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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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Recent advances in brain cholesterol dynamics : transport, domains, and alzheimer's disease

TL;DR: Recent contributions to the understanding of brain cholesterol dynamics are examined, focusing on extracellular and intracellular lipid carrier proteins, membrane cholesterol domains, and emerging evidence linking an association between cholesterol dynamics and Alzheimer's disease.
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BACE1 gene deletion: impact on behavioral function in a model of Alzheimer's disease.

TL;DR: Results suggest that while excess Abeta is functionally pathological, BACE1-mediated processing of APP and other substrates play a role in "normal" learning, memory and sensorimotor processes.
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Rosiglitazone Treatment Prevents Mitochondrial Dysfunction in Mutant Huntingtin-expressing Cells: POSSIBLE ROLE OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR-γ (PPARγ) IN THE PATHOGENESIS OF HUNTINGTON DISEASE*

TL;DR: Evidence indicates that PPARγ activation by rosiglitazone attenuates mitochondrial dysfunction in mutant huntingtin-expressing striatal cells, and this could be an important therapeutic avenue to ameliorate the mitochondrial dysfunction that occurs in HD.
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Serotonin stimulates mitochondrial transport in hippocampal neurons

TL;DR: It is shown that the neuromodulator serotonin (5-HT) greatly enhances mitochondrial movement in the axons of rat hippocampal neurons in vitro and suggests that 5-HT may mediate the redistribution of energy sources within responsive neurons.
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Insulin-like growth factor I (IGF-I) and cognitive decline in older persons.

TL;DR: It is suggested that IGF-I levels below 9.4 nmol/l are negatively associated with both the level and decline of information processing speed.
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