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Vitamin B3 and green tea protect against Alzheimer’s disease

Vitamin B3 and green tea protect against Alzheimer’s diseaseVitamin B3, found in protein-rich foods, is important for energy metabolism, circulation, and protection of nerve cells. Getting enough vitamin B3, combined with drinking green tea that contains a specific antioxidant, appears to provide additional protection for nerve cells. This suggests that the combination of vitamin B3 and green tea may protect against the development of Alzheimer’s disease through synergistic effects, according to a study published in GeroScience.

As the population ages, more and more people are affected by Alzheimer’s disease. Firstly, cells, including nerve cells, become less efficient at producing energy. During energy metabolism, more free radicals are generated, which can attack and damage healthy cells, including nerve cells. Alzheimer’s disease is characterized by oxidative stress, where there are too many free radicals and too few protective antioxidants. During aging and periods of insufficient sleep, the brain’s ability to clear harmful components decreases, leading to accumulations of proteins (beta-amyloid plaques) between nerve cells and tangling of other proteins (tau) inside the cells. Alzheimer’s disease is also associated with insulin resistance in the brain, which is why it is sometimes called type 3 diabetes.
Symptoms of Alzheimer’s disease arise from declining brain function, as nerve cells in multiple regions of the brain slowly deteriorate. Today, it is the leading cause of dementia. It is well known that diet and nutrient deficiencies play an important role in Alzheimer’s disease. Researchers at the University of California have specifically found that two simple nutrients, which are often easy to obtain in sufficient amounts from the diet, protect against Alzheimer’s disease through different mechanisms.

Vitamin B3 for energy metabolism and numerous enzymatic processes

Vitamin B3 (niacin) is primarily found in protein-rich foods such as meat, poultry, fish, and eggs, as well as whole grains, beans, nuts, seeds, and kernels. The liver can also synthesize niacin from the amino acid tryptophan with the help of vitamin B6, which should also be supplied through the diet.
Vitamin B3 is converted in the liver into the coenzymes NAD (nicotinamide adenine dinucleotide in oxidized form) and NADH (in reduced form), which are essential for cellular energy metabolism, including the high energy demands of nerve cells. The active form, NAD, is also involved in more than 400 biochemical processes affecting mental balance, blood sugar, circulation, skin, and mucous membranes.
However, aging, genetic variations, and liver stress can make it harder to convert niacin from food or supplements into NAD. A low-protein diet, alcohol misuse, high blood sugar, diuretics, immunosuppressive drugs, and certain intestinal disorders such as Crohn’s disease can also make it difficult to get enough B3 or convert it into NAD. Therefore, many people, especially older adults, have an increased need for vitamin B3.
Previous studies have shown that B3 deficiency increases the risk of Alzheimer’s disease, Parkinson’s disease, schizophrenia, and other neurological disorders. It is best to get enough B3 from the diet, but as mentioned, several factors can increase the need for supplementation. According to the researchers, vitamin B3’s protective effect against Alzheimer’s disease appears to be enhanced when combined with green tea.

Vitamin B3 and green tea have a unique synergistic effect on nerve cell health

Green tea contains a flavonoid called epigallocatechin gallate (EGCG), which is a very powerful antioxidant. This function is important in preventing Alzheimer’s disease, which is characterized by cell damage caused by free radicals and oxidative stress.
The University of California researchers conducted a study on nerve cells from mouse brains. These cells were cultured in the lab and exposed to vitamin B3 and the antioxidant EGCG. The study revealed that the combination of B3 and EGCG boosted a specific energy molecule called GTP (guanosine triphosphate) that is found in brain nerve cells. GTP provides a type of energy that helps remove harmful substances linked to Alzheimer’s disease. This cellular self-cleaning process is called autophagy. The study also suggested that the ability of cells to perform autophagy declines with aging and as a result of oxidative stress.
The combination of B3 and EGCG from green tea appears to enhance GTP levels in nerve cells, helping to remove harmful proteins such as beta-amyloid and tau, which are involved in Alzheimer’s disease development. Overall, it may counteract various damages to nerve cells associated with aging.
The researchers hypothesize that combining higher B3 intake with EGCG from green tea could increase levels of GTP to those seen in young cells. They emphasize that this was a laboratory study using mouse cells, and more research, including human studies, is needed before specific therapies can be recommended.
Nevertheless, getting enough vitamin B3 is advisable for Alzheimer’s prevention. Drinking 2-4 cups of green tea daily, preferably with or after meals, may also help, as the bitter compounds both enhance nutrient absorption and help regulate blood sugar.

Synergistic effects of vitamin B3 and green tea on the brain and nerve cells

  • Supports energy utilization in nerve cells
  • Boosts GTP in nerve cells, aiding autophagy to remove harmful proteins and components
  • Antioxidant effect countering cell damage from free radicals and oxidative stress
  • Supports nutrient absorption and blood sugar regulation

References:

R.A. Santana et al. Treatment of age-related decreases in GTP levels restores endocytosis and autophagy. GeroScience. 2025

David Nield. Green Tea and a Vitamin Supplement Could Protect Against Alzheimer´s . Science Alert 2025

Raymond Chong et al. Niacin Enhancement for Parkinson´s Disease: An Effectiveness Trial. Frontiers in Aging Neuroscience. 2021

Lehmann S. et al. Enhancing NAD salvage metabolism is neuroprotective in a Pink1 model of Parkinson´s disease. Biology Open 2016


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