Biomarkers and evolution in Alzheimer disease

Stanley I. Rapoport; Peter T. Nelson

doi:10.1016/j.pneurobio.2011.07.006

Biomarkers and evolution in Alzheimer disease

Stanley I. Rapoport, Peter T. Nelson

Research output: Contribution to journal › Comment/debate

31 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 language	English
Pages (from-to)	510-513
Number of pages	4
Journal	Progress in Neurobiology
Volume	95
Issue number	4
DOIs	https://doi.org/10.1016/j.pneurobio.2011.07.006
State	Published - 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.

Funding

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.

Funders	Funder number
National Institutes of Health (NIH)	R21 AG036875
National Institutes of Health (NIH)
National Institute on Aging
Institute of Neurological Disorders and Stroke National Advisory Neurological Disorders and Stroke Council	R01NS061933
Institute of Neurological Disorders and Stroke National Advisory Neurological Disorders and Stroke Council

Keywords

Alzheimer
Association
Biomarker
Brain
Cortex
Evolution
Metabolism
Neuroplasticity

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.pneurobio.2011.07.006

Cite this

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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.",

keywords = "Alzheimer, Association, Biomarker, Brain, Cortex, Evolution, Metabolism, Neuroplasticity",

author = "Rapoport, {Stanley I.} and Nelson, {Peter T.}",

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.",

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language = "English",

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pages = "510--513",

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AU - Rapoport, Stanley I.

AU - Nelson, Peter T.

N1 - 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.

PY - 2011/12

Y1 - 2011/12

N2 - 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.

AB - 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.

KW - Alzheimer

KW - Association

KW - Biomarker

KW - Brain

KW - Cortex

KW - Evolution

KW - Metabolism

KW - Neuroplasticity

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SN - 0301-0082

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JO - Progress in Neurobiology

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Biomarkers and evolution in Alzheimer disease

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

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