Evidence map›Paper›PMID 19775776›Full record

ReviewNeurobiology of aging2011

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

George Bartzokis

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurobiology of aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 318 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
318citing papers in PubMed, 2 pooled it
11.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

318 citing papers in PubMed, 2 syntheses or guidelines pooled it, 569 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
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  6. Review
  7. Superficial white matter and gray matter jointly support cognition among older adults in India.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  17. bioRxiv : the preprint server for biology · 2025
    Article
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  19. Review
  20. Article

258 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

George BartzokisDepartment of Psychiatry and Biobehavioral Sciences, The David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA. gbar@ucla.edu
Neurobehavioral Systems · US

Funding

Brain Iron in Aging AdultsR01AG027342 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BARTZOKIS, GEORGE · 2007 to 2011
$2.1M
Brain Development on Adults with SchizophreniaR01MH066029 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BARTZOKIS, GEORGE · 2004 to 2008
$2.1M
NIA NIH HHS AG027342NIA NIH HHS R01 AG027342NIMH NIH HHS MH066029NIMH NIH HHS R01 MH066029
6 · The paper itself

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.

Indexed as

AgedAgingAlzheimer DiseaseHomeostasisHumansMyelin SheathOligodendroglia

Identifiers

PMID19775776
PMCPMC3128664
OpenAlexW2130418945

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.