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
TL;DR: In this paper, a single-blind study was conducted to investigate whether the progression of dementia could be slowed by the trivalent ion chelator, desferrioxamine.
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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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Long-term effects of Aβ42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial
Clive Holmes,Clive Holmes,Delphine Boche,David Wilkinson,David Wilkinson,Ghasem Yadegarfar,Ghasem Yadegarfar,Vivienne Hopkins,Antony James Bayer,Roy W. Jones,Roger Bullock,Seth Love,James Neal,Elina Zotova,James A. R. Nicoll +14 more
TL;DR: Although immunisation with Abeta(42) resulted in clearance of amyloid plaques in patients with Alzheimer's disease, this clearance did not prevent progressive neurodegeneration and there was no evidence of improved survival.
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The effect of age on the non-haemin iron in the human brain.
B Hallgren,P Sourander +1 more
TL;DR: The most extensive and systematic investigations of histologically demonstrable iron in the brain were conducted by SPATZ (1922), which found a fine granular deposit of iron in individual oligodendroglia cells and nerve cells, mainly in the globus pallidus and in the red zone of substantia nigra.
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Ubiquitin-dependent sorting into the multivesicular body pathway requires the function of a conserved endosomal protein sorting complex, ESCRT-I.
TL;DR: It is demonstrated that ubiquitination serves as a signal for sorting into the multivesicular body pathway and proposed that ESCRT-I represents a conserved component of the endosomal sorting machinery that functions in both yeast and mammalian cells to couple ubiquitin modification to protein sorting and receptor downregulation in the MVB pathway.
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The metallobiology of Alzheimer's disease.
TL;DR: Compounds that interdict metal-ion binding to Abeta dissolve brain deposits in vitro and one such compound, clioquinol, inhibits Abeta deposition in the Tg2576 mouse model for AD and could be useful clinically.
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Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease.
Gorazd B. Stokin,Concepción Lillo,Tomás L. Falzone,Richard G. Brusch,Edward Rockenstein,Stephanie L. Mount,Rema Raman,Peter Davies,Eliezer Masliah,David S. Williams,Lawrence S.B. Goldstein +10 more
TL;DR: Reductions in microtubule-dependent transport may stimulate proteolytic processing of β-amyloid precursor protein, resulting in the development of senile plaques and Alzheimer's disease.