| Literature DB >> 21801803 |
Stanley I Rapoport1, Peter T Nelson.
Abstract
Brain regions and their highly neuroplastic long axonal connections that expanded rapidly during hominid evolution are preferentially affected by Alzheimer disease. There is no natural animal model with full disease pathology (neurofibrillary tangles and neuritic amyloid plaques of a severity seen in Alzheimer's disease brains). Biomarkers such as reduced glucose metabolism in association neocortex, defects in long white matter tracts, RNA neurochemical changes, and high CSF levels of total and phosphorylated tau protein, which are helpful to identify MCI and preclinical Alzheimer disease patients, may also provide insights into what brain changes led to this disease being introduced during hominid evolution. Published by Elsevier Ltd.Entities:
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Year: 2011 PMID: 21801803 PMCID: PMC5878862 DOI: 10.1016/j.pneurobio.2011.07.006
Source DB: PubMed Journal: Prog Neurobiol ISSN: 0301-0082 Impact factor: 11.685