ReviewActa neuropathologica communications2023
Myelin in Alzheimer's disease: culprit or bystander?
Review in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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.
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Who cites it
41 citing papers in PubMed, 54 citations in OpenAlex.
- Neurologic dance training and home exercise improve motor-cognitive dual-task function similarly, but through potentially different mechanisms, among breast cancer survivors with chemotherapy-induced neuropathy: Initial results of a randomized, controlled clinical trial.Journal of Alzheimer's disease : JAD · 2025Trial
- A Novel Nogo-A Receptor Antagonist Peptide Impedes Alzheimer's Disease Pathology by Nogo-A/NgR/ROCK Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- When myelin breaks, tau aggregates - a new perspective on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Altered T1w/T2w-FLAIR Ratio in White Matter Hyperintensities as an Indicator of Structural Integrity Loss: Association with Alzheimer's Disease and Vascular Dementia.medRxiv : the preprint server for health sciences · 2026Article
- Cortical gray-white matter contrast alterations precede amyloid-β positivity and macrostructural changes in older adults without dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- CYP46A1 activation by low-dose efavirenz uncovers the link between brain cholesterol metabolism, energetics, and vasculature.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Dysregulated oligodendrocyte and myelin dynamics as an early pathological feature of neuropil degeneration in Alzheimer's disease: an ultrastructural study.Acta neuropathologica communications · 2026Article
- Investigation of the myelin-amyloid interplay in Alzheimer's disease: insights from novel dsCMA imaging in mouse and human brains.Acta neuropathologica communications · 2026Article
- A DERIVED RELAXATION CONTRAST FROM SYNTHETIC MRI FOR DETECTING NETWORK MICROSTRUCTURAL VULNERABILITY.bioRxiv : the preprint server for biology · 2026Article
- Dynamic thermodynamic-informational entropic relationship (TIER) models of selective vulnerability to neurodegeneration.bioRxiv : the preprint server for biology · 2026Article
- Multimodal MRI Reveals Cerebral and Vascular Amyloid-Driven Myeloarchitectural Disorganization in a Mouse Model of Alzheimer's Disease.NMR in biomedicine · 2026Article
- Rising energetic cost of walking predicts cognitive impairment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The evolution of phonemic verbal fluency test: bridging tradition with contemporary insights.Frontiers in psychology · 2026Review
- Dual Mechanisms of Cognitive Function and Pathological Improvements by the Selective S1PR1/5 Modulator Siponimod in 3xTg-AD Mice.Molecular neurobiology · 2025Article
- Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Review
- Pyruvate kinase deficiency links metabolic perturbations to neurodegeneration and axonal protection.Molecular metabolism · 2025Article
- Dysregulated synaptic gene expression in oligodendrocytes of spinal and bulbar muscular atrophy.JCI insight · 2025Article
- The Role of Oligodendrocytes in Neurodegenerative Diseases: Unwrapping the Layers.International journal of molecular sciences · 2025Review
- APOE genotype determines cell-type-specific pathological landscape of Alzheimer's disease.Neuron · 2025Article
- Are Oligodendrocytes the Culprits or Victims in Alzheimer's Disease.Physiological research · 2025Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder with neuronal and synaptic losses due to the accumulation of toxic amyloid β (Αβ) peptide oligomers, plaques, and tangles containing tau (tubulin-associated unit) protein. While familial AD is caused by specific mutations, the sporadic disease is more common and appears to result from a complex chronic brain neuroinflammation with mitochondriopathies, inducing free radicals' accumulation. In aged brain, mutations in DNA and several unfolded proteins participate in a chronic amyloidosis response with a toxic effect on myelin sheath and axons, leading to cognitive deficits and dementia. Αβ peptides are the most frequent form of toxic amyloid oligomers. Accumulations of misfolded proteins during several years alters different metabolic mechanisms, induce chronic inflammatory and immune responses with toxic consequences on neuronal cells. Myelin composition and architecture may appear to be an early target for the toxic activity of Aβ peptides and others hydrophobic misfolded proteins. In this work, we describe the possible role of early myelin alterations in the genesis of neuronal alterations and the onset of symptomatology. We propose that some pathophysiological and clinical forms of the disease may arise from structural and metabolic disorders in the processes of myelination/demyelination of brain regions where the accumulation of non-functional toxic proteins is important. In these forms, the primacy of the deleterious role of amyloid peptides would be a matter of questioning and the initiating role of neuropathology would be primarily the fact of dysmyelination.
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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.