SynthesisAlzheimer's & dementia : the journal of the Alzheimer's Association2018
DNA damage-associated oligodendrocyte degeneration precedes amyloid pathology and contributes to Alzheimer's disease and dementia.
Synthesis in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Fish consumption and cognitive function in aging: a systematic review of observational studies.GeroScience · 2026Pooled it
- Review
- Age-Related Decline in Myelin Markers and Oligodendrocyte Density in Rhesus Macaque Prefrontal Cortex.eNeuro · 2026Article
- Spatially resolved transcriptome-metabolome integration reveals region-specific glial lipid dysregulation associated with Alzheimer's pathology.bioRxiv : the preprint server for biology · 2026Article
- Dying oligodendrocytes persist without mitochondria.bioRxiv : the preprint server for biology · 2026Article
- Multiscale proteomic modeling reveals protein networks driving Alzheimer's disease pathogenesis.Cell · 2025Article
- Myelin dysfunction in aging and brain disorders: mechanisms and therapeutic opportunities.Molecular neurodegeneration · 2025Review
- The many connections of UFMylation with Alzheimer's disease: a comprehensive review.Molecular neurodegeneration · 2025Review
- NETSseq reveals inflammatory and aging mechanisms in distinct cell types, driving cerebellar decline in ataxia telangiectasia.Frontiers in neuroscience · 2025Article
- The Dual Role of Amyloid Beta-Peptide in Oxidative Stress and Inflammation: Unveiling Their Connections in Alzheimer's Disease Etiopathology.Antioxidants (Basel, Switzerland) · 2024Review
- Myelin Pathology in Alzheimer's Disease: Potential Therapeutic Opportunities.Aging and disease · 2024Review
- Beyond Amyloid: A Machine Learning-Driven Approach Reveals Properties of Potent GSK-3β Inhibitors Targeting Neurofibrillary Tangles.International journal of molecular sciences · 2024Article
- Article
- Imaging crossing fibers in mouse, pig, monkey, and human brain using small-angle X-ray scattering.Acta biomaterialia · 2023Article
- Sting and p53 DNA repair pathways are compromised in Alzheimer's disease.Scientific reports · 2023Article
- Cerebral Gray and White Matter Monogalactosyl Diglyceride Levels Rise with the Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- White matter injury, cholesterol dysmetabolism, and APP/Abeta dysmetabolism interact to produce Alzheimer's disease (AD) neuropathology: A hypothesis and review.Frontiers in aging neuroscience · 2023Article
- Apolipoprotein E ε4 Mediates Myelin Breakdown by Targeting Oligodendrocytes in Sporadic Alzheimer Disease.Journal of neuropathology and experimental neurology · 2022Article
- Greater Diffusion Restriction in White Matter in Preclinical Alzheimer Disease.Annals of neurology · 2022Article
- Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer's Disease.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
introductionIn looking for novel non-amyloid-based etiologies for Alzheimer's disease, we explore the hypothesis that age-related myelin loss is an attractive explanation for age-associated cognitive decline and dementia.
methodsWe performed a meta-analysis of data in the National Alzheimer's Coordinating Center database accompanied by quantitative histopathology of myelin and oligodendrocytes (OLs) in frontal cortices of 24 clinically characterized individuals. Pathological findings were further validated in an Alzheimer's disease mouse model and in culture.
resultsMyelin lesions increased with cognitive impairment in an amyloid-independent fashion with signs of degeneration appearing before neuronal loss. Myelinating OLs in the gray matter showed greater vulnerability than those in white matter, and the degenerative changes correlated with evidence of DNA damage. Similar results were found in myelinating OL cultures where DNA damage caused aberrant OL cell cycle re-entry and death. DISCUSSION: We present the first comprehensive analysis of the cell biology of early myelin loss in sporadic Alzheimer's disease.
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Registered trials
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.