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Biomarkers and evolution in Alzheimer disease
Stanley I Rapoport1, Peter T Nelson
1Brain 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
Progress in Neurobiology
|August 2, 2011
Summary
Alzheimer disease preferentially impacts brain regions with rapid expansion during human evolution. Biomarkers may reveal evolutionary origins of Alzheimer disease, despite the lack of a perfect animal model.
Area of Science:
- Neuroscience
- Evolutionary Biology
- Pathology
Background:
- Alzheimer disease (AD) disproportionately affects specific brain regions and their extensive axonal connections, which underwent rapid expansion during hominid evolution.
- Currently, no natural animal model fully replicates the severe neurofibrillary tangles and neuritic amyloid plaques characteristic of human AD brains.
Purpose of the Study:
- To explore the link between brain regions affected by Alzheimer disease and their evolutionary expansion during hominid development.
- To investigate how biomarkers of Alzheimer disease might offer insights into its evolutionary origins.
Main Methods:
- Analysis of brain regions and axonal connections affected by Alzheimer disease in the context of hominid evolution.
- Review of existing biomarkers for identifying mild cognitive impairment (MCI) and preclinical Alzheimer disease.
Main Results:
- Specific brain regions and their long, neuroplastic axonal connections that evolved rapidly in hominids are preferentially targeted by Alzheimer disease.
- Identified biomarkers include reduced neocortical glucose metabolism, white matter tract defects, altered RNA neurochemistry, and elevated cerebrospinal fluid (CSF) tau protein levels.
Conclusions:
- The evolutionary trajectory of specific brain structures may predispose them to Alzheimer disease pathology.
- Biomarkers used for clinical diagnosis could also illuminate the evolutionary emergence of Alzheimer disease in the human lineage.
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