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Alzheimer's disease as homeostatic responses to age-related myelin breakdown
Author(s):
George Bartzokis
Publication date
Created:
August 2011
Publication date
(Print):
August 2011
Journal:
Neurobiology of Aging
Publisher:
Elsevier BV
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Abstract
The amyloid hypothesis (AH) of Alzheimer's disease (AD) posits that the fundamental cause of AD is the accumulation of the peptide amyloid beta (Aβ) in the brain. This hypothesis has been supported by observations that genetic defects in amyloid precursor protein (APP) and presenilin increase Aβ production and cause familial AD (FAD). The AH is widely accepted but does not account for important phenomena including recent failures of clinical trials to impact dementia in humans even after successfully reducing Aβ deposits. Herein, the AH is viewed from the broader overarching perspective of the myelin model of the human brain that focuses on functioning brain circuits and encompasses white matter and myelin in addition to neurons and synapses. The model proposes that the recently evolved and extensive myelination of the human brain underlies both our unique abilities and susceptibility to highly prevalent age-related neuropsychiatric disorders such as late onset AD (LOAD). It regards oligodendrocytes and the myelin they produce as being both critical for circuit function and uniquely vulnerable to damage. This perspective reframes key observations such as axonal transport disruptions, formation of axonal swellings/sphenoids and neuritic plaques, and proteinaceous deposits such as Aβ and tau as by-products of homeostatic myelin repair processes. It delineates empirically testable mechanisms of action for genes underlying FAD and LOAD and provides "upstream" treatment targets. Such interventions could potentially treat multiple degenerative brain disorders by mitigating the effects of aging and associated changes in iron, cholesterol, and free radicals on oligodendrocytes and their myelin. Copyright © 2009 Elsevier Inc. All rights reserved.
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Author and article information
Journal
Title:
Neurobiology of Aging
Abbreviated Title:
Neurobiology of Aging
Publisher:
Elsevier BV
ISSN (Print):
01974580
Publication date Created:
August 2011
Publication date (Print):
August 2011
Volume
: 32
Issue
: 8
Pages
: 1341-1371
Article
DOI:
10.1016/j.neurobiolaging.2009.08.007
PMC ID:
3128664
PubMed ID:
19775776
SO-VID:
673a4f37-b746-43d9-b80a-c64995f8e285
Copyright ©
© 2011
License:
https://www.elsevier.com/tdm/userlicense/1.0/
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