive, I think they continue deserve mention in the article stating clearly that current best practice does not recommend a role in treatment.  Also, the section on vitamin E should be restored based on the AAGP info.  --Ipeltan 12:58, 9 August 2006 (UTC)


 * PBT2 does not meet a proposed requirments of section - "Laboratory-based therapy targets", since safety studies in healthy humans (Phase 1 A & B) indicate that PBT2 is well tolerated at doses proposed for Alzheimer’s treatment --Igoruha 6:58, 12 August 2006 (UTC)


 * Phase I studies are to determine safety, not efficacy. The fact that PBT2 has complete a phase I study (citation please) offers no evidence that it will have any effect at all on clinical Alzheimer's.  The only evidence to suggest a role in Alzheimer's remains the laboratory data.--Ipeltan 14:52, 13 August 2006 (UTC)


 * I am ready to help edit the potential treatments. I would think it makes sense to have the text be brief and proportional to the testing that has been done in clinical settings in humans (note I said "in clinical settings", and not just "in humans", otherwise we might end up with 10,000 words on THC, dudes).  If compounds get approved, they should have their own entry.  If we think these potential treatments deserve more space, then we can work toward a new entry.  What do we think about the links to the clinicaltrials.gov for the Phase 3 compounds?  The diabetes, lupus erythematosus, and hypertension entries have considerably less of the potential treatments, although the "Treatment Research" has a few sentences in the Lupus article.  "Diabetes Management" is a separate entry and "anti hypertensives" also has a separate entry (with references to a bunch of categories of treatments).  What say ye?  --Chrispounds 13:57, 18 August 2006 (UTC)

I support phase III drugs only when they are very promising (i.e. not me-too cholinesterase inhibitors). I have adhered to this policy on rivaroxaban and ximelagatran. Only in extreme cases would I support phase II trials/drugs.

For phase III studies there are usually peer-reviewed studies that are more useful (IMHO) than links to clinicaltrials.gov. In addition it would remove the suggestion that Wikipedia aids in the recruitment of study subjects. JFW | T@lk  21:44, 26 August 2006 (UTC)


 * Geriatrics & Aging had a good review article back in March on upcoming therapies. It is accessible through Medscape, and we could use as a quick summary for tramiprosate and r-flurbiprofen. This does not have a PMID, but it looks okay and seems to get at most of the different strategies out there.  I have not seen much on Xaliproden for alzheimer's beyond the Phase 3 on clinicaltrials.gov  --Chrispounds 19:21, 28 August 2006 (UTC)


 * The fruit juice study is a single observational study and is just barely enough to be mentioned. The blueberry data is not experimental in humans.  We might have a tiny mention, but the article is getting ponderous. --Chrispounds 15:42, 2 September 2006 (UTC)

I took a big hack at the potential treatments section removing the table and pointing at journal articles as references. In terms of space on the page, Potential and current treatments are closer to being in balance. I may take a crack at the Risk Reducers since they are eating up a lot of page space as well. having "blueberries" and each of the current pharmalogical therapies having the same line space is a bit crazy --Chrispounds 15:42, 2 September 2006 (UTC)


 * Since when adult stem cells stoped being considered as a potential treatment ????????
 * --Igoruha 22:32, 4 September 2006 (UTC)


 * I would like to think stem cells are a potential treatment, but I could not find a record of patients who have been treated with stem cells. Another of the great hopes in medicine--gene therapy--had a trial with 8 patients back in 2004.    I am a big proponent of using multiple Randomized controlled trial (with significant outcomes on primary endpoints) to qualify something as a treatment.  Observational studies (in the proper population) can suggest a research direction and may hint at protective effects, but one would hope to see that verified in an RCT.  The current stem cell treatments page does not list AD as a treatment area.  Gene therapy has a passing mention to AD.  If you think we should mention these treatments, I would hope we could say that they have very limited exposure in humans. --Chrispounds 14:25, 5 September 2006 (UTC)

Discuss it first
I just posted a paragraph on "First Alzheimer patch" (in Potential Ttreatments section). I anyone wants to delete or move it, please discuss it first. --Igoruha 6:47, 12 August 2006 (UTC)


 * This is not a "potential treatment" but merely a different form of administration for an already existing drug. Not only is the information in the wrong place, but there's no reason for this to deserve it's own paragraph, much less a long one. The paragraph is longer than the entire paragraph on the entire class of drugs to which Rivestigmine belongs! A sentence in the section on acetylcholinesterase inhibitors would be appropriate, but no more.--Ipeltan 14:52, 13 August 2006 (UTC)


 * Thank you for providing an explanation before taking action. In a way I agree with you. But, I posted it in "potential treatment" because by potential treatments I understand some exiting progress in new therapies for AD. Such as: advances in adult stem cell research; advances in the earliest stages of drug discovery through post-marketing studies; and also advances that include: positive results from the first Alzheimer "patch". By potential treatments I understand not only drugs with new targets or a new mechanism of action, but also new methods of delivery. For these reasons I ask not to change it. --Igoruha 19:24, 13 August 2006 (UTC)


 * I think he was trying to say that a new delivery system for a crappy drug, and indeed an entire crappy mode of thinking about drug treatment of this disease, is not that exciting. These people have brains full of dead or dying neurons. Dumping a little more of this or that neurotransmitter on them, a little nerve gas here or there by pill or by patch, is not an answer. We've spent decades now and billions for treatments that change things so little that it takes a big statistical study even to tell the difference between treatment and placebo. We've seeing changes of something like +1 in a score of 30 on the MMSE. For 6 months. By contrast, the vaccine trials that you mention below in the next section, really is a new mode of thinking, and deserves some of the space you used (and shouldn't have used) for the patch. S B Harris 00:49, 27 August 2006 (UTC)


 * Is it time to cut down some of the talk page? --Chrispounds 19:21, 28 August 2006 (UTC)

Question - ADDL
Why there is no mention about ADDLs ? Follow this link to find out more one ADDLs and their relationship to AD: http://alzheimers.about.com/od/research/a/ADDLs.htm --Igoruha 21:00, 21 August 2006 (UTC)


 * About.com is a secondary source. I'd prefer a peer-reviewed primary source on the utility of ADDLs in Alzheimer's. JFW | T@lk  08:26, 3 September 2006 (UTC)

Fruity
This paper made headlines by suggesting that fruit juice intake may reduce incidence of AD by 75%. JFW | T@lk  08:25, 3 September 2006 (UTC)

Mechanism
Would anybody be interested representing the mechanism of AD as a schematic diagram ? --Igoruha 22:38, 4 September (UTC)


 * I can help out and might have a starting point from the amyloid hypothesis perspective. I would say we will need to re-write the Disease Mechanism section to reflect the growing influence of amyloid and tau.  William Summers, the champion of tacrine, has said he favors the oxidative injury theory and that amyloid and tau might be "tombstones derived from cellular debris." (p 444)   The Geriatrics and Aging article  has a nice diagram that we could start with.  If we include some of the details of gamma and beta secretase we might have a really cool image.  --Chrispounds 14:52, 5 September 2006 (UTC)
 * has a great picture of the disease. --Chrispounds 02:51, 12 September 2006 (UTC)

Cholinesterase Inhibitors
I really like how the author shows that cholinesterase inhibitors are essentially ineffective. I added another reference from the British Medical Journal 2005 that further supports this concept. It's very important to get this point out there. The pharmaceutical companies are making billions of dollars off patients who believe that these drugs slow the progression of the disease. Not only is this false, but these drugs do next-to-nothing aside from causing diarrhea in 40% of the old folk who take them. Thanks!E4043 04:33, 15 September 2006 (UTC)

AlzheimUr CENTRE
[Copied from: User talk:Nunquam Dormio

Dear Nunquam, I have introduced a link of a weblog that deals with a Centre for treatment of Alzheimer AlzheimUr CENTREand it has been removed. Do you know the reasons?

Sincerely, jsmjsm User talk:Jsmjsm


 * The short answer is No, I don't. I looked at your edit and decided it was on balance OK. User talk:Ipeltan obviously felt otherwise. I think, as the article currently stands, a blog about the design of a centre seems a little tangential. There's probably a whole wikipedia article to be written about design for Alzheimer's, both for architecture and for implements. I remember reading somewhere that certain colours of dining plate are useful for Alzheimer's sufferers as the contrast helps them see what they're eating. So probably the thing to do is to make it clearer how the link relates to the article. These are my thoughts so far. Nunquam Dormio 15:13, 22 September 2006 (UTC)


 * It seems to me a blog about the ongoing development of a particular Alzheimer's disease "center" isn't appropriate for an encyclopedia article on Alzheimer's disease. There are hunderds if not thousands of centers, clinics etc. that provide Alzheimer's treatment that would also deserve mention. Frankly, I wasn't able to understand exactly what the purpose of the blog, although this was not my reason for removing the link, where the AlzheimeUr Centre is located, nor what its purpose is going to be.  Is it a residence facility, a research center, a treatment clinic, or a day/respite service?  As Nunquam Dormio suggested, you might wish to a separate article on design for Alzheimer's.  You could also add some material to the treatment section about lifestyle/living accomdations for patients. The social impact section of the main article is extremely weak; you might be able to make a contribution to this section as well.  It also seems you have access to some great Alzheimer's histology images.  These would be a major addition to the article if you'd be willing to add them. --Ipeltan 23:19, 22 September 2006 (UTC)


 * "Our weblog emerges from the wish to offer an insight into the process of creating ideas for the AlzheimUr Centre. This centre is the reference for the region of Murcia (Spain) to provide a comprehensive attention to the illness of dementia. This weblog is an added tool to the project. Besides proofing the elaboration of different criteria that guide the development of the work, it tries to encourage interactivity with a system of commentaries. This is done in order to enrich the project with significant suggestions. Interdisciplinary collaboration is believed to be an essential part of the architect’s work. Working sessions every day are based on different programmes to develop specific contents and objectives. At the beginning of the first ten days the approach will be very intuitive. Then it will formulate the brief which, without being completely defined, suggests aims and important interests which the project will be based on." Quoted from the first post of the weblog.

I hope this answers your questions on purpose of the blog, location of the centre, etc. Definitely, the design for an Alzheimer Centre is something much more complex than deciding the colours of the dining plates. It requires the strong collaboration of architects, doctors, patients and families. There is not much information on it and this weblog is recollecting facts on this theme. It is a pity to remove information of Wikipedia under such misunderstandings, so I would appreciate if you reconsider your action or somebody more qualified gives an opinion. Sincerely, jsmjsm User talk:Jsmjsm

I've started a Design for Alzheimer's section. Add to it as you will. Nunquam Dormio 11:05, 24 September 2006 (UTC)

Determining AD
I think we should add a section on the techniques (tests) used to determine the severity of AD's symtoms. Here is a list of a few that I found, if anybody can find them available online please provide a link: - Mini-Mental State Examination (MMSE) - Disability Assesement in Dememntia (DAD) - ADAS-Cog - Caregiver Stress scale (CSS) - Clinician's Global Impression of Change (CGI-C)

Igoruha 13:45, 22 September 2006 (UTC)


 * Given the length of the article, we could mention the more common tests (MMSE, perhaps Clock drawing and ADAS-Cog) and then create a page of neuropsychiatric tests. Some of these tests are Alzheimer's specific, but other tests are general neurological tests. Others I have heard of include the ADCS-Activities of Daily Living, Clinical Dementia Rating (CDR-Sum of Boxes), Neuropsychiatric Inventory Questionnaire (NPI), Brief Cognitive Rating Scale, Global Deterioriation Scale, and Clock Drawing. Some of these have been used in clinical settings to measure functional, cognitive or global changes.  A Medscape article looks at some of the tests in a diagnostic battery. --Chrispounds 22:42, 22 September 2006 (UTC)

Section order
First, I want to compliment User:Chrispounds. He's taken on some really tedious jobs and done a great job. His work is taking this article to a new level.

Second, a comment on the recent peer-review based edit. Although the normal layout places external links below references, I've asked for a discussion of this at WP:MEDMOS. Given the length of medical article ref sections and the relatively greater general utility of external links to references in these articles -- a situation that is different than a concisely referenced article on most topics -- it seems appropriate to use a different section order. I feel like the external links section belongs above references because it adds significantly to this article, wheras the references section has no stand-alone value.

Kraepelin
I found a newer source that gives some credit to Kraepelin, however the first cases in his own textbook are credited to Alois Alzheimer. This seems to be fairly convincing that he credited Alzheimer with the disease.--Chrispounds 01:36, 3 October 2006 (UTC)
 * and now I have cited the reference. It was a busy morning when I added the text. --Chrispounds 23:07, 28 October 2006 (UTC)

THC
As entertaining as the THC studyat scripps might be, it does provide the level of clinical evidence and years of testing in humans that the Potential Treatments for Alzheimer's requires. I will keep zapping it out if it comes back. —The preceding --Chrispounds 21:39, 10 October 2006 (UTC)


 * This information is based on a valid scientific study that has been referred in respected news networks (CNN, Reuters). It has nothing to do with being entertaining but with being a potential treatment for the disease. Who are you to decide about this case? Is it a common Wikipedia policy to censor facts if some people don't like them? I will put the information back on the article because there is no valid reason for it to not be there. Jnx 21:03, 10 October 2006 (UTC)


 * The length of this article (which has been discussed) is getting to the point where we have to decide what stays and what goes. Reading back at the discussion to the Potential treatments section about 6 weeks ago, we had discussed that a randomized control trial would be necessary for a something to make it into the potential treatments on this page.  It may be time to do a split to create a page with potential treatments (things that that can show activity in a lab, animal model, human testing) and then summarize the relevant ones (lots of human testing, close to being approved) on this page.  Many potential treatments are just not going to be approved by regulatory bodies and the things that have not been tested in at least Healthy Patients in clinical trials are at least 5 years from the market.  Personally, I did work with a cannabinoid to treat agigation in Alzheimer's in 1999, but it is 7 years later and the product is not much closer to being approved.  --Chrispounds 21:39, 10 October 2006 (UTC)


 * The length of this article is not a valid reason to censor this information. Could the fact that it is the controversial THC that was considered possibly superior to expensive commercially available drugs have anything to do with the fact that this information somehow disappears from the page? It certainly shouldn't have an effect on it whatsoever. I find it strange you joke about this subject being entertaining since everyone knows how expensive and difficult Alzheimer's disease is to treat. Jnx 21:55, 10 October 2006 (UTC)
 * I belive it should be left in. The article is not long enough that one paragraph is going to topple it. Wikipedia should be a complete resource. -Ravedave (help name my baby) 22:09, 10 October 2006 (UTC)


 * Look at the reference list. Only a handful are NOT from scientific articles (with PMID links).  Just this week in Neurology there was a paper on mediteranean diet that has not yet been included, but that has been in a peer-reviewed journal.  The THC hypothesis for "treating" Alzheimer's has not even been verified in the literature.  Yes, AD is costly (one of the non-scientific sources has good data on that), but I would hope that we could focus people on what is likely or probably effect and not on unproven therapies.  Notice the comment on Vitamin E and its risks.  We mention Gingko and the huge trial it has running.  I think the Potential therapies page is the way to go with this and I will leave THC here until I can move it to where it can be seen with information of the same quality.  Of course, given the status of the "war on drugs," some therapies may not have their day in a clinical trial.  AVE 1625 is a cannabinoid from sanofi-aventis and is currently in phase 1 for Alzheimer's.  When that gets to late Phase 2, we should be glad to add it to this page.  --Chrispounds 22:17, 10 October 2006 (UTC)


 * It is not the length of the article per se that means the THC information does not belong in this article but rather the poor relation of the data to actual treatment. (See potential treatments above for a discussion on this very topic that reached consensus among article editors.) The data on THC is based purely on biochemical data and does not include animal studies much less human trials.  Despite the statements in the press release linked as the reference, the relevance of this study to potential treatments is therefore extremely uncertain.


 * The standards for compounds like PBT2, green tea, and blueberry extract apply equally to THC. The data relating these compounds to reductions in Alzheimer's symptoms are extremely poor but are, nevertheless far better than for THC.  Editors of this article reached a consensus that the literature on compounds and others like them was insufficient to support a treatment role in Alzheimer's for inclusion. Ravedave and Jnx, if you wish to re-address the topic of standards for potential treatment inclusion in the main article, please do so.  But until a new consensus is reached about the prequisites for including a potential treatment in the main article, I am deleting the THC paragraph.  A new article on potential treatments would be an appropriate place for THC and every other of the hundreds of compounds that can alter the behavior of amyloid-beta.--Ipeltan 03:22, 11 October 2006 (UTC)
 * Is green tea also a considerably superior inhibitor of amyloid plaque aggregation to several currently approved drugs for treating the disease as the study for THC claims? If not I think this fact alone makes THC a different case and certainly a potential treatment. I do realize that this article is of a very high quality as far as Wikipedia articles go and I understand the points you made but I certainly hope research for THC continues. As far as I can see, according to this study it could provide a lot cheaper and possibly even better treatment for AD than drugs currently commercially available. Jnx 20:43, 11 October 2006 (UTC)
 * The current therapies do not target amyloid, so it does not take much to beat them. Two Phase 3  compounds have effects against amyloid in animal models and have shown to change CSF levels in humans.  THC could be "possibly even better", but it would need to make it through at least 6 years of clinical testing and be successful to be marketed. In the recent AAGP paper, THC was not even mentioned--and they did mention many different "potential treatments." --Chrispounds 14:06, 12 October 2006 (UTC)


 * Then what does it mean that "formation of amyloid plaque is the primary pathological marker for Alzheimer's disease." I have a strong feeling it means that the formation of amyloid plaque has a lot to do with the symptoms of Alzheimer's, especially since in the article you can read that "majority of researchers support the alternative hypothesis that amyloid is the primary causative agent." We are talking about potential treatments here and this finding certainly makes THC a potential treatment. Wikipedia is supposed to be a complete resource, not an abstract of AAGP paper.


 * Read this (straight from the press release): '''"The cholinergic system - the nerve cell system in the brain that uses acetylcholine (Ach) as a neurotransmitter - is the most dramatic of the neurotransmitter systems affected by Alzheimer's disease. Levels of acetylcholine, which was first identified in 1914, are abnormally low in the brains of Alzheimer's patients. Currently, there are four FDA-approved drugs that treat the symptoms of Alzheimer's disease by inhibiting the active site of acetylcholinesterase, the enzyme responsible for the degradation of acetylcholine.


 * When we investigated the power of THC to inhibit the aggregation of beta-amyloid," Janda said, "we found that THC was a very effective inhibitor of acetylcholinesterase. In addition to propidium, we also found that THC was considerably more effective than two of the approved drugs for Alzheimer's disease treatment, donepezil (Aricept ®) and tacrine (Cognex ®), which reduced amyloid aggregation by only 22 percent and 7 percent, respectively, at twice the concentration used in our studies.


 * Also, the only drugs listed by name in the Wikipedia article are the ones that affect the levels of acetylcholine. Still you say that current therapies do not target the amyloid? Why do you say that?


 * If this doesn't convince you that THC is a potential treatment worth mentioning I'd like to hear what the administrators have to say about this subject. --Jnx 14:42, 12 October 2006 (UTC)


 * AGREE - Because THC has been reported as a potential treatment, we should provide the reader with the information. It is UP TO THEM to decide wether or not they believe it.  We should present the neutral view, and allow our readers to decide. --by97aa 13:00, 13 October 2006 (UTC)


 * There seems to be a fundamental misunderstanding here about the evidence that makes something a potential treatment for a disease. Jnx, your comments indicate misunderstandings about the pathogenesis of AD. Specifically, amyloid aggregation does not represent a good surrogate marker for disease state.  There also seems to be a fundamental misunderstanding about what constitutes a reference for this article. By97aa, I disagree with you strongly.  In a scientific or medical encyclopedia article, it is up to the authors to decide whether the claims advanced in a research article are valid before including them.  Jnx, Wikipedia is an encyclopedia, not a "complete resource."  This means that information is included selectively based on its importance and validity. Since this issue seems important to maintaining a quality article I'll address these questions at length, starting with the latter.


 * News articles covering research may be adjunctive; press releases should never be used as a source. Here's why: setting aside the fact that a reporter's knowledge of Alzheimer's may be limited to his/her few hours writing the article, the news media interest in research is calibrated only in part by the importance, reliability, and quality of a study. Another major factor for a reporter is interest for the general public. Therefore, claims that a controlled substance may be a treatment for Alzheimer's may be newsworthy without being an important or valid study.


 * Press releases' intention is to increase awareness of the article and therefore to increase the prestige of the researcher and sponsoring institution. While a press release may promote an important, valid, and/or clinically relevant study, a study is not automatically important, valid, or clinicially relevant because a press release is issued.  It's more obvious with a "classic" press release: are the statements here true simply because they are in a press release?  Of course not. Are they false because they are in a press release?  No.  The risk with a scientific press release is to not recognize that scientific press release have the same underlying goal as political press releases and therefore require a similarly high index of suspicion when judging truth claims made therein.  To make this judgment, we need to consider the primary data, the study itself.


 * The simple fact that research has been published does not make its data valid or its conclusions true. Note first that this article appears in a new, practically unknown, and very low impact journal. We next note that the data derives from pure biochemical studies. That is to say the data does not derive from studying cells, animals, or humans, but proteins in solution and computer models of protein behavior.  Even if the mechanism of Alzheimer's pathogenesis were precisely known, such data would have extremely low relevance to treatment, defined as whether a compound alters disease course or symptoms.  But the pathogenesis of Alzheimer's is not understood.  While amyloid beta is almost certainly involved, how and why remains unclear despite 20+ years of research.  When or even whether Abeta aggregation is pathogenic is less clear; whether AChE-mediated Abeta aggregation is important is essentially unknown.  Furthermore, the mechanism of AChE inhibitors is not well understood either but is not generally understood to have to do with Abeta aggregation.  To summarize this study, purely biochemical tests revealed that THC interferes with a process not generally understood to be involved in the pathogenesis or symptomotology of Alzheiemer's.


 * For all these reasons, this study does not provide nearly strong enough evidence for listing THC as a potential treatment. To be fair, a much stronger study was published in the high-impact Journal of Neuroscience in 2005 that indicated a cannabinoid receptor agonist could alter pathologic changes and symptoms in a rat model of Alzheimer's.  But this article still doesn't support THC's inclusion because it still doesn't meet the standards previously established by consensus that require data showing efficacy in human patients. We decided on this requirement because biochemical (amyloid beta levels and aggregation) and pathological (amyloid plaque count) surrogate markers have such a poor correlation with Alzheimer's disease risk, severity/symptoms, and progression. Similarly, even the best Alzheimer's animal models are so dramatically different from the real human disease that even dramatic effects in these animals have very dubious relevance to actual treatment.


 * Sorry for the long post, but I feel this debate has highlighted a number of problems that threaten the authoritativeness of this article. I've reverted the article one last time, and am invoking WP:3RR on myself.--Ipeltan 04:53 05:04, 14 October 2006 (UTC)


 * Actually, I think it's better to await a response that addresses the issues I've raised in these posts.--Ipeltan 05:14, 14 October 2006 (UTC)


 * There is no reason to not have THC mentioned as a potential treatment for the disease. Wikipedia is supposed to be a complete, neutral encyclopedia, not just a collection of what you want to have included in the article. Many of the points you try to make are really weak in my opinion. CNN and Reuters both thought this study was worth telling about (http://today.reuters.com/news/articlenews.aspx?type=healthNews&storyID=2006-10-10T223447Z_01_N10385225_RTRUKOC_0_US-MARIJUANA.xml&WTmodLoc=HealthNewsHome_C2_healthNews-7, http://www.cnn.com/2006/HEALTH/10/05/pot.alzheimers.reut/index.html). One thing is for sure, you really don't seem to want THC to be included.


 * As I said in my previous post, I'd really like to hear what the administrators have to say about this subject. --Jnx 09:32, 14 October 2006 (UTC)


 * In order to defend inclusion of THC, you would need to respond substantively to my points explaining why they're weak. I've already addressed why Reuters is not a good arbiter of research validity.  (Note that the CNN article is actually just the Reuters article posted to CNN, by the way.)  This isn't at all about THC per se, but rather what evidence constitutes a basis for calling something a potential treatment.  I've asked User:Jfdwolff to weigh in.--Ipeltan 15:53, 14 October 2006 (UTC)


 * I have already made my points. Refer to my earlier postings on this thread; You haven't explained why they're weak either. You earlier said that THC is the same as green tea as far as treatments for Alzheimer go, which simply isn't true. Chrispounds straight-out lied about the current treatments. You say that some press release involving a POLITICAL CAMPAIGN has something to do with a scientific press release about a study - what kind of argument is that? Scripps Research Institute is one of the biggest research institutes in the world, by the way.


 * You are trying to hide this fact from the public, why, I don't know. In my opinion what you are trying to do is against all the fundamental policies of Wikipedia. And who is JFW? I am asking an administrator to take a stance. I am interested to know what kind of encyclopedia Wikipedia really is. --Jnx 16:16, 14 October 2006 (UTC)


 * The basis for me to make claims about currently marketed compounds comes from the FDA approved label. Amyloid is not mentioned in any of them, and their understood mechanism is cholinergic not amyloid.  The Scripps article about cannabinoids (which have been looked at in other places too ) does not present any findings about clinical effects in humans. Even if you had sourced the item the right way (refering to the scientific journal article) or with multiple references, several of us who work on this page do not see that evidence as equivalent to the other information that is listed.  I think it is 100% about the science and 0% about the politics.  We did the same thing to blueberries a few weeks ago.  --Chrispounds 22:27, 14 October 2006 (UTC)


 * Include THC in this article as a potential treatment.82.181.41.37 02:22, 15 October 2006 (UTC)


 * Researchers at the Scripps Research Institute in California found that marijuana's active ingredient, delta-9-tetrahydrocannabinol, or THC, can prevent an enzyme called acetylcholinesterase from accelerating the formation of "Alzheimer plaques" in the brain more effectively than commercially marketed drugs. (From the corrected Reuters article). Chrispounds, you are a liar. Why should we believe anything you say? --Jnx 10:36, 15 October 2006 (UTC)


 * Jnx, please be civil. JFW is the administrator you requested and one of the leaders of the medicine Wikiproject.  Chrispounds is precisely correct. Even if THC is the best inhibitor of AChE-induced Abeta aggregation the world has ever seen, AChE-induced Abeta aggregation isn't generally understood to play any role in the progression of Alzheimer's disease.  Similarly, to suggest that THC was better than current pharmaceuticals for Alzheimer's was disingenuous on the part of the researchers (and the reporter who paraphrased the press release).  The understanding of why commercially marketed drugs work (see the treatment section of this FDA article) is increased acetylcholine levels, not interference with Abeta aggregation. Essentially, this study showed that THC better inhibits a process that drugs like rivastigmine are not even targeting.--Ipeltan 14:54, 15 October 2006 (UTC)


 * In my opinion I have been civil, more civil than you and Chrispounds. The JFW link you previously provided took me to "Just Fuckin Works" Wikipedia article. Furthermore, I'd also like an opinion from someone who has no ties to FDA or the medicine/drug industry because I think their view on this might be biased.


 * Rivastigmine wasn't one of the approved drugs the THC study evaluated, still Chrispounds said that "The current therapies do not target amyloid, so it does not take much to beat them." In my opinion that is straight-out lying, since there are several approved drugs that precisely target amyloid and those were evaluated in the study. --Jnx 15:44, 15 October 2006 (UTC)


 * As far as I can see after reading the article, rivastigmine is an AChE-inhibitor. In the press release of the study we can read that "THC was a very effective inhibitor of acetylcholinesterase". What is the difference between these two AChE-inhibitors if THC better inhibits a process rivastigmine doesn't even target according to you? --Jnx 16:20, 15 October 2006 (UTC)

Any treatment that is not (1) in phase III trials, or (2) being regarded by the research community as a very promising lead should not be in this article. This is a general purpose encyclopedia; cholinesterase inhibition is miles ahead of THC. I'm also suspicious that anything involving cannabinoids will make it into Wikipedia out of its sheer urban legend index. JFW | T@lk  19:24, 15 October 2006 (UTC)


 * We are talking about a disease that has no cure. We are talking about a disease that is very expensive to treat and most commercially available drugs have severe side effects and are not very effective. We are talking about a disease that kills more than 65000 people every year, and many can't afford the treatment.


 * Are you really telling me this lead is not promising or did I understand something wrong? At least Reuters reported that "The researchers said their discovery could lead to more effective drug treatment for Alzheimer's, the leading cause of dementia among the elderly." THC was found to be more effective AChE-inhibitor than commercially available drugs, does that not make this finding a very promising lead in your opinion?


 * Are you really telling me this scientifically proven fact is not worth telling people about? --Jnx 20:38, 15 October 2006 (UTC)


 * That the study could lead to a "more effective drug treatment" is not a fact but a contention and unlikely based on current knowledge and the study's own data. THC was actually NOT shown to be a more effective AChE inhibitor than existing drugs: it was only compared to approved drugs for AChE-mediated amyloid aggregation (which I've already pointed out is NOT how those drugs improve disease symptoms). Here's what the authors actually said about THC's ability to inhibit AChE in the report: "Steady-state kinetic analysis of THC inhibition revealed that THC competitively inhibits AChE (Ki = 10.2 M) (Figure 3A). This level of inhibition is relatively modest..."


 * And yes, that this study does not belong in this article is the consensus of the editors and a Wikiproject medicine administrator. You're welcome to tell people about it in other forums. The paragraph has been removed. Although I respect that you disagree with this consensus, please abide by it. Thank you for raising this issue and pursuing it until a clearer consensus was reached on when a potential treatment belongs in this article.--Ipeltan 01:58, 16 October 2006 (UTC)


 * This is what the study actually says: We have demonstrated that THC competitively inhibits AChE and, furthermore, binds to the AChE PAS and diminishes A aggregation. In contrast to previous studies aimed at utilizing cannabinoids in Alzheimer's disease therapy,8-10 our results provide a mechanism whereby the THC molecule can directly impact Alzheimer's disease pathology. We note that while THC provides an interesting Alzheimer's disease drug lead, it is a psychoactive compound with strong affinity for endogenous cannabinoid receptors. It is noteworthy that THC is a considerably more effective inhibitor of AChE-induced A deposition than the approved drugs for Alzheimer's disease treatment, donepezil and tacrine, which reduced A aggregation by only 22% and 7%, respectively, at twice the concentration used in our studies.7 Therefore, AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer's disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing A aggregation, thereby simultaneously treating both the symptoms and progression of Alzheimer's disease. The administrator still has not replied to my questions. I will add the information back into the article. There is no valid reason to not include THC as a potential treatment. --Jnx 08:47, 16 October 2006 (UTC)


 * You asked for an administrative review, and JFW, a Dutch physician who is also an administrator for the English Wikipedia said that THC does not belong. You seem to have ignored the process that you requested.  --Chrispounds 12:25, 16 October 2006 (UTC)


 * I also asked for non-biased opinion, and furthermore, I asked JFW questions to which he hasn't replied yet. I have asked Jimbo Wales to give an opinion on this subject. --Jnx 12:29, 16 October 2006 (UTC)


 * The request was removed from Jimbo's talk page, as the headers clearly state that isn't the place for disputes. He listed this on AN:I, as well, and continued to claim that no one neutral has gotten involved yet when his request was rejected there. --InShaneee 15:03, 16 October 2006 (UTC)


 * You can remove the THC study from the article as far as I'm concerned. I thought my claims had something to back them up but apparently they didn't. Sorry for the interference. --Jnx 15:10, 16 October 2006 (UTC)


 * can someone summarize? how did Jnx arrive at this new conclusion????68.192.13.46 22:18, 16 October 2006 (UTC)


 * InShaneee told him to shut up at . Nice administrating, InShaneeeeeeeee. 195.148.156.16 06:01, 17 October 2006 (UTC)


 * Just so you know a link to the full text of the article is available in the citation in the last paragraph of this article: Health_issues_and_the_effects_of_cannabis.


 * Feel free to the article text, it is short and to the point. I wrote it after reading the study. HighInBC 16:04, 16 October 2006 (UTC)


 * Oh, and my 2 cents is that it deserves a short mention with citation links. It is a widely accepted study that states within it that it is a potential treatment. HighInBC 16:08, 16 October 2006 (UTC)


 * I have tried a different wording than before. It is well sourced. If you object, please explain why. HighInBC 05:07, 17 October 2006 (UTC)


 * That's a well-written paragraph. However, numerous editors of this article and a Wikimedicine administrator have explained in detail in the above discussion why this study and all other biochemically-demonstrated "potential treatments" do not belong in this article.  I'll take one more shot at it.  I wasted some time trying to explain what makes a quality study and the difference between published data and proven facts.  These points were irrelevant.


 * Here's what's relevant: it is the consensus policy in this article -- established during this discussion and also during a separate, previous discussion -- that the definition of "potential treatment" used by this article requires: 1) advanced research trials in human subjects supporting clinical use; 2) wide use in clinical or popular practice for treating Alzheimer's; or 3) the general acceptance in the fields of neurology and Alzheimer's research that a particular modality is a major hope for successful treatment. Familiarity with the field is helpful but not necessary to assert category three; you might, for instance, cite a review article published in a major medical journal.


 * Just like blueberries, green tea, and several hundred other compounds that have been shown in biochemical studies to interfere with one of Alzheimer's postulated mechanism of pathogenesis, THC does not come close to meeting the requirements for inclusion that have been set forth. This is as clear as I can be on these issues. If you start and flesh out an article on "Mechanistic approaches to Alzheimer's treatment," I will add a link to it from the main article.--Ipeltan 05:41, 18 October 2006 (UTC)


 * I submit to your superior persistence, while I think this reference is relevant I am not going to spend a disproportionate amount of time insisting upon it. If another editor feels as I do about this reference I encourage that editor to revert the addition, otherwise I step down from the arguement. HighInBC 06:13, 18 October 2006 (UTC)

This potential treatment should be included because Wikipedia rules state that a neutral point of view must be presented to the reader. "All Wikipedia articles must be written from a neutral point of view (NPOV), representing fairly and without bias all significant views that have been published by a reliable source." It should be up to the reader of the page to decide wether or not they believe that TCH is an effective potential treatment. by97aa 15:04, 18 Octover 2006 (UTC)


 * Well if you see it removed again, put it back. The claim that consensus is to remove does not seem accurate. HighInBC 22:06, 18 October 2006 (UTC)


 * Editors who have been posting on this page for months and who have added significant content throughout the page have unanimously said that it should be removed. A Wikimedicine administrator has said it should be removed.  We had an established standard which has not been refuted and previous deletions based on the standard have not been addressed.  The "post THC" side has only used the persistence in reposting and seem to ignore when well-published researchers have said that it is not a treatment.  --Chrispounds 00:11, 19 October 2006 (UTC)


 * I would like to support Chrispounds in his comment above, and respectfully ask not to disregard the consensus that long time editors came to. I do acknowledge that the THC post belongs to a group of potential (or possible) treatments for the Alzheimer's, and I support the enthusiasm of those of you who want to see it in the main article. But please understand "Potential Treatments" section was not meant for "THC" and like posts (since we did not intend to have postings of every study that comes out, no matter how "potential" it can be), Chrispuonds, with support of other editors, changed the title to "Treatments in clinical development," to avoid the growing confusion. I'd like to remind that Wikipedia is an encyclopedia not a research forum; if anyone interested is really interested in THC discussion I invite you to the www.alzforum.org. Igoruha 20:46, 18 October, 2006 (UTC)


 * While editors in the past have come to a consensus that can be applied to this situation, it seems clear that the current consensus is not to exclude this statement. Consensus can change, and you have reverted it's removal from 3 editors putting it in now. HighInBC 01:09, 19 October 2006 (UTC)


 * Do you even know how many potential treatments there are for the AD ? Do you want start posting any treatment that appears in the sceintific literature ? There are literally hunderds of the promising treatments for the AD. Tell me what do you want to do, either we keep "Potential Treatments" and then it would take atleast another 5 pages just to list all of them, or we change title to "Treatments in clinical development" and keep only those that are in the clinical phase trials right now. We simply can not list potential treatments because it would take too much space.

Igoruha 22:32, 18 October, 2006 (UTC)


 * I disagree that 3 editors have put it in. Three people who think THC belongs in the AD article have put it in, but their credibility with respect to Alzheimer's has not been demonstrated. Also consider that we are not censoring the information about Alzheimer's and THC--since the editors here have left it to the editors of the THC page to include it on that page without removing it. The standards we (the AD editors) have established on this page are not being respected and at least two administrators have agreed with us.  You have tried to argue with NPOV, but this has been established to be very weak because you have failed to argue for other potential treatments over THC.  Also, the editors understanding of the disease is poor when they did not understand that the current therapies do not target amyloid, and thus the paper they support demonstrates weakness in its scholarship. I would ask you to carefully these points and to remove the THC content from this page. --Chrispounds 02:54, 19 October 2006 (UTC)


 * Wow. I just stumbled across this on AN/I and this is inane. The cited study on THC is not at the level of proposing a meaningfully potential treatment; it's a couple of experiments and a docking pose. None of those who propose to mention this study - excluding the literally hundreds of similar studies on less, erm, popular molecules - have demonstrated significant familiarity with the Alzheimer's literature or with the drug discovery process. Contrary to claims of POV exclusion of the THC data, it is in fact giving undue weight to a very minor and preliminary study to leave it in, so I've removed it once. Consensus is clear among those who are familiar with the subject. (I only wish the data on aggregation inhibition by psilocin had ever been published...) Opabinia regalis 03:42, 19 October 2006 (UTC)


 * Ok. HighInBC 03:57, 19 October 2006 (UTC)


 * I think we are going to a dangerous direction when we let people decide which scientific studies are good and which are not. I also wonder will THC ever get proper attention from the research community if people in scientific circles consider THC "entertaining" or "erm, popular".. While I am not going to add THC again, it does strike me as a surprise that there are hundreds of compounds that have been found to be considerably superior to drugs currently on the market. 195.148.156.16 08:14, 19 October 2006 (UTC)


 * I have been told by those opposed to the addition that it is not bias against illegal drugs. I can only take their word for it. However the bias(intentional or not) of the scientific community to experiment on these drugs is evident, mostly through the prohibition from governments to do human tests.


 * In some cases Wikipeida is capable of being more nuetral than society as a whole, other times it is limited to the level of societies neutrality(due to the requirement of verifiability). This is not a bad thing, an encyclopedia should reflect societies current beleifs, regardless of the accuracy.


 * I don't agree with the removal, but I do not think any editors are introductin their own bias here. HighInBC 13:51, 19 October 2006 (UTC)

More than 200 people in the U.S. alone die tomorrow because of this disease. How many will die tomorrow? --Jnx 23:23, 21 October 2006 (UTC)

Reference section formatting
Some articles with long lists of references use the syntax to make two columns. Thought you might want to try it out. - User:Samsara (talk • contribs) 15:23, 11 October 2006 (UTC)
 * I was thinking the same thing, implemented. -Ravedave (help name my baby) 15:38, 11 October 2006 (UTC)
 * Very nice. Makes the External links that much closer to the text. --Chrispounds 17:04, 11 October 2006 (UTC)

Let's shorten the discussion page
I think it would be a good idea to maybe summarize and/or reiterate the conclusions that we came to for editing the main page, and also keep some ideas/suggestions for the future development of the main article. Or maybe have some sort of FAQ and answers & ideas for the future improvment/projects. Is anyone else thinks it'd be a good idea ? -Igoruha 16:56, 13 October 2006 (UTC)


 * I did an archive pass that moved a lot of the threads from 2004 out of here. We can move more threads over to it. It would seem that the editors here have a lot to say.  --Chrispounds 03:42, 12 October 2006 (UTC)


 * is it time to wipe the slate clean and start afresh? --Chrispounds 23:08, 28 October 2006 (UTC)


 * I would not mind. I see no point of keeping past discussions, which probably nobody reads anyway. Igoruha 19:23, 28 October 2006(UTC)