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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Head trauma and in vivo measures of amyloid and neurodegeneration in a population-based study
Michelle M. Mielke,Rodolfo Savica,Heather J. Wiste,Stephen D. Weigand,Prashanthi Vemuri,David S. Knopman,Val J. Lowe,Rosebud O. Roberts,Mary M. Machulda,Yonas E. Geda,Ronald C. Petersen,Clifford R. Jack +11 more
TL;DR: Self-reported head trauma with at least momentary loss of consciousness or memory was associated with greater amyloid deposition, suggesting that head trauma may be associated with Alzheimer disease–related neuropathology.
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Iron Level and Myelin Content in the Ventral Striatum Predict Memory Performance in the Aging Brain
Tineke K. Steiger,Tineke K. Steiger,Nikolaus Weiskopf,Nikolaus Weiskopf,Nico Bunzeck,Nico Bunzeck +5 more
TL;DR: It is shown, that age-related high levels of iron are accompanied by a negative correlation of iron and myelin in the ventral striatum, which predicted individual memory performance, and suggests that ventral Striatum iron accumulation is linked to demyelination and impairments in declarative memory.
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Multimodal imaging improves brain age prediction and reveals distinct abnormalities in patients with psychiatric and neurological disorders.
Jaroslav Rokicki,Jaroslav Rokicki,Thomas Wolfers,Thomas Wolfers,Wibeke Nordhøy,Natalia Tesli,Daniel Quintana,Daniel Quintana,Dag Alnæs,Geneviève Richard,Ann-Marie Glasø de Lange,Ann-Marie Glasø de Lange,Ann-Marie Glasø de Lange,Martina J. Lund,Linn B. Norbom,Linn B. Norbom,Ingrid Agartz,Ingrid Melle,Terje Nærland,Geir Selbæk,Geir Selbæk,Karin Persson,Jan Egil Nordvik,Emanuel Schwarz,Ole A. Andreassen,Ole A. Andreassen,Tobias Kaufmann,Lars T. Westlye,Lars T. Westlye +28 more
TL;DR: In this paper, the authors implemented a multimodal model to estimate brain age using different combinations of cortical area, thickness and sub-cortical volumes, cortical and sub cortical T1/T2-weighted ratios, and cerebral blood flow (CBF) based on arterial spin labeling.
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Regional brain shrinkage over two years: Individual differences and effects of pro-inflammatory genetic polymorphisms
Ninni Persson,Paolo Ghisletta,Cheryl L. Dahle,Andrew R. Bender,Yiqin Yang,Peng Yuan,Ana M. Daugherty,Naftali Raz +7 more
TL;DR: The results replicate the pattern of brain shrinkage observed in previous studies, with a notable exception of the LPFC, thus casting doubt on the unique importance of prefrontal cortex in aging.
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Chemical inducers and transcriptional markers of oligodendrocyte differentiation
Lara Joubert,Isabelle Foucault,Yves Sagot,Lilia Bernasconi,François Duval,Chantal Alliod,Marie-José Frossard,Rosanna Pescini Gobert,Marie-Laure Curchod,Catherine Salvat,Anthony Nichols,Sandrine Pouly,Christian Rommel,Arthur Roach,Rob Hooft van Huijsduijnen +14 more
TL;DR: It is confirmed the view that ErbB2 is a natural signaling component that is required for OPC proliferation, whereas Erb B2 inhibition or genetic knockdown results in OPC differentiation.
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.