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Connecting mechanism of proteotoxicity: from worm to mouse
Author(s) -
Dillin Andrew
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.lb213
Subject(s) - proteotoxicity , mechanism (biology) , biology , disease , evolvability , scope (computer science) , neuroscience , protein aggregation , medicine , microbiology and biotechnology , evolutionary biology , computer science , philosophy , epistemology , pathology , programming language
The greatest risk factor for nearly all neurodegenerative diseases is aging. The central hypothesis of our work is that continual production of aggregation prone proteins eventually leads to age onset proteotoxicity and disease. The key area of research to address is to understand the molecular mechanisms that prevent proteotoxicity during early life that become compromised with age. To address this question, I will present our results in C. elegans that point towards a protective disaggregation activity and a protective aggregation activity that are regulated by the aging program. Next, I will describe our work in which we have discovered the same protective mechanisms exist in mammals. Finally, I will broaden the scope of my presentation to illustrate that other pathways of aging also regulate age onset proteotoxicity in simple and more complex model systems such as C. elegans and mice and elaborate their mechanism of action.