Here’s some health news on the Alzheimer’s front: a special form of vitamin B1 could help stop the progression of Alzheimer’s symptoms. The plaque-destroying vitamin is called benfotiamine and the medical community is excited about its performance when it comes to protecting memory function.
Benfotiamine is a fat-soluble form of thiamine. It’s considered a potent antioxidant that has been used over the past decade to treat pain symptoms. In Germany, benfotiamine is actually licensed for use as a treatment for nerve pain caused by sciatica.
But benfotiamine is also useful in preserving brain health. It turns out benfotiamine is linked to Alzheimer’s prevention because of its involvement in glucose metabolism. When your brain cells need fuel, they metabolize glucose. Sometimes, for a variety of reasons, metabolism slows down in your brain. When this happens, it seems to open the door for Alzheimer’s disease to take hold. Or at least, this is what researchers at the Department of Neurology and Neuroscience at Weill Cornell Medical College think may be the case.
Scientists there have discovered that patients with Alzheimer’s are often deficient in thiamine. This thiamine deficiency seems to encourage plaque formation in the brain. People who have low levels of thiamine have also been found to have trouble with their memory. Reverse this vitamin shortage, however, and the opposite is likely to happen, the Cornell researchers reasoned.
When the theory was tested on mice, those treated with benfotiamine showed diminished levels of plaque and their memory problems had reversed. It could be that this form of B1 could offer a safe and effective way to reverse memory-destroying plaque in the brain, helping to stop the progression of Alzheimer’s.
Benfotiamine is generally considered safe. Talk to your doctor if you’re thinking about trying the supplement. For those who can’t seem to absorb enough thiamine, benfotiamine may be a better option. It’s easier for the body to break down and utilize.
Source(s) for Today’s Article:
Gibson, G.E., et al, “Abnormal thiamine-dependent processes in Alzheimer’s Disease. Lessons from diabetes,” Mol Cell Neurosci. July 2013; 55: 17-25.