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Open AccessJournal ArticleDOI

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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Symmetric temporal abnormalities on MR imaging in amyotrophic lateral sclerosis with dementia.

TL;DR: A symmetric pattern of frontotemporal atrophy and anteromedial subcortical hyperintensities in the temporal lobes on T2WI could be characteristic of ALSD.
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Cytoskeletal transition at the paranodes: the Achilles' heel of myelinated axons.

TL;DR: A model in which the myelinated axons depend on the axon-glial junctions to stabilize the cytoskeletal transition at the paranodes, which is likely to be particularly susceptible to damage induced by demyelinating diseases such as multiple sclerosis is proposed.
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Formation of amyloid-β oligomers in brain vascular smooth muscle cells transiently exposed to iron-induced oxidative stress

TL;DR: In this paper, the authors studied cellular accumulation of amyloid-β peptide (Aβ) processing in vascular smooth muscle cells during recovery after exposure to ferrous ions using cells cultured from Tg2576 mice.
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Paul Flechsig’s System of Myelogenetic Cortical Localization In the Light of Recent Research in Neuroanatomy and Neurophysiology Part II

TL;DR: In man, too, the motor centers of the type of Fritsch and Hitzig are restricted to the precentral gyrus and the immediately adjacent part of the first frontal convolution, and the central sulcus here too is the posterior boundary of the motor zone.
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