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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Temporal memory deficits in Alzheimer's mouse models: rescue by genetic deletion of BACE1.
Masuo Ohno,Lei Chang,Wilbur Tseng,Holly Oakley,Martin Citron,William L. Klein,Robert Vassar,John F. Disterhoft +7 more
TL;DR: Trace fear conditioning is a useful assay to test the mechanisms and therapeutic interventions for Aβ‐dependent deficits in temporal associative memory and suggests that lowering soluble Aβ oligomers by inhibiting BACE1 may be beneficial for alleviating cognitive disorders in AD.
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Iron in Chronic Brain Disorders: Imaging and Neurotherapeutic Implications
TL;DR: This article focuses on the imaging of brain iron and the underlying physiology and metabolism relating to iron deposition and the potential implications of iron-related toxicity to neurotherapeutic development.
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Remyelination occurs as extensively but more slowly in old rats compared to young rats following gliotoxin-induced CNS demyelination.
TL;DR: It is shown that remyelination of lysolecithin‐induced demyelinations in the spinal white matter of old adult rats can be extensive, with longer survival times than have previously been examined, indicating that remYelination need not occur rapidly for it to be extensive.
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The Drosophila beta-amyloid precursor protein homolog promotes synapse differentiation at the neuromuscular junction.
TL;DR: It is shown that APPL was transported to motor axons and that its overexpression caused a dramatic increase in synaptic bouton number and changes in synapse structure, and a model by which APPL, in conjunction with activity-dependent mechanisms, regulates synaptic structure and number is proposed.