Article: CD38 Inhibitor Reverses Age-Related NAD+ Decline and Metabolic Dysfunction: Preclinical Findings

PrevNext
Mitochondrial Health Preclinical

CD38 Inhibitor Reverses Age-Related NAD+ Decline and Metabolic Dysfunction: Preclinical Findings

Synopsis

Aging is characterized by the development of metabolic dysfunction and frailty. Recent studies show that a reduction in nicotinamide adenine dinucleotide (NAD+) is a key factor for the development of age-associated metabolic decline. The enzyme CD38, which breaks down NAD+, plays a key role in this decline. Using a powerful, specific CD38 inhibitor called 78c, researchers reversed age-related NAD+ loss in mice and improved metabolic health markers such as glucose tolerance, muscle and heart function, and exercise ability. The benefits depended on NAD+ levels and were blocked if NAD+ synthesis was inhibited. Increased NAD+ activated longevity-related proteins (sirtuins, AMPK, PARPs) and suppressed pathways that harm health span (mTOR-S6K, ERK). Additionally, DNA damage linked to aging was reduced. This suggests targeting CD38 to maintain NAD+ is a promising way to prevent or reverse aging-related metabolic decline.

Journal

Cell Metabolism

Share

Read more

Alzheimer's Disease

The Effects of NAD+ Boosting in Mitochondrial DNA Depletion Syndrome: Preclinical Findings

Synopsis Patients with mtDNA depletion syndrome 3 (MTDPS3) often die young from liver failure due to severely reduced mitochondrial DNA. Research into treatments has been difficult because MTDPS3 ...

Read more
Healthy Aging & Longevity

Muscle Loss and Reduced Physical Performance in Emery–Dreifuss Muscular Dystrophy: Preclinical Findings

Synopsis Autosomal Emery–Dreifuss muscular dystrophy (EDMD) is caused by mutations in the lamin A/C gene (LMNA), which encodes nuclear envelope proteins. The disease typically causes muscle wastin...

Read more