Nicotinamide mononucleotide (NMN) supplementation rescues cerebromicro

DesignPreclinical intervention study in aged mice with in-vivo neurovascular and cognitive testing plus endothelial-cell experiments

Population24-month-old C57BL/6 mice and aged-derived cerebromicrovascular endothelial cells

SampleMultiple aged and control mouse cohorts; see publication

InterventionNMN supplementation for 2 weeks in aged mice

EndpointsNeurovascular coupling and cerebral blood-flow responses; Endothelial nitric-oxide-mediated dilation; Spatial working memory; Gait coordination; Mitochondrial reactive oxygen species and bioenergetics

What the publication reported

This study tested short-term NMN supplementation in very old mice to examine age-related neurovascular dysfunction.

NMN improved neurovascular-coupling responses and endothelial function in the aged mice and was associated with better spatial working-memory and gait measures. Cell experiments supported mitochondrial and oxidative-stress mechanisms.

The results are preclinical. Improved cognitive tests in aged mice do not establish that NMN prevents cognitive decline or vascular dementia in people.

Key findings

Neurovascular-coupling responses improved in NMN-treated aged mice.
Endothelial nitric-oxide-mediated vasodilation improved.
Spatial working-memory and gait-coordination measures improved in the mouse model.
Mitochondrial oxidative-stress and bioenergetic measures were altered in supporting cell experiments.

What it cannot establish

Mouse aging model only.
Cognitive tasks in mice are not equivalent to human cognitive outcomes.
Two-week intervention does not address long-term effects.
Mechanistic cell findings and animal behavior cannot establish prevention or treatment of human cognitive impairment.

HealthspanX claim boundary: This study does not establish that NMN prevents cognitive decline, improves memory in humans, or treats vascular cognitive impairment or dementia.

Source identifiers

DOI: 10.1016/j.redox.2019.101192
PubMed: PMID 31015147
Trial registration: Not applicable.
Publication type: Preclinical animal study
Publication: Redox Biology, 2019. 24:101192

Transparency

Funding: Supported by grants from the American Heart Association; Oklahoma Center for the Advancement of Science and Technology; National Institute on Aging (R01-AG047879, R01-AG038747, R01-AG055395, R01-AG043483); National Institute of Neurological Disorders and Stroke (R01-NS056218, R01-NS100782); National Heart, Lung, and Blood Institute (R01-HL132553); National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK098656); the NIA-supported Oklahoma Nathan Shock Center (3P30AG050911-02S1); Oklahoma Shared Clinical and Translational Resources (GM104938); Presbyterian Health Foundation; and the NIA Geroscience Training Program (T32AG052363). David A. Sinclair was also supported by the Glenn Foundation for Medical Research and NIH grants R37 AG028730, R01 AG019719, R21 DE027490, and R01 DK100263.
Declared interests: David A. Sinclair disclosed numerous founder, equity, board, advisory, consulting, investment, and patent relationships, including MetroBiotech and other biotechnology companies; a Harvard/Mayo patent licensed to Elysium Health was also disclosed. The publication's declaration provides the complete list.

HealthspanX observation: This paper is important neurovascular mechanistic evidence but cannot be translated into a human cognition claim.

Interpretive status: Mechanistic contextAged-mouse neurovascular intervention with functional and cognitive readouts; relevant mechanistically but not evidence of human cognitive or vascular benefit.

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Source fields verified 20 September 2026