In recent years, cell senescence has fallen into the biomedical limelight, with these ‘zombie cells’ serving up a rich source of opportunities for innovative therapeutic development in aging and age-related diseases.

An in-depth look into cell senescence and how these zombie cells contribute to developments in age-related diseases and aging.

Researchers fight off childhood neurodegenerative disease characteristics rooted in NAD+ deficiency, mitochondrial damage, and senescence

Boosting NAD+ levels helps stave off childhood neurodegenerative disease rooted in NAD+ deficiency, senescence, and mitochondrial damage.

Longevity

Nanocrystals with nicotinamide riboside and resveratrol enhance NAD+ levels in mouse organs

NAD+ boosting nanocrystals containing nicotinamide riboside and resveratrol help with heart damage and dysfunction following injury in mice.

Cardiovascular

Boosting NAD+ after injury suppresses tissue damage and scarring.

NMN boosts NAD+ levels to reduce DNA damage and subsequent kidney tissue scarring in mice with potential translatability to people.

Others

This indicator can facilitate research and clinical trials of drugs that target age-related diseases

An indicator to evaluate drugs that target aged cells can help with research for anti-aging and age-related disease purposes.

Supplementing with the antioxidant precursor combination provides a simple and effective means to enhance human health.

Supplementing with the antioxidant precursors in GlyNAC reduces oxidative stress and improves physical and cognitive function in aged adults.

Increasing NAD+ levels could represent a promising and safe therapeutic strategy for chemotherapy medicine-related neurotoxicity

Cisplatin chemotherapy-induced cognitive impairment from neurotoxicity is ameliorated with NAD+-boosting nicotinamide mononucleotide (NMN).

Cancer

A drug cocktail reduces brain inflammation and improves cognitive function in aged mice

A drug cocktail reduces brain inflammation by eliminating aged, non-proliferating cells to improve cognitive function in aged mice.

Neurological

Stimulating a longevity-linked protein with nicotinamide mononucleotide (NMN) reduces tissue scarring progression and subsequent kidney disease.

Stimulating the SIRT1 protein with nicotinamide mononucleotide (NMN) attenuates the progression of kidney scarring by diminishing the activity of the HIF-2a protein.

This plant-derived molecule may be beneficial in age-related neurological disorders

The plant-derived molecule fisetin improves oxidative stress-induced cognitive dysfunction in mice.

Nicotinamide mononucleotide (NMN) reduces heart scarring to restore the blood-pumping organ’s size and thickness in mice

Treatment with the NAD+ boosting molecule called NMN alleviates heart enlargement and blood pumping capabilities in chemically-induced heart scarring.

Rats with increased blood pressure and stroke predisposition have decreased NAD+ levels

NMN supplementation stimulates a cell damage cleanup process called autophagy to increase the survival of stroke-prone rats.

Quercetin enhances blood vessel generation and reduces heart fat accumulation in mice.

Quercetin treatment improves fatty diet-induced heart function in mice by stimulating blood vessel generation.

Sirtuin proteins are not required for the NAD+ precursor nicotinamide riboside to enhance liver regeneration

Liver regeneration does not require sirtuin proteins for liver regeneration, and boosting NAD+ with its precursor NR suffices to regenerate the liver.

Dr. Dudley Lamming discusses how restricting protein building blocks called branch chain amino acids extends male but not female mouse lifespan and the potential application to human diets.

Dr. Dudley Lamming discusses his group's study of low branch chain amino acid dietary restrictions extending male but not female healthy mouse lifespan.

Studies

NEWS

NMN Alleviates Kidney Tissue Scarring in Rodents

NMN Improves Mouse Heart Dysfunction Caused by Scarring

Study Shows NMN Delays Stroke in Rodents

Dr. Dudley Lamming on Dietary Restriction of Branch Chain Amino Acids Extending Male Mouse Lifespan