Cited by 239Alzheimer's disease research and treatmentsAutophagy in Disease and TherapyMitochondrial Function and Pathology

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Nicotinamide forestalls pathology and cognitive decline in Alzheimer mice: evidence for improved neuronal bioenergetics and autophagy procession

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Liu, Dong, Pitta, Michael, Jiang, Haiyang, Lee, Jong-Hwan, Zhang, Guofeng, Chen, Xinzhi, Kawamoto, Elisa M., Mattson, Mark P.·2013·Neurobiology of Aging

DOI 10.1016/j.neurobiolaging.2012.11.020PMC PMC3596471

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Abstract

Impaired brain energy metabolism and oxidative stress are implicated in cognitive decline and the pathologic accumulations of amyloid β-peptide (Aβ) and hyperphosphorylated tau in Alzheimer's disease (AD). To determine whether improving brain energy metabolism will forestall disease progress in AD, the impact of the β-nicotinamide adenine dinucleotide precursor nicotinamide on brain cell mitochondrial function and macroautophagy, bioenergetics-related signaling, and cognitive performance were studied in cultured neurons and in a mouse model of AD. Oxidative stress resulted in decreased mitochondrial mass, mitochondrial degeneration, and autophagosome accumulation in neurons. Nicotinamide preserved mitochondrial integrity and autophagy function, and reduced neuronal vulnerability to oxidative/metabolic insults and Aβ toxicity. β-Nicotinamide adenine dinucleotide biosynthesis, autophagy, and phosphatidylinositol-3-kinase signaling were required for the neuroprotective action of nicotinamide. Treatment of 3xTgAD mice with nicotinamide for 8 months resulted in improved cognitive performance, and reduced Aβ and hyperphosphorylated tau pathologies in hippocampus and cerebral cortex. Nicotinamide treatment preserved mitochondrial integrity, and improved autophagy-lysosome procession by enhancing lysosome/autolysosome acidification to reduce autophagosome accumulation. Treatment of 3xTgAD mice with nicotinamide resulted in elevated levels of activated neuroplasticity-related kinases (protein kinase B [Akt] and extracellular signal-regulated kinases) and the transcription factor cyclic adenosine monophosphate (AMP) response element-binding protein in the hippocampus and cerebral cortex. Thus, nicotinamide suppresses AD pathology and cognitive decline in a mouse model of AD by a mechanism involving improved brain bioenergetics with preserved functionality of mitochondria and the autophagy system.

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Authors: Liu, D., Pitta, M., Jiang, H., Lee, J.-H., Zhang, G., Chen, X., Kawamoto, E. M., & Mattson, M. P.
Affiliations: National Institute on Aging (US)
Konkuk University (KR)
National Institutes of Health (US)
Corresponding author: Mattson, Mark P.
ORCID: Liu, Dong
Jiang, Haiyang
Zhang, Guofeng
Chen, Xinzhi
Kawamoto, Elisa M.
Mattson, Mark P.
Venue: Neurobiology of Aging
Publisher: Elsevier BV
Published: 2013-06
Volume: 34
Issue: 6
Pages: 1564-1580
ISSN: 0197-4580 (ISSN-L)
DOI: 10.1016/j.neurobiolaging.2012.11.020
PMC: PMC3596471
OpenAlex: W1996656477
Cited by: 238
References: 101
Citations by year: 2026: 11 · 2025: 29 · 2024: 23 · 2023: 19 · 2022: 21 · 2021: 37 · 2020: 16 · 2019: 17 · 2018: 17 · 2017: 13 · 2016: 10 · 2015: 10 · 2014: 8 · 2013: 7
FWCI: 5.36
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Aging (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Intramural Research Program of the National Institute on Aging
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: nicotinamide, Alzheimer's disease, brain energy metabolism, mitochondrial function, autophagy, oxidative stress, amyloid-beta, hyperphosphorylated tau, 3xTg-AD mice, cognitive decline, phosphatidylinositol 3-kinase signaling, AMPK, lysosomal acidification, neuroprotection, hippocampus
MeSH terms: Alzheimer Disease, Animals, Autophagy, Cells, Cultured, Cognition Disorders, Disease Models, Animal, Energy Metabolism, Mice, Inbred C57BL, Mice, Transgenic, Neurons, Niacinamide, Vitamin B Complex, Oxidative Stress, Mice, Rats

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Nicotinamide forestalls pathology and cognitive decline in Alzheimer mice: evidence for improved neuronal bioenergetics and autophagy procession

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