ArticleBiochemistry2009
Myelin basic protein binds to and inhibits the fibrillar assembly of Abeta42 in vitro.
Article in Biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- From scavenger to victim: mechanism and treatment of microglial ferroptosis in white matter injury disease.Frontiers in immunology · 2026Review
- 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
- The Role of Oligodendrocyte Lineage Cells in the Pathogenesis of Alzheimer's Disease.Neurochemical research · 2025Review
- Alzheimer's-linked axonal changes accompany elevated antidromic action potential failure rate in aged mice.Brain research · 2024Article
- Myelin Basic Protein Attenuates Furin-Mediated Bri2 Cleavage and Postpones Its Membrane Trafficking.International journal of molecular sciences · 2024Article
- The multifaceted role of quaking protein in neuropsychiatric disorders and tumor progression.Frontiers in neuroscience · 2024Review
- Inhibition of NMDA Receptor Activation in the Rostral Ventrolateral Medulla by Amyloid-β Peptide in Rats.Biomolecules · 2023Article
- Advances in Amyloid-β Clearance in the Brain and Periphery: Implications for Neurodegenerative Diseases.Experimental neurobiology · 2023Review
- 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
- New Insights into the Molecular Interplay between Human Herpesviruses and Alzheimer's Disease-A Narrative Review.Brain sciences · 2022Review
- The role of myelin damage in Alzheimer's disease pathology.Archives of medical science : AMS · 2020Article
- Association of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease.JAMA neurology · 2017Article
- Gene Expression of Quaking in Sporadic Alzheimer's Disease Patients is Both Upregulated and Related to Expression Levels of Genes Involved in Amyloid Plaque and Neurofibrillary Tangle Formation.Journal of Alzheimer's disease : JAD · 2016Article
- N-terminal region of myelin basic protein reduces fibrillar amyloid-β deposition in Tg-5xFAD mice.Neurobiology of aging · 2015Article
- Inflammation Combined with Ischemia Produces Myelin Injury and Plaque-Like Aggregates of Myelin, Amyloid-β and AβPP in Adult Rat Brain.Journal of Alzheimer's disease : JAD · 2015Article
- The formation of tau pore-like structures is prevalent and cell specific: possible implications for the disease phenotypes.Acta neuropathologica communications · 2014Article
- Oral delivery of bioencapsulated proteins across blood-brain and blood-retinal barriers.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- The absence of myelin basic protein promotes neuroinflammation and reduces amyloid β-protein accumulation in Tg-5xFAD mice.Journal of neuroinflammation · 2013Article
- Fine mapping of the amyloid β-protein binding site on myelin basic protein.Biochemistry · 2013Article
- Nucleobindin 1 caps human islet amyloid polypeptide protofibrils to prevent amyloid fibril formation.Journal of molecular biology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The deposition of amyloid beta-protein (Abeta) fibrils into plaques within the brain parenchyma and along cerebral blood vessels is a hallmark of Alzheimer's disease. Abeta peptides are produced through the successive cleavage of the Abeta precursor protein by beta- and gamma-secretase, producing peptides between 39 and 43 amino acids in length. The most common of these are Abeta40 (the most abundant) and Abeta42. Abeta42 is more fibrillogenic than Abeta40 and has been implicated in early Abeta plaque deposition. Our previous studies determined that myelin basic protein (MBP) was capable of inhibiting fibril formation of a highly fibrillogenic Abeta peptide containing both E22Q (Dutch) and D23N (Iowa) mutations associated with familial forms of cerebral amyloid angiopathy [Hoos, M. D., et al. (2007) J. Biol. Chem. 282, 9952-9961]. In this study, we show through a combination of biochemical and ultrastructural techniques that MBP is also capable of inhibiting the beta-sheet fibrillar assembly of the normal Abeta42 peptide. These findings suggest that MBP may play a role in regulating the deposition of Abeta42 and thereby also may regulate the early formation of amyloid plaques in 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.