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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27-Hydroxycholesterol Promotes Oligodendrocyte Maturation – Implications for Hypercholesterolemia Associated Brain White Matter Changes
Vilma Alanko,Tania Quintela-López,Adhara Gaminde-Blasco,Raúl Loera-Valencia,Alina Solomon,Ingemar Björkhem,Angel Cedazo-Minguez,Silvia Maioli,Graziella Tabacaru,María Latorre-Leal,Carlos Matute,Miia Kivipelto,Elena Alberdi,Anna Matton +13 more
TL;DR: Vilma Alanko Karolinska Institutet Tania Quintela-López University of the Basque Country: Universidad del Pais Vasco Adhara Gaminde-Blasco University of
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Computerized cognitive training and physical exercise : effects on cognitive and brain function in older adults
ten Brinke,Lisanne Femke +1 more
TL;DR: In this article, the authors present a Table of Table of Contents of the Table of contents of the paper "A Table of the Contents of a Table" for the paper this article.
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Key brain cell interactions and contributions to the pathogenesis of Alzheimer’s disease
TL;DR: In this paper , the authors discuss the interactions between different brain cells, from physiological conditions to their pathological reactions in Alzheimer's disease, and how this basic knowledge can be crucial for developing new therapeutic strategies.
Journal ArticleDOI
Decreased myelin content of the fornix predicts poorer memory performance beyond vascular risk, hippocampal volume, and fractional anisotropy in nondemented older adults.
Katherine J. Bangen,Katherine J. Bangen,Lisa Delano-Wood,Lisa Delano-Wood,Sean C.L. Deoni,Alexandra L. Clark,Alexandra L. Clark,Nicole D. Evangelista,Samantha N. Hoffman,Scott F. Sorg,Scott F. Sorg,Sophia Holmqvist,Jessica R. Osuna,Jessica R. Osuna,Alexandra J. Weigand,Amy J. Jak,Amy J. Jak,Mark W. Bondi,Mark W. Bondi,Melissa Lamar +19 more
TL;DR: In this article, fornix fractional anisotropy (FA) and diffusion tensor imaging (DTI) were used to measure FA in older adults without dementia, and linear regression models revealed that lower FA was associated with poorer memory functioning.
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.
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.
Journal ArticleDOI
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.