title: Biomarkers and evolution in Alzheimer disease.
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.
authors.affiliation: Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S-126, Bethesda, MD 20892, USA. sir@helix.nih.gov
authors.forename: Stanley I
authors.initials: SI
authors.lastname: Rapoport
authors.forename: Peter T
authors.initials: PT
authors.lastname: Nelson
mesh_terms: D000544:Alzheimer Disease / Q000134:cerebrospinal fluid / Q000150:complications / Q000175:diagnosis; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid; D000818:Animals; D005075:Biological Evolution; D015415:Biomarkers / Q000134:cerebrospinal fluid*; D006801:Humans; D016874:Neurofibrillary Tangles / Q000473:pathology; D058225:Plaque, Amyloid / Q000209:etiology
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers