Cited by 546Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Alzheimer's disease as homeostatic responses to age-related myelin breakdown

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Bartzokis, George·2011·Neurobiology of Aging

DOI 10.1016/j.neurobiolaging.2009.08.007PMC PMC3128664

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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.

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“…substrate (caused by he rate-limiting BACE1 cleavage of APP described above) rives the increased A 42/40 ratio observed in both PS1 utations as well as in wild type PS1 (Yin et al., 2007) and einforces the preeminence of the BACE1 cleavage of APP n the production of A (McConlogue et al., 2007).”
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Authors: Bartzokis, G.
Affiliations: University of California, Los Angeles (US)
Corresponding author: Bartzokis, George
Venue: Neurobiology of Aging
Publisher: Elsevier BV
Published: 2011-08
Volume: 32
Issue: 8
Pages: 1341-1371
ISSN: 0197-4580 (ISSN-L)
DOI: 10.1016/j.neurobiolaging.2009.08.007
PMC: PMC3128664
OpenAlex: W2130418945
Cited by: 546
References: 411
Citations by year: 2026: 27 · 2025: 39 · 2024: 23 · 2023: 41 · 2022: 38 · 2021: 33 · 2020: 43 · 2019: 31 · 2018: 31 · 2017: 34 · 2016: 40 · 2015: 36 · 2014: 31 · 2013: 31 · 2012: 31
FWCI: 2.43
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Aging (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (R01AG027342, AG027342)
National Institute of Mental Health (MH066029, R01MH066029)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: Alzheimer's disease, amyloid hypothesis, amyloid-beta, myelination, oligodendrocytes, remyelination, white matter, axonal transport, neuritic plaques, tau protein, amyloid precursor protein, presenilin, familial Alzheimer's disease, late-onset Alzheimer's disease, brain aging, iron, cholesterol, free radicals, treatment goals
MeSH terms: Aged, Aging, Alzheimer Disease, Homeostasis, Humans, Myelin Sheath, Oligodendroglia

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Alzheimer's disease as homeostatic responses to age-related myelin breakdown

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