A study published in the Journal of Neuroscience (2008 Nov 5;28(45):11500–11510) examined the effects of nicotinic acid (vitamin B3) in a mouse model genetically engineered to develop Alzheimer’s-like pathology. The researchers compared three groups: transgenic mice given nicotinic acid in their drinking water, transgenic mice that received no supplementation, and a group of normal (non–disease-model) mice.
After four months, the mice receiving nicotinic acid showed increased levels of proteins involved in stabilizing neuronal microtubules—structures essential for maintaining normal nerve cell function. The supplemented mice also demonstrated reduced accumulation of phosphorylated tau, a protein strongly associated with neurofibrillary tangles in Alzheimer’s disease.
Functionally, the untreated transgenic mice developed significant memory impairment. In contrast, the transgenic mice receiving nicotinic acid performed memory tasks comparably to the normal control mice, suggesting preservation of cognitive function in this animal model.
While this study does not establish clinical benefit in humans, it suggests that vitamin B3 may influence pathways involved in neuronal structure and tau-related pathology. These findings support further investigation into the role of niacin and related metabolic pathways in neurodegenerative disease
