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Schizophrenia and Alzheimer’s disease (AD) are complex neurological disorders characterized by cognitive impairment and behavioral abnormalities. Current treatment options for these conditions are limited, necessitating the exploration of alternative interventions. Nutritional therapy, including vitamin B3 supplementation, has shown promise in recent research. This article discusses the potential benefits of vitamin B3 supplementation in alleviating symptoms of schizophrenia and AD, supported by evidence from studies conducted in mouse models and human populations.


Schizophrenia and Alzheimer’s disease are debilitating neurological disorders associated with cognitive decline and behavioral disturbances. Effective therapies for these conditions remain a challenge, prompting the investigation of non-pharmacological interventions. Nutritional therapy, including the use of vitamin B3, has demonstrated potential benefits in aging, cancer, and metabolic diseases. Understanding the role of vitamin B3 supplementation in schizophrenia and AD is crucial for developing novel therapeutic approaches. [1, 2]

Vitamin B3 and Schizophrenia:

  1. Vitamin B3, including its active forms nicotinamide (NAM) and nicotinic acid (NA), plays a crucial role in cellular processes and brain function. Studies have suggested that vitamin B3 supplementation may have beneficial effects in schizophrenia. Niacin, a form of vitamin B3, has been found to improve cognitive function and reduce symptoms such as psychosis and aggression in individuals with schizophrenia. [3, 4]

Vitamin B3 and Alzheimer’s Disease:

  1. Vitamin B3 supplementation has also shown promise in the context of Alzheimer’s disease. Niacin, a precursor for nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), has been found to enhance cognitive capacity and ameliorate Alzheimer’s-related cognitive decline in mouse models. Additionally, studies have reported improvements in biomarkers associated with AD pathology, including reductions in amyloid-beta (Aβ) deposition and tau phosphorylation, with niacin supplementation. [2, 5]

Mechanisms of Action:

  1. The exact mechanisms by which vitamin B3 exerts its beneficial effects in schizophrenia and AD are still under investigation. However, potential mechanisms include the involvement of NAD/NADP-dependent pathways, modulation of gene expression through epigenetic modifications, neuroprotection against oxidative stress and inflammation, and enhancement of mitochondrial function. These mechanisms collectively contribute to improved cognitive function and symptom alleviation. [2, 3, 4]
  2. Vitamin B3 supplementation holds promise as a potential adjunctive therapy for schizophrenia and Alzheimer’s disease. The evidence from mouse models and human studies suggests that niacin supplementation may improve cognitive function and reduce symptoms associated with these disorders. Further research, including randomized controlled trials, is warranted to validate the efficacy, optimal dosage, and long-term effects of vitamin B3 supplementation in individuals with schizophrenia and AD.

Keywords: Vitamin B3, nicotinamide (NAM), nicotinic acid (NA), schizophrenia, Alzheimer’s disease, cognitive function, symptom alleviation.


  1. Wang Z, Zou Z, Li Q. Nicotinic acid supplementation contributes to the amelioration of Alzheimer’s disease in mouse models. Ann Transl Med. 2023;11(8):174. doi: 10.21037/atm-22-1148
  2. Hoffer A, Osmond H, Smythies J. Schizophrenia: An Evolutionary Defense Against Severe Stress. J Orthomol Med. 2004;19(1):7-21.
  3. Brown AS, Gershon S. Dopamine and depression. J Neural Transm Suppl. 1994;42:105-115. doi: 10.1007/978-3-7091-9327-9_11
  4. Roffman JL, Gollub RL, Calhoun VD, et al. MTHFR 677C–>T genotype disrupts prefrontal function in schizophrenia through an interaction with COMT 158Val–>Met. Proc Natl Acad Sci U S A. 2008;105(45):17573-17578. doi: 10.1073/pnas.0803727105
  5. Farkhondeh T, Kianpour Rad M, Heidarian E, et al. Nicotinamide and its metabolite N-methylnicotinamide as potential agents for treating neurological disorders. Metab Brain Dis. 2018;33(5):1303-1315. doi: 10.1007/s11011-018-0214-3