Scientists from the University of Maryland School of Medicine found nicotinamide mononucleotide (NMN) prevented cognitive impairment and loss of brain volume in diabetic rats.(fotografixx | iStock)
Diabetes increases a person’s chance of experiencing cognitive decline. Scientists have linked this effect with decreased nicotinamide adenine dinucleotide (NAD+) levels in the brain.
Researchers from the University of Maryland boosted NAD+ levels in diabetic rats with nicotinamide mononucleotide (NMN), which improved and prevented diabetes-induced cognitive impairments. The results were published in the International Journal of Molecular Sciences.
In the US, the percentage of adults affected by diabetes has risen to 9.1% in 2018 from around 6% in 2000. Increasing evidence suggests diabetes raises the risk of cognitive-decline-led dementia in animal models and humans. Scientists have associated decreased NAD+ levels in the brain with this cognitive decline. With an increasing portion of the US population with diabetes, therapeutic options for this disease become increasingly important.
The study showed that NMN administration prevents cognitive decline from diabetes along with loss of neurons in rats’ hippocampus, a region of the brain associated with memory. NMN treatment also prevented diabetes-induced reductions in SIRT1 — a protein involved in the maintenance of cellular health — and preserved the function of the cell’s powerhouse, the mitochondria.
Researchers found that the CA1 region, a specific area of the hippocampus associated with memory, had increased volume and number of neurons in diabetic rats after they received NMN treatment.
The findings demonstrated that giving diabetic rats NMN improved their cognition. Scientists tested rats’ cognitive function by a method called the “Y maze,” where animals with better cognitive functions prefer to explore new arms of the maze. Similar to normal rats, NMN-fed diabetic rats spent more time exploring the new arm than diabetic rats, indicating NMN improved cognition in diabetic rats.
Other results show that NMN improved cellular reactions involving oxygen in the cell’s powerhouse, the mitochondria. This indicated improved generation of energy through the molecule adenosine triphosphate, ATP, with NMN treatment.
The scientists said in their study that NMN compensated for the loss of NAD+ in the brain in diabetes and thereby prevented cognitive impairment and loss of neurons in the region of the brain associated with memory, the hippocampus. They also stated these results paralleled the preservation of mitochondrial function and the activation of SIRT1, a protein involved in cellular health maintenance.
“The study suggests that medications that prevent NAD+ depletion induced by diabetes mellitus and molecules that activate SIRT1 may provide a therapeutic intervention for diabetic neurodegeneration in the central nervous system,” stated the authors in their study.