Biomarkers and evolution in Alzheimer disease

Stanley I. Rapoport, Peter T. Nelson

Research output: Contribution to journalComment/debate

29 Scopus citations

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.

Original languageEnglish
Pages (from-to)510-513
Number of pages4
JournalProgress in Neurobiology
Volume95
Issue number4
DOIs
StatePublished - Dec 2011

Bibliographical note

Funding 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.

Keywords

  • Alzheimer
  • Association
  • Biomarker
  • Brain
  • Cortex
  • Evolution
  • Metabolism
  • Neuroplasticity

ASJC Scopus subject areas

  • Neuroscience (all)

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