Could Vitamin Supplementation Help Alzheimer’s Patients?
Niacin, a form of vitamin B3 used to treat cardiovascular disease, helps immune cells in the brain fight neurodegenerative diseases such as Alzheimer’s in mice models, according to recent studies. Researchers hope that human clinical trials will swiftly follow.
Could Vitamin Supplementation Help Alzheimer’s Patients?
Could Vitamin Supplementation Help Alzheimer’s Patients?
Niacin, a form of vitamin B3 used to treat cardiovascular disease, helps immune cells in the brain fight neurodegenerative diseases such as Alzheimer’s in mice models, according to recent studies. Researchers hope that human clinical trials will swiftly follow.
Niacin, a form of vitamin B3 used to treat cardiovascular disease, helps immune cells in the brain fight neurodegenerative diseases such as Alzheimer’s in mice models, according to recent studies. Researchers hope that human clinical trials will swiftly follow.
Researchers say they hope to launch a clinical trial to test bumetanide, a diuretic approved in 2002, but how it might improve neural functioning is unclear.
A new study links a variant of the apolipoprotein E gene called APOE ε4 to better memory in older age, even in the presence of amyloid plaques—a possible explanation for the variant’s persistence despite its association with an increased risk of Alzheimer’s disease.
Pharmaceutical companies ramp up efforts to get the brain’s immune cells to help treat Alzheimer’s disease and other conditions, but not everyone agrees the approach will be effective.
These “coarse-grained” plaques resemble those that clog up the brain’s blood vessels in a different disease, pointing to links between the vascular system and the neurodegenerative disease.
New studies show that elevated levels of a form of tau called p-tau217 can accurately distinguish Alzheimer’s disease from other forms of dementia, and perhaps even predict it.
A new study shows that the brains of Alzheimer’s disease patients have a greater viral load, while another study in mice shows infection leads to amyloid-β build up.