The inhibition of IGF-1 signaling promotes proteostasis by enhancing protein aggregation and deposition

• Published in: The FASEB journal Vol. 30; no. 4; p. 1656
• Main Authors: Moll, Lorna, Ben-Gedalya, Tziona, Reuveni, Hadas, Cohen, Ehud
• Format: Journal Article
• Language: English
• Published: United States 01.04.2016
• Subjects: Amyloid beta-Peptides - antagonists & inhibitors; Amyloid beta-Peptides - metabolism; Animals; Blotting, Western; Caenorhabditis elegans - drug effects; Caenorhabditis elegans - metabolism; Cell Line, Tumor; Cells, Cultured; CHO Cells; Cricetinae; Cricetulus; Gene Expression - drug effects; Homeostasis - drug effects; Homeostasis - physiology; Insulin-Like Growth Factor I - metabolism; Mice; Molecular Chaperones - genetics; Molecular Chaperones - metabolism; Neurodegenerative Diseases - metabolism; NIH 3T3 Cells; Organic Chemicals - pharmacology; PC12 Cells; Prions - antagonists & inhibitors; Prions - metabolism; Proteasome Endopeptidase Complex - metabolism; Proteins - metabolism; Pyrogallol - analogs & derivatives; Pyrogallol - pharmacology; Rats; Reverse Transcriptase Polymerase Chain Reaction; Signal Transduction - drug effects; Signal Transduction - physiology; Thioamides - pharmacology; neurodegeneration; chaperones; aggresome; protein degradation

The discovery that the alteration of aging by reducing the activity of the insulin/IGF-1 signaling (IIS) cascade protects nematodes and mice from neurodegeneration-linked, toxic protein aggregation (proteotoxicity) raises the prospect that IIS inhibitors bear therapeutic potential to counter neurode...