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Open AccessJournal ArticleDOI

Neurodegenerative disease: A proteostatic boost.

Darran Yates
- 19 Jan 2018 - 
- Vol. 19, Iss: 2, pp 61-61
TLDR
Promoting mitochondrial proteostasis counteracts Aβ aggregation in worms and an Alzheimer disease mouse model and links to a mitochondrial stress response that may be conserved across species.
Abstract
Amyloid-β (Aβ)-induced proteotoxicity is linked to a mitochondrial stress response that may be conserved across species, and promoting mitochondrial proteostasis counteracts Aβ aggregation in worms and an Alzheimer disease mouse model.

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Citations
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Microglial priming of antigen presentation and adaptive stimulation in Alzheimer’s disease

TL;DR: The change in functionality of microglia from innate to adaptive immune response in the context of neuroprotection, which may help in the search of novel immune therapy in AD is focused on.
Journal ArticleDOI

Phagocytosis of full-length Tau oligomers by Actin-remodeling of activated microglia

TL;DR: It is suggested that microglia modified actin cytoskeleton for phagocytosis and rapid clearance of Tau oligomers in Alzheimer’s disease condition and the peri-membrane polymerization of actin filament and co-localization of Iba1 relate to the microglial movements forPhagocyTosis.
References
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Journal ArticleDOI

Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity

TL;DR: Evidence of a conserved mitochondrial stress response signature present in diseases involving amyloid-β proteotoxicity in human, mouse and Caenorhabditis elegans that involves the mitochondrial unfolded protein response and mitophagy pathways is provided.
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