Cited by 968Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeurogenesis and neuroplasticity mechanisms

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Age-related myelin breakdown: a developmental model of cognitive decline and Alzheimer’s disease

Bartzokis, George·2004·Neurobiology of Aging

DOI 10.1016/j.neurobiolaging.2003.03.001

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Abstract

A hypothetical model of Alzheimer's disease (AD) as a uniquely human brain disorder rooted in its exceptional process of myelination is presented. Cortical regions with the most protracted development are most vulnerable to AD pathology, and this protracted development is driven by oligodendrocytes, which continue to differentiate into myelin producing cells late into the fifth decade of life. The unique metabolic demands of producing and maintaining their vast myelin sheaths and synthesizing the brain's cholesterol supply make oligodendrocytes especially susceptible to a variety of insults. Their vulnerability increases with increasing age at differentiation as later-differentiating cells myelinate increasing numbers of axonal segments. These vulnerable late-differentiating cells drive the protracted process of intracortical myelination and by increasing local cholesterol and iron levels, progressively increase the toxicity of the intracortical environment forming the basis for the age risk factor for AD. At older ages, the roughly bilaterally symmetrical continuum of oligodendrocyte vulnerability manifests as a progressive pattern of myelin breakdown that recapitulates the developmental process of myelination in reverse. The ensuing homeostatic responses to myelin breakdown further increase intracortical toxicity and results in the relentless progression and non-random anatomical distribution of AD lesions that eventually cause neuronal dysfunction and degeneration. This process causes a slowly progressive disruption of neural impulse transmission that degrades the temporal synchrony of widely distributed neural networks underlying normal brain function. The resulting network "disconnections" first impact functions that are most dependent on large-scale synchronization including higher cognitive functions and formation of new memories. Multiple genetic and environmental risk factors (e.g. amyloid beta-peptide and free radical toxicity, head trauma, anoxia, cholesterol levels, etc.) can contribute to the cognitive deficits observed in aging and AD through their impact on the life-long trajectory of myelin development and breakdown. This development-to-degeneration model is testable through imaging and post mortem methods and highlights the vital role of myelin in impulse transmission and synchronous brain function. The model offers a framework that explains the anatomical distribution and progressive course of AD pathology, some of the failures of promising therapeutic interventions, and suggests further testable hypotheses as well as novel approaches for intervention efforts.

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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: 2004-01
Volume: 25
Issue: 1
Pages: 5-18
ISSN: 0197-4580 (ISSN-L)
DOI: 10.1016/j.neurobiolaging.2003.03.001
OpenAlex: W1981000616
Cited by: 968
References: 274
Citations by year: 2026: 31 · 2025: 37 · 2024: 49 · 2023: 40 · 2022: 50 · 2021: 46 · 2020: 50 · 2019: 48 · 2018: 40 · 2017: 47 · 2016: 42 · 2015: 48 · 2014: 40 · 2013: 58 · 2012: 43
FWCI: 3.43
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Aging (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (P50AG016570, AG 16570)
National Institute of Mental Health (MH6357-01A1)
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 › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: Alzheimer's disease, myelination, oligodendrocytes, myelin breakdown, cognitive decline, brain aging, cortical development, cholesterol, iron, neuronal synchronization, memory impairment, amyloid-beta, free radical toxicity, head trauma, anoxia
MeSH terms: Aging, Alzheimer Disease, Animals, Brain, Cognition Disorders, Disease Models, Animal, Humans, Myelin Sheath, Neurons, Oligodendroglia, Risk Factors, Cell Death

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Age-related myelin breakdown: a developmental model of cognitive decline and Alzheimer’s disease

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