Alzheimer's disease as homeostatic responses to age-related myelin breakdown
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TLDR
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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Is Alzheimer's Also a Stem Cell Disease? - The Zebrafish Perspective
TL;DR: A plausible way to circumvent the AD phenotypes could be to mobilize the endogenous stem cells by enhancing their proliferative and neurogenic capacity as well as to provide the newborn neurons the potential to survive and integrate into the existing circuitry.
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Local molecular and global connectomic contributions to cross-disorder cortical abnormalities
Justine Y. Hansen,Golia Shafiei,Jacob W. Vogel,Kelly Smart,Carrie E. Bearden,Martine Hoogman,Barbara Franke,Daan van Rooij,Jan K. Buitelaar,Carrie R. McDonald,Sanjay M. Sisodiya,Lianne Schmaal,Dick J. Veltman,Odile A. van den Heuvel,Dan J. Stein,Theo G.M. van Erp,Christopher R.K. Ching,Ole A. Andreassen,Tomas Hajek,Nils Opel,Gemma Modinos,André Aleman,Ysbrand D. van der Werf,Neda Jahanshad,Sophia I. Thomopoulos,Paul M. Thompson,Richard E. Carson,Alain Dagher,Bratislav Misic +28 more
TL;DR: Using MRI morphometry from the ENIGMA consortium, the authors constructed maps of cortical abnormalities for thirteen neurodevelopmental, neurological, and psychiatric disorders from N = 21,000 participants and N = 26,000 controls, collected using a harmonised processing protocol.
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Full diffusion characterization implicates regionally disparate neuropathology in Mild Cognitive Impairment
Erin L. Boespflug,Judd M. Storrs,Sara Sadat-Hossieny,James C. Eliassen,Marcelle D. Shidler,Matthew M. Norris,Robert Krikorian +6 more
TL;DR: Findings suggest disparate pathology of temporal stems and fornix white matter in association with early memory impairment in MCI and highlight the methodological importance of evaluating the full tensor, rather than only summative metrics in research using DTI.
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Disruption of thalamic connectivity in Alzheimer's disease: a diffusion tensor imaging study.
Qing-Yong Zhu,Si-Wei Bi,Xiu-Ting Yao,Zhi-Yan Ni,Ying Li,Boyu Chen,Guo-Guang Fan,Xiu-Li Shang +7 more
TL;DR: The DTI analyses indicate that the integrity of thalamic connectivity is progressively disrupted following cognitive decline in AD and that DTI parameters in the column and body of the fornix show promise as potential markers for the early diagnosis of AD and for monitoring disease progression.
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Terahertz Imaging and Electromagnetic Model of Axon Demyelination in Alzheimer's Disease
Woon-Gi Yeo,Ogan Gurel,Nandhini Srinivasan,Paul D. King,Niru K. Nahar,Sungchan Park,Norman L. Lehman,Kubilay Sertel +7 more
TL;DR: It is demonstrated that the THz reflection spectra reveal detectable differences between postmortem brain tissues exhibiting Alzheimer's disease and normal controls, and a simplified electromagnetic model of white matter axons exhibiting various degrees of demyelination is presented to support this hypothesis through full-wave electromagnetic simulations.
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.
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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.