Reference - Detail
|Author||Rangaraju S, Solis GM, Andersson SI, Gomez-Amaro RL, Kardakaris R, Broaddus CD, Niculescu AB 3rd, Petrascheck M.|
|Title||Atypical antidepressants extend lifespan of Caenorhabditis elegans by activation of a non-cell-autonomous stress response.|
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.
|MeSH||Aging / drug effects* Aging / physiology Animals Antidepressive Agents, Second-Generation / pharmacology* Caenorhabditis elegans / physiology* Caenorhabditis elegans Proteins / metabolism Catalase / metabolism Fluoxetine / pharmacology Histamine H1 Antagonists / pharmacology Life Expectancy* Longevity / drug effects* Longevity / physiology Mianserin / analogs & derivatives Mianserin / pharmacology Oxidative Stress / drug effects* Peroxiredoxins / metabolism Reactive Oxygen Species / metabolism Serotonin Antagonists / pharmacology Serotonin Uptake Inhibitors / pharmacology Superoxide Dismutase / metabolism Synaptic Transmission / drug effects|
|WOS Category||GERIATRICS & GERONTOLOGY CELL BIOLOGY|
|C.elegans||tm776 tm760 tm1146|