Glucose metabolism is reduced “drastically” in brain tissue of patients with Alzheimer’s disease (AD). This abnormality may precede any brain symptoms by decades. Diabetes, with disturbed glucose metabolism, is a risk factor for AD.
The brain cell pathology of AD is similar to that of thiamine (vitamin B-1) deficiency. Thiamine, important in glucose metabolism, does not function properly in brains of patients with AD. Therefore, chemicals which inhibit an enzyme called cholinesterase benefit AD patients, but thiamine treatment does not benefit those patients even though it is a mild cholinesterase inhibitor.
Benfotiamine and fursultiamine, related to thiamine with superior bioavailability, are both tested in this study to see if they improve symptoms in a mouse model of AD. Benfotiamine benefits diabetic retinopathy and neuropathy; there is less evidence for the benefit from fursultiamine. After treatment, animals were tested for learning ability in a water maze. (Times were recorded of how long it took to find a submerged platform for them to rest on.) The animal’s brains were then tested by counting amyloid plaques under the microscope. Amyloid plaques with tangled fibers are a hallmark of AD.
Benfotiamine improved the cognitive functioning in the mouse model of AD and reduced the number of brain plaques. Huperzine A, a cholinesterase inhibitor used as a control for comparison, significantly improved the learning times in the water maze and reduced the number of amyloid plaques. Fursultiamine did not have a significant beneficial effect.
CONCLUSION: Benfotiamine was of benefit in a mouse model of AD, probably by a mechanism independent of thiamine. Any increase in thiamine levels was too small to be the cause of the improvements.
NOTE: Read about the effects of benfotiamine in heart attacks (myocardial infarction.)
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Sum mary #583.