Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity

Nature

Volumn 552, Issue 7684, 2017, Pages 187-193

  Sorrentino, Vincenzo ^a   Romani, Mario ^a   Mouchiroud, Laurent ^a   Beck, John S ^b   Zhang, Hongbo ^a   D'Amico, Davide ^a   Moullan, Norman ^a   Potenza, Francesca ^a   Schmid, Adrien W ^a   Rietsch, Solène ^a   Counts, Scott E ^b   Auwerx, Johan ^a  

^a EPFL   (Switzerland)

^b MICHIGAN STATE UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID BETA PROTEIN; MITOCHONDRIAL PROTEIN; NICOTINAMIDE; NICOTINAMIDE ADENINE DINUCLEOTIDE; NICOTINAMIDE-BETA-RIBOSIDE;

CELLS AND CELL COMPONENTS; EXPERIMENTAL STUDY; INDUCED RESPONSE; MOLECULAR ANALYSIS; NERVOUS SYSTEM DISORDER; PEPTIDE; PROTEIN; PROTEOMICS; RODENT; TOXICITY;

ALZHEIMER DISEASE; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; BIOINFORMATICS; CELL STRESS; CONTROLLED STUDY; FITNESS; HUMAN; HUMAN TISSUE; LIFESPAN; MALE; MITOCHONDRION; MITOPHAGY; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN HOMEOSTASIS; TRANSLATION REGULATION; ANALOGS AND DERIVATIVES; ANIMAL; CAENORHABDITIS ELEGANS; DISEASE MODEL; DRUG EFFECT; GENETICS; HOMEOSTASIS; MEMORY; METABOLISM; OXIDATIVE PHOSPHORYLATION; PATHOLOGY; PHYSIOLOGY; PROTEIN SYNTHESIS; PROTEINOSIS; TRANSGENIC MOUSE; UNFOLDED PROTEIN RESPONSE;

CAENORHABDITIS ELEGANS; MUS MUSCULUS;

ALZHEIMER DISEASE; AMYLOID BETA-PEPTIDES; ANIMALS; CAENORHABDITIS ELEGANS; DISEASE MODELS, ANIMAL; HOMEOSTASIS; HUMANS; MALE; MEMORY; MICE; MICE, TRANSGENIC; MITOCHONDRIA; MITOCHONDRIAL DEGRADATION; NAD; NIACINAMIDE; OXIDATIVE PHOSPHORYLATION; PROTEIN AGGREGATION, PATHOLOGICAL; PROTEIN BIOSYNTHESIS; PROTEOSTASIS; UNFOLDED PROTEIN RESPONSE;

EID: 85038255288     PISSN: 00280836     EISSN: 14764687     Source Type: Journal    
DOI: 10.1038/nature25143     Document Type: Article

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