Alzheimer's disease as homeostatic responses to age-related myelin breakdown
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This work delineates empirically testable mechanisms of action for genes underlying FAD and LOAD and provides "upstream" treatment targets and reframes key observations such as axonal transport disruptions, formation of axonal swellings/sphenoids and neuritic plaques, and proteinaceous deposits as by-products of homeostatic myelin repair processes.Citations
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Synthesis and characterization of water soluble choline labeled cadmium selenide/zinc selenide/zinc sulfide luminescent quantum dots
TL;DR: Water soluble choline-labeled CdSe/ZnSe /ZnS quantum dot (QD) bioconjugates were synthesized by attaching a thiolated choline analogue to the core-shell QD surface.
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Emotional Dysregulation in Mild Behavioral Impairment Is Associated with Reduced Cortical Thickness in the Right Supramarginal Gyrus.
TL;DR: In this article, the authors investigated the relationship between mild behavioral impairment (MBI) and surface area, cortical thickness, and volume in the temporal and parietal lobes, which are strongly associated with dementia and emotional disorders.
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27‐hydroxycholesterol promotes oligodendrocyte maturation: Implications for hypercholesterolemia‐associated brain white matter changes
TL;DR: In this article , the authors investigated the effects of 27-hydroxycholesterol (27-OH) in cultured oligodendrocytes and found that 27-OH induces cell death of immature O4+ /GalC+ oligod endrocyte along with stimulating differentiation of PDGFR+ oligodegmented progenitors (OPCs).
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Cell type-specific histone acetylation profiling of Alzheimer’s disease subjects and integration with genetics
TL;DR: In this paper , the authors profile genome-wide histone 3 lysine 27 acetylation (H3K27ac) of 3 major brain cell types from hippocampus and dorsolateral prefrontal cortex (dlPFC) of subjects with and without Alzheimer's disease (AD) and confirm that single nucleotide polymorphisms associated with late onset AD (LOAD) show a strong tendency to reside in microglia-specific gene regulatory elements.
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Higher levels of myelin are associated with higher resistance against tau pathology in Alzheimer's disease
TL;DR: In this article , the authors investigated whether the level of myelination in fiber-tracts and cortex is predictive of region-specific tau accumulation, and they found that higher myelinated cortical regions show lower tau-PET uptake in spatially corresponding areas and regions connected by highly myelinate fiber tracts show lower rates of tau spreading.
References
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The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
John Hardy,Dennis J. Selkoe +1 more
TL;DR: It has been more than 10 years since it was first proposed that the neurodegeneration in Alzheimer's disease (AD) may be caused by deposition of amyloid β-peptide in plaques in brain tissue and the rest of the disease process is proposed to result from an imbalance between Aβ production and Aβ clearance.
Journal ArticleDOI
Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families
Elizabeth H. Corder,Ann M. Saunders,Warren J. Strittmatter,Donald E. Schmechel,P. C. Gaskell,Gary W. Small,A. D. Roses,Jonathan L. Haines,Margaret A. Pericak-Vance +8 more
TL;DR: The APOE-epsilon 4 allele is associated with the common late onset familial and sporadic forms of Alzheimer9s disease (AD) in 42 families with late onset AD.
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Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment.
Robert D. Terry,Eliezer Masliah,David P. Salmon,Nelson Butters,Richard DeTeresa,Robert Hill,Lawrence A. Hansen,Robert Katzman +7 more
TL;DR: Both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of patients with Alzheimer's disease and 9 neuropathologically normal subjects reveal very powerful correlations with all three psychological assays.
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Alzheimer's Disease Is a Synaptic Failure
TL;DR: Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid β protein.
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Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory.
Ganesh M. Shankar,Shaomin Li,Tapan Mehta,Amaya Garcia-Munoz,Nina E. Shepardson,Imelda M. Smith,Francesca Brett,Michael A. Farrell,Michael J. Rowan,Cynthia A. Lemere,Ciaran M. Regan,Dominic M. Walsh,Bernardo L. Sabatini,Dennis J. Selkoe +13 more
TL;DR: It is concluded that soluble Aβ oligomers extracted from Alzheimer's disease brains potently impair synapse structure and function and that dimers are the smallest synaptotoxic species.