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.
Bibliographical noteFunding Information:
This work was supported by the Intramural Program of the National Institute of Aging , NIH (SIR) and by NIH Grants # R01 NS061933 and R21 AG036875 to PTN. Neither author has a conflict of interest with regard to this paper.
ASJC Scopus subject areas
- Neuroscience (all)