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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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
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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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Plasmalogen metabolism-related enzymes in rat brain during aging: influence of n-3 fatty acid intake.
TL;DR: The increase of brain Pls content in the first part of the life may be related to the high increase of DHAP-AT activity, probably stimulated by DHA, and dietary DHA may not oppose the physiologic aging.
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Cellular and subcellular localizations of nonheme ferric and ferrous iron in the rat brain: a light and electron microscopic study by the perfusion-Perls and -Turnbull methods.
TL;DR: With advancing age, both Fe(III) and Fe(II) became more extensively distributed and accumulated more numerously in oligodendrocytes and astrosol, suggesting that age-related increases in Fe( II) accumulation may raise the risk of tissue damage in the normal brain.
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Age-related changes in the proportion of amyloid precursor protein mRNAs in Alzheimer's disease and other neurological disorders.
Seigo Tanaka,Li Liu,Jun Kimura,Satoshi Shiojiri,Yasuyuki Takahashi,Nobuya Kitaguchi,Shigenobu Nakamura,Kunihiro Ueda +7 more
TL;DR: It is found that the ratio of (APP770 mRNA+APP751 mRNA)/APP695 mRNA in the frontal cortex increased approximately 1.5-fold in AD compared with other neurodegenerative or cerebrovascular disorders, which led to the idea that a relative increase in KPI-harboring APPs over a K PI-lacking APP may perturb normal degradation of APPs, thereby leading to deposition of beta A4 protein as amyloid.
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Abnormal expression of neurofilament proteins in dysmyelinating axons located in the central nervous system of jimpy mutant mice.
Takahiro Gotow,Jean François Leterrier,Yoshiyuki Ohsawa,Tsuyoshi Watanabe,Kyoko Isahara,Riichi Shibata,Kazuhiro Ikenaka,Yasuo Uchiyama +7 more
TL;DR: The results suggest that myelination regulates both the expression and phosphorylation of neurofilament proteins, and is essential for the cytoplasmic organization of myelinated axons.
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Overcoming failure to repair demyelination in EAE: γ-secretase inhibition of Notch signaling
TL;DR: The results suggest that inhibiting the non-myelin permissive environment maintained by Notch pathways within the mature CNS offers a new strategy for treating autoimmune demyelination, including MS.