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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The connectomics of brain disorders
TL;DR: This work considers how brain-network topology shapes neural responses to damage, highlighting key maladaptive processes and the resources and processes that enable adaptation, and shows how knowledge of network topology allows for predictive models of the spread and functional consequences of brain disease.
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The Cellular Phase of Alzheimer’s Disease
TL;DR: Evidence supporting a long, complex cellular phase consisting of feedback and feedforward responses of astrocytes, microglia, and vasculature is reviewed.
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Intramuscular desferrioxamine in patients with Alzheimer's disease
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White matter characterization with diffusional kurtosis imaging.
TL;DR: A physically meaningful interpretation of DKI metrics in white matter regions consisting of more or less parallel aligned fiber bundles is provided by modeling the tissue as two non-exchanging compartments, the intra-axonal space and extra-AXonal space.
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Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer's Disease.
Wei Ting Chen,Wei Ting Chen,Ashley Lu,Ashley Lu,Katleen Craessaerts,Katleen Craessaerts,Benjamin Pavie,Carlo Sala Frigerio,Carlo Sala Frigerio,Carlo Sala Frigerio,Nikky Corthout,Xiaoyan Qian,Jana Lalakova,Malte Kühnemund,Iryna Voytyuk,Iryna Voytyuk,Leen Wolfs,Leen Wolfs,Renzo Mancuso,Renzo Mancuso,Evgenia Salta,Evgenia Salta,Sriram Balusu,Sriram Balusu,An Snellinx,An Snellinx,Sebastian Munck,Aleksandra Jurek,José Fernández Navarro,Takaomi C. Saido,Inge Huitinga,Inge Huitinga,Joakim Lundeberg,Mark Fiers,Mark Fiers,Mark Fiers,Bart De Strooper,Bart De Strooper,Bart De Strooper +38 more
TL;DR: Genome-wide spatial transcriptomics analysis provides an unprecedented approach to untangle the dysregulated cellular network in the vicinity of pathogenic hallmarks of AD and other brain diseases.
References
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Is there remyelination during aging of the primate central nervous system
Alan Peters,Claire Sethares +1 more
TL;DR: Support for the proposal that remyelination is occurring in the aging cerebral cortex of the monkey, short internodal lengths of myelin have been found in the nerve bundles passing through the cortices of old monkeys and inappropriately thin sheaths occur around some axons.
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Beneficial effects of pioglitazone on cognitive impairment in MPTP model of Parkinson's disease
TL;DR: Chronic administration of pioglitazone in MPTP-lesioned rats improved cognitive performance in passive avoidance task and cued version of the Morris water maze test and reduced oxidative stress.
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Phospholipid composition and levels are altered in Down syndrome brain.
TL;DR: The results suggest either a decrease in membrane phospholipids due to a loss of dendrites and dendritic spines, or a general defect in brain lipid metabolism in older DS subjects, likely are related to the Down syndrome condition rather than to Alzheimer neuropathology.
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Absence of functional peroxisomes from mouse CNS causes dysmyelination and axon degeneration
Leen Hulshagen,Olga Krysko,Astrid Bottelbergs,Steven Huyghe,Rüdiger Klein,Paul P Van Veldhoven,Peter P. De Deyn,Rudi D'Hooge,Dieter Hartmann,Myriam Baes +9 more
TL;DR: It is reported that a substantial fraction of the latter Nes-Pex5 knock-out mice survive into adulthood but develop progressive motoric and coordination problems, impaired exploration, and a deficit in cognition and die before the age of 6 months.
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In vivo actions of fibroblast growth factor-2 and insulin-like growth factor-I on oligodendrocyte development and myelination in the central nervous system.
TL;DR: In vivo evidence is provided that FGF‐2 and IGF‐I control the numbers of oligodendrocytes in the brain and, respectively, retard and promote myelination.