Open AccessAtypical antidepressants extend lifespan of Caenorhabditis elegans by activation of a non‐cell‐autonomous stress response
Author(s) -
Rangaraju Sunitha,
Solis Gregory M.,
Andersson Sofia I.,
GomezAmaro Rafael L.,
Kardakaris Rozina,
Broaddus Caroline D.,
Niculescu Alexander B.,
Petrascheck Michael
Publication year - 2015
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/acel.12379
Subject(s) - oxidative stress , caenorhabditis elegans , biology , mechanism (biology) , reactive oxygen species , oxidative phosphorylation , neuroscience , microbiology and biotechnology , pharmacology , genetics , endocrinology , biochemistry , gene , philosophy , epistemology
Summary Oxidative stress has long been associated with aging and has recently been linked to psychiatric disorders, including psychosis and depression. We identified multiple antipsychotics and antidepressants that extend Caenorhabditis elegans lifespan and protect the animal from oxidative stress. Here, we report that atypical antidepressants activate a neuronal mechanism that regulates the response to oxidative stress throughout the animal. While the activation of the oxidative stress response by atypical antidepressants depends on synaptic transmission, the activation by reactive oxygen species does not. Lifespan extension by atypical antidepressants depends on the neuronal oxidative stress response activation mechanism. Neuronal regulation of the oxidative stress response is likely to have evolved as a survival mechanism to protect the organism from oxidative stress, upon detection of adverse or dangerous conditions by the nervous system.