Valter D. Longo (born October 9, 1967) is an Italian-American bio-gerontologist and cell biologist known for his studies on the role of starvation and nutrient response genes on cellular protection aging and diseases and for proposing that longevity is regulated by similar genes and mechanisms in many eukaryotes. He is currently a professor at the USC Davis School of Gerontology with a joint appointment in the department of Biological Sciences as well as serving as the director of the USC Longevity Institute.
Originally from Genoa, Italy, Valter Longo attended the University of North Texas majoring in Biochemistry.
In 1992 he joined the laboratory of “calorie restriction” pioneer Roy Walford at UCLA where he studied calorie restriction and aging of the immune system. He completed his PhD work in Biochemistry studying antioxidant enzymes and anti-aging genes under Joan Valentine at UCLA in 1997 and his postdoctoral training in the neurobiology of Alzheimer’s disease under Caleb Finch at the University of Southern California.
Since 1997 he has been a faculty member at the USC Davis School of Gerontology and Ethel Percy Andrus Gerontology Center.
In his 1997 doctoral thesis he described a new way to study aging in Saccharomyces cerevisiae (chronological life span) and described in parallel with the work of others in Caenorhabditis elegans the first aging regulatory pathway which, in yeast, involved Ras, adenylate cyclase and protein kinase A, protective transcription factors and antioxidant enzymes.
In 2001, he led the USC team that discovered that inhibition of the growth stimulating Mammalian target of rapamycin/S6 kinase pathway by deletion of the SCH9 gene caused a 3-fold life span extension in yeast. Analogous genes including adenylate cyclase, PKA, Tor and S6K were recently shown to regulate also aging in mice.
In 2008 the Longo laboratory showed that inactivation of the Tor-S6K and Ras-PKA pathways is responsible for a major portion of the effects of calorie restriction on life span and together with calorie restriction causes a 10 fold life span extension in S. cerevisiae.