The DOI matches its Crossref record, with a small difference in title or year; 411 of the 411 references it cites were found in a registry or an index.
Alzheimer's disease as homeostatic responses to age-related myelin breakdown
Open accessAbstract
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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“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
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“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]
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“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]
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“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
In the citing paper
“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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The Cellular Phase of Alzheimer’s Disease
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Metadata
- 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)
- 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
- 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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