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
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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Prefrontal white matter volume is disproportionately larger in humans than in other primates
TL;DR: Using magnetic resonance imaging brain scans from 11 primate species, gray, white and total volumes for both prefrontal and the entire cerebrum on each specimen suggest that connectional elaboration played a key role in human brain evolution.
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A Systems Level Analysis of Transcriptional Changes in Alzheimer's Disease and Normal Aging
TL;DR: The transcriptional network in AD was characterized, identifying 12 distinct modules related to synaptic and metabolic processes, immune response, and white matter, nine of which were related to disease progression, and presenilin 1 (PSEN1) is highly coexpressed with canonical myelin proteins, suggesting a role for PSEN1 in aspects of glial-neuronal interactions related to neurodegenerative processes.
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Concurrence of TDP-43, tau and α-synuclein pathology in brains of Alzheimer's disease and dementia with Lewy bodies
Shinji Higashi,Eizo Iseki,Ryoko Yamamoto,Michiko Minegishi,Hiroaki Hino,Koshiro Fujisawa,Takashi Togo,Omi Katsuse,Hirotake Uchikado,Yoshiko Furukawa,Kenji Kosaka,Heii Arai +11 more
TL;DR: This study will provide a more in-depth understanding of the various pathogenic pathways leading to neurodegenerative disorders and suggest that TDP-43 pathology found in this study may be related in some way to AD and LB pathology.
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Overexpression of Alzheimer's Disease Amyloid-β Opposes the Age-dependent Elevations of Brain Copper and Iron
Christa J. Maynard,Roberto Cappai,Roberto Cappai,Irene Volitakis,Robert A. Cherny,Robert A. Cherny,Anthony R. White,Anthony R. White,Konrad Beyreuther,Colin L. Masters,Colin L. Masters,Ashley I. Bush,Ashley I. Bush,Ashley I. Bush,Qiao-Xin Li,Qiao-Xin Li +15 more
TL;DR: It is demonstrated that overexpression of the carboxyl-terminal fragment of APP, containing Aβ, results in significantly reduced copper and iron levels in transgenic mouse brain, while overexposure of the APP in Tg2576 transgenic mice results inificantly reduced copper, but not iron, levels prior to the appearance of amyloid neuropathology and throughout the lifespan of the mouse.
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Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans.
Kunihiro Uryu,Xiao-Han Chen,Daniel Martinez,Kevin D. Browne,Victoria E. Johnson,David I. Graham,Virginia M.-Y. Lee,John Q. Trojanowski,Douglas H. Smith +8 more
TL;DR: Brain tissue from 18 cases who died after TBI and from 6 control cases was examined using immunohistochemistry to show rapid axonal accumulation of proteins implicated in neurodegenerative diseases including Alzheimer's disease and the synucleinopathies.