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

Bartzokis, George

doi:10.1016/j.neurobiolaging.2009.08.007

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

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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Disturbances in myelin are associated with an increased rate of AD progression and byproducts of homeostatic myelin maintenance can promote the formation of amyloid plaques.
“Consistent with this possibility, disturbances in myelin have been associated with an increased rate of AD progression and byproducts of homeostatic myelin maintenance can promote the formation of amyloid plaques (Bartzokis, 2007, 2011).”
From Down Syndrome Developmental Brain Transcriptome Reveals Defective Oligodendrocyte Differentiation and Myelination (2016) · cites this paper as Bartzokis, 2011
Section 2.2 associates more severe myelin damage with the trajectory of decline into AD, but does not establish that myelin disturbances increase the rate of progression. Section 5 proposes that Aβ released during unsuccessful myelin repair could contribute to a mature neuritic plaque, supporting the claim's qualified plaque-formation mechanism. Page numbers were not available in our copy. (LLM, conf=0.85)
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Myelin damage likely precedes and contributes to amyloid plaque buildup in early AD.
“This is notable because myelin damage likely precedes and contributes to amyloid plaque buildup in early AD.55–57”
From TET2-mutant myeloid cells mitigate Alzheimer’s disease progression via CNS infiltration and enhanced phagocytosis in mice (2025) · cites this paper as [55]
Aβ load correlates better with age than disease severity in AD.
“the Aβ load, which has been our main target, correlates better with age than disease severity in AD [291,292,293]”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [291]
Age-associated myelin breakdown is seen in MRI scans of patients from age 50 on, which is accentuated in APOE4 patients.
“Age-associated myelin breakdown is seen in MRI scans of patients from age 50 on, which is accentuated in APOE4 patients (Scheltens et al. , 1992; Bartzokis, 2011).”
From Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer’s Disease (2020) · cites this paper as Bartzokis, 2011
MRI data indicate that individuals with the APOEε4 risk allele have accentuated myelin breakdown in AD.
“magnetic resonance imaging (MRI) data indicate that individuals with the risk allele APOEε4 have accentuated myelin breakdown in AD [128, 129].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [128]

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“This pattern of DTI-based findings is consistent with data demonstrating that myelin and its components such as cholesterol and myelin proteins are reduced early in the AD process [64, 65] and with a recently proposed theory suggesting that disruption of myelin integrity is an early event in the course of AD [66].”
Result
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Estrogenic plants: to prevent neurodegeneration and memory loss and other symptoms in women after menopause
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“Another possible explanation presented by the authors focused on myelin damage [52], which has been shown to promote Aβ oligomerization, eventually contributing to amyloid deposition [53].”
Background

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: Health Sciences › Medicine › Physiology › 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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