Talk:Biology of depression/Archive 1

Untitled
One para was removed from the 4 or so on monoamine theories so I copied the old longer version to here for later use. Cheers, Casliber (talk · contribs) 20:42, 28 September 2008 (UTC)

Guild of Copy Editors Revisions
I am copy editing this article, which has included rearranging and organizing a large amount of material, as part of the Guild of Copy editors project (http://en.wikipedia.org/w/index.php?title=Category:All_articles_needing_copy_edit&pagefrom=Bannu#mw-pages) Thank you for your indulgence of these much needed changes. --BenJonson (talk) 13:05, 5 April 2013 (UTC)
 * Excellent. If you have any content-related questions, please ask -- I'm moderately knowledgeable about this topic and might be able to help out. Looie496 (talk) 15:51, 5 April 2013 (UTC)

Large Scale Brain Network Theory
Njbetz (talk) 14:59, 23 April 2013 (UTC)

Twin studies
Why doesn't the genetics section say anything about twin studies? Wouldn't that help establish if genetics is a big factor in depression? Sonicsuns (talk) 00:57, 13 June 2013 (UTC)
 * This article is sketchy in lots of ways. Twin studies would definitely be a legitimate thing to cover --  is a useful source, though there might be more recent ones. Looie496 (talk) 01:21, 13 June 2013 (UTC)

Neuroreceptor imaging
The study concluded about D1 receptors that

"PET assessments of D1 receptor binding have emphasized the stri- atum due to the relatively low specific-to-nonspecific binding in extra-striatal tissues. The extant PET data are suggestive of a decrease in D1 receptor availability in the striatum. Postmortem studies, in contrast, have focused on extrastriatal regions. The percentage of D1-expressing neurons together with D1 mRNA expression was reported to be increased by 25% in the CA3 region of the hippocampus (Pantazopoulos et al., 2004) in BD subjects versus controls, but to not differ from controls in the amygdala of MDD subjects (Xiang et al., 2008). The hypothesis that the D1 receptor function is decreased in the striatum of depressed patients receives some support from a rat model of anhedonia. Anhedonic rats show a decreased dopaminergic response in the nucleus accumbens (NAc) to palatable food concurrent with decreased sensitivity of the D1 receptor (Scheggi et al., 2011). Fur- ther, in rhesus monkeys, electroconvulsive therapy (ECT) resulted in in- creased dopaminergic neurotransmission in the striatum together with transient increases in D1 receptor binding (Landau et al., 2011)."

Should this not be mentioned in the Biology of Depression Article? Petergstrom (talk) 07:16, 18 November 2016 (UTC)
 * Thanks for talking here. I read the paper - (won't be able to use that magic link much longer). .  First, it is focused on one way of looking at receptors, and that is PET, and they make clear the limitations of that approach and how provisional all the results to date are.  (as in this bit you have copied - the author says that PET is blind outside the striatum....      And if you are not aware, all our animal models for depression completely suck.  People say we have cured rats of cancer thousands of times; we have cured rats of depression millions of times.  I am ranting though.  What do you propose to do with this paper?  Do you want summarize each receptor?    I guess we could say something like, "As of 2013, using the PET imaging technology and reagents available at that time, it appeared that the D1 receptor may be underexpressed in the striatum of people with MDD."  is that what you are looking for? Jytdog (talk) 09:04, 18 November 2016 (UTC)

Yes that actually looks pretty good. Petergstrom (talk) 16:04, 18 November 2016 (UTC)
 * This was not acceptable.  If  - and if it is a big if - we are going to get into detail, we cannot omit the specifics of the detection technology and its limitations.  People don't understand how limited our tools are for doing neuroscience and we cannot have content that imagines we have perfect technology to assess things in living human brains.  We don't.  Jytdog (talk) 01:15, 19 November 2016 (UTC)

How about this "===Receptor binding===

As of 2012, efforts to determine differences in neurotransmitter receptor expression or for function in the brains of people with MDD using Positron emission tomography had shown inconsistent results. Using the PET imaging technology and reagents available, it appears that the D1 receptor may be underexpressed in the striatum of people with MDD. "

-- 2601:646:8100:3F68:C91A:53E0:E950:684A (talk) 04:10, 19 November 2016 (UTC)
 * That is better but the ref published in 2013, and why so much WP:WEIGHT on one receptor? Please do answer.  thx Jytdog (talk) 04:22, 19 November 2016 (UTC)

frontal gyrus
Other bit of content:

Another meta-analysis yielded similar results, finding that during resting states the middle frontal gyrus and superior frontal gyrus were hypoactive. The hypoactivity was reversed with SSRI treatment.

OK, so we again have a mangled ref. it is also from 2008; not from 2016.

This is from about the same date as the Hamilton ref, but it is much more ambivalent about the amygdala stuff, noting that some of the studies showed no increased activation in the amygdala in emotional tasks (no left/right distinction). We need to summarize what the literature says - the whole of it (or at least a chunk of it), not just pick paper X for A and paper Y for Z.  About the content.. this paper is proposing complicated network effects under different states. it also wonderfully clear about the limitations. They wrote "However, currently our understanding of the complexity of interregional physiology may be insufficient to allow us to fully explain why some regions may show both increases and decreases in activation, for example in the right middle frontal gyrus in the studies conducted at rest" Where is that in the content? Jytdog (talk) 06:25, 5 December 2016 (UTC)

amygdala
One source source states: : "whereas the aggregate effect size calculated from studies that included only medicated individuals indicated that amygdala volume was significantly increased in depressed relative to healthy persons, studies with only unmedicated depressed individuals showed a reliable decrease in amygdala volume in depression."

That was roughly what I wrote

Another states"More specifically, dorsal prefrontal regions are commonly described as under-active with increases in activity of subgenual cingulate and subcortical regions."

I wrote that the prefrontal regions were hypoactive

Another source said "Our emotion meta-analysis showed clusters of altered and increased activation in left thalamus/parahippocampus and left amydgala/globus pallidus, while right anterior cingulate/putamen, right amygdala showed a relative decreased activation."

This is pretty much what I wrote

Petergstrom (talk) 04:40, 5 December 2016 (UTC)


 * Content was added as follows:


 * The amygdala is smaller than controls in unmedicated depressed persons, and similar size in medicated depressed persons. One meta analysis found that although the left amygdala was hyperactive, the left amygdala was hypoactive during emotional processing tasks.


 * First of all the refs are mangled. Look at the dates.  I explained to you how to use the autofill function with the PMID; if you would do that these kinds of errors would not happen.


 * Secondly the first ref, which is actually from 2008 (not 2016) paints a more nuanced picture than what you present - much more tentative. It talks about tendencies and suggestions, not flat black and white facts as this content says. But really it is from 2008, and there two recent reviews,  and  that cite this paper.


 * The second ref is indeed from 2015; . We need to deal with fMRI-based work carefully because of this. In any case the content here "One meta analysis found that although the left amygdala was hyperactive, the left amygdala was hypoactive during emotional processing tasks" ...  this isn't correct.   This paper found the following: right amygdala has less activity during emotional processing and left amygdala has more; no apparent differences in the either-side amygala during the cognitive task, and left amygdala to be more active in the resting state and no difference in the right.


 * The second ref has a pretty nice discussion of issues that hinder study of the biology of depression (depression rating scales are not great; individual studies don't record data the same way; issue of medicated vs unmedicated (and kind of medication, etc). likewise fRMI is often used in this work and the literature is all messed up due to a flaw in the software that almost all academics use to analyze their data.     am thinking it would be useful to have a discussion of this in the article.  i may add that,but anybody is welcome to. Jytdog (talk) 05:47, 5 December 2016 (UTC)

Ah that makes sense. I will try adding it with the suggestions. I did use the Autofill using the link not the PMID, I guess there was an error with that. Petergstrom (talk) 07:13, 5 December 2016 (UTC)

Networks
This page originally had a brain region section and a large scale network theory section, however there is no section on circuits which I think might be more relevant as most studies don't describe findings using individual brain regions or in the context of large scale network theories. Would it be a better idea to remove the brain region section and replace it with circuits or what?\\Petergstrom (talk) 09:19, 5 December 2016 (UTC)

Weird Sections
The following section on the raphe is a bit tangential, with weak sourcing, and little content relating it to depression. The literature relating the RN to depression is massive, so it could be easily expanded and reinstated.Petergstrom (talk) 06:25, 4 April 2018 (UTC) The section on ventricles is outdated, as it contradicts a number of recent studies observing more nuance is degenerative v. developmental models of depression, as well as studies observing nuanced effects of depression and ventricular enlargement(e.g. the ENIGMA consortium reported enlarged ventricles only in early onset depression )Petergstrom (talk) 06:32, 4 April 2018 (UTC)

Raphe nuclei
The sole source of serotonin in the brain is the raphe nuclei, a group of small nerve cell nuclei in the upper brain stem, located directly at the mid-line of the brain. There is some evidence for neuropathological abnormalities in the rostral raphe nuclei in depression. Despite their small size, they reach very widely through their projections, and are involved in a very diverse set of functions. Most antidepressants are serotonergic.

Ventricles
Multiple studies have found evidence of ventricular enlargement in people who have depression, particularly enlargement of the third ventricle. These observations are interpreted as indicating loss of neural tissue in brain regions adjacent to the enlarged ventricle, leading to suggestions that cytokines and related mediators of neurodegeneration may play a role in giving rise to the disease.