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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.
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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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Apolipoprotein E genotype and age-related myelin breakdown in healthy individuals: Implications for cognitive decline and dementia

TL;DR: In later-myelinating regions, the severity and rate of myelin breakdown in healthy older individuals are associated with APOE status and support the hypothesis that this process may contribute to age at onset of AD.
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Age-related changes in ethanolamine glycerophospholipid fatty acid levels in rat frontal cortex and hippocampus.

TL;DR: Hippocampus and frontal cortex underwent specific age-induced modifications in PmE and PE acyl composition, which could produce different effects on the functional ability of these two structures involved in the processes of specific memorization.
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