A new study from Indiana University found that niacin limits Alzheimer’s disease progression.
This finding identifies a potential novel therapeutic target for Alzheimer’s disease, which can be modulated by FDA-approved drugs.
The study is published in Science Translational Medicine and was conducted by Gary Landreth et al.
In the study, the team examined how niacin affects amyloid plaques in Alzheimer’s disease.
Niacin, which sustains metabolism throughout the body, is mainly obtained through a typical diet; it also can be taken in supplements and cholesterol-lowering drugs.
The brain, however, uses niacin in a different manner. In the brain, niacin interacts with a highly-selective receptor, HCAR2, present in immune cells physically associated with amyloid plaques.
When niacin—used in this project as the FDA-approved Niaspan drug—activates the receptor, it stimulates beneficial actions from these immune cells.
Past epidemiology studies of niacin and Alzheimer’s disease showed that people who had higher levels of niacin in their diet had diminished risk of the disease.
Niacin is also currently being used in clinical trials in Parkinson’s disease and glioblastoma.
In a recent study from UC San Diego and published in the Journal of Experimental Medicine, researchers found that a new drug that could prevent Alzheimer’s disease by modulating, rather than inhibiting, a key enzyme involved in forming amyloid plaques in the brain.
They demonstrated that the drug is safe and effective in animals, paving the way for future clinical trials in humans.
A key hallmark of Alzheimer’s disease involves the formation of amyloid plaques composed of small protein fragments known as amyloid-β (Aβ) peptides.
Some of these fragments are particularly prone to forming amyloid plaques, and their production is elevated in patients with mutations predisposing them to early-onset Alzheimer’s disease.
In that study, the team developed a novel drug and tested it on mice, rats, and monkeys.
Repeated low doses of the drug completely eliminated amyloid-β production in mice and rats without causing any toxic side effects.
The drug was also safe and effective in monkeys, reducing amyloid-β levels by up to 70%.
The researchers then tested the drug in a mouse model of early-onset Alzheimer’s disease, treating the animals either before or shortly after they began to form amyloid plaques.
In both cases, the novel drug decreased plaque formation and reduced plaque-associated inflammation, which is thought to contribute to the development of the disease.
These findings suggest that the drug could be used to prevent Alzheimer’s disease, either in patients with genetic mutations that increase susceptibility to the disease or in cases where amyloid plaques have been detected by brain scans.
The team says future clinical trials will determine whether this promising drug is safe in humans and could be used to effectively treat or prevent Alzheimer’s disease.
If you care about Alzheimer’s, please read studies about the likely cause of Alzheimer’s disease , and new non-drug treatment that could help prevent Alzheimer’s.
For more information about brain health, please see recent studies about diet that may help prevent Alzheimer’s, and results showing that some dementia cases could be prevented by changing these 12 things.
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