User:Kdgaffney/sandbox

I am thinking of adding to the Hirano body page. I was able to find articles published that have related hirano bodies to Alzheimer's disease; and, I think it I could update the page with how hirano bodies actually are associated to Alzheimer's disease. It would give hirano bodies more importance. It would also be more information about hirano bodies that could be useful to give the reader more of an idea in how they are relevant. Possible sources to start with-
 * 1. A. Hirano, Hirano bodies and related neuronal inclusions. Neuropathol. Appl. Neurobiol. 20, 3-11 (1994).
 * 2. A. Hirano, H. Zimmerman, Alzheimer's neurofibrillary changes: a topographic study. Arch. Neurol. 7, 227-242 (1962).
 * 3. S. Mitake, K. Ojika, A. Hirano, Hirano bodies and Alzheimer's disease. Kaohsiung J. Med. Sci. 13, 10-18 (1997).
 * 4. D. P. Perl, Neuropathology of Alzheimer's disease. Mt. Sinai J. Med. 77, 32-42 (2010).

Background
The eponym ‘Hirano bodies’ was not introduced until 1968, by Schochet et al., three years after Hirano first observed the proteins.

They were first described in the CA1 in patients with amyotrophic lateral sclerosis and parkinsonism-dementia complex (ALS-PDC). Hirano bodies (Hb) are found mostly in the neuronal processes in the pyramidal layer in the Sommer’s sector (CA1) of the hippocampus, mostly arising from age related changes in the microfilament system. Hirano described their structure to contain “epitopes of actin, actin-associated proteins, tau, middle molecular weight neurofilaments subunit and a C-terminal fragment of β-amyloid precursor protein”.

Alzheimer's Disease
The Sommer’s sector (CA1) of the hippocampus has been described to be influential in the formation of new memories, as well as, containing inclusion bodies that contribute to a hallmark of Alzheimer’s disease (AD), intellectual deficit. Alzheimer’s neurofibrillary tangles show a preference to form in the CA1, which is one of the major areas in which Hb’s have been observed. There are a larger number of Hb’s found in people with Alzheimer’s disease than those without the disease. Additionally many processes of Alzheimer’s neurofibrillary tangles have been observed to contain Hirano bodies.

Hirano bodies are described as cytoplasmic paracrystalline lattices, which are a main form of a pathological feature seen in a broad spectrum of neurodegenerative diseases, such as Alzheimer’s disease. There is an upregulation of a macroautophagic pathway related to AD that can be related to an actin aggregate thought to be an intermediate in the formation of Hirano bodies. More specifically the actin and actin binding proteins seen in Hirano bodies are a significant feature of an Alzheimer’s disease brain. Additionally, variations in the locational characteristics of β-amyloid precursor proteins seen in Alzheimer’s disease are connected to Hirano bodies. It was observed that Hirano bodies are a specific site of a C-terminal fragment of β-amyloid precursor proteins.