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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Dissertation
The role of hypertension and inflammation on the cognitive symptoms of Alzheimer’s disease patients.
TL;DR: The possible synergistic effect of blood pressure, markers of vascular health asymmetric dimethylarginine (ADMA) and Fetuin-A, and markers of inflammation upon cognition was assessed.
Journal ArticleDOI
Axonal Conduction Velocity in CA1 Area of Hippocampus is Reduced in Mouse Models of Alzheimer's Disease.
TL;DR: An age-dependent reduction in VC is reported in area CA1 in two amyloid-β precursor protein transgenic mouse models, line 41 and APP/PS1, and in a tauopathy model, rTg4510.
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White Matter Dementia: Origin, Development, Progress, and Prospects
TL;DR: The idea of WMD promises to continue as a useful construct informing the study of dementia and the understanding of brain-behavior relationships and emerging data are identifying new opportunities for dementia prevention by avoidance of acquired vascular and traumatic white matter insults.
Journal Article
Reproducibility and use of myelin imaging methods for the study of adolescent brain development
TL;DR: This dissertation examines the reproducibility and application of two recently developed MRI techniques with sensitivity to myelin content in white matter using in vivo and simulated data.
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Protective Effects of Fish (Alaska Pollock) Protein Intake against Short-Term Memory Decline in Senescence-Accelerated Mice
Yuki Murakami,Ryota Hosomi,Ayano Nishimoto,Toshimasa Nishiyama,Munehiro Yoshida,Kenji Fukunaga +5 more
TL;DR: In this article , the effects of FO and FP on brain function were investigated in senescence-accelerated mouse-prone 10 (SAMP10) mice, and the results suggest that FP intake prevents age-related cognitive dysfunction by maintaining axonal morphology in the Hipp of SAMP10 mice.
References
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Journal ArticleDOI
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.
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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.