symptoms of Alzheimer’s –vs– fat soluble form of vitamin B1
— Mini-Mental Status Examination = measurement of cognitive function.
Maximum score is 30 points.
Score of 20 to 24 suggests mild dementia,
Score of 13 to 20 suggests moderate dementia,
Score of 12 and below indicates severe dementia.
The score of a person with Alzheimer’s declines 2 to 4 points each year
— benfotiamine = a fat soluble form of the water soluble B vitamin called Thiamine, also known as Vitamin B1, has better bioavailability than thiamine, and does better at getting into the brain
Xiaoli Pan, et al. Zhongshan Hospital, Shanghai, China……..
—– “A disturbance of brain glucose metabolism is one of the most important pathophysiological features, and precedes the overt symptoms of Alzheimer’s disease by decades…..”
—– “Both the Thiamine diphosphate level and the activity of Thiamine diphosphate-dependent enzymes are significantly reduced in blood and brain autopsy samples from Alzheimer’s disease patients….Thiamine diphosphate reduction is a significant biomarker for Alzheimer’s disease diagnosis……disruption of thiamine metabolism directly contributes to Alzheimer’s disease pathogenesis by perturbing glucose utilization and by activating multiple pathophysiological cascades in the brain.”
—– “The better bioavailability and the pharmacological effects via multiple mechanisms against abnormal glucose metabolism and its consequences may explain why benfotiamine administration but not thiamine supplementation had a long-term beneficial effect on cognitive ability in Alzheimer’s disease patients.”
—– “befotiamine has beneficial effects against abnormal glucose metabolism and its consequences via multiple mechanisms, including the elimination of oxidative stress and the inhibition of glycogen synthase kinase-3, which are both considered to be major pathogenic factors that cause neurodegeneration in Alzheimer’s disease“
“Here, we report that long-term administration of benfotiamine improved the cognitive ability of patients with Alzheimer’s disease.”
“Five patients with mild to moderate Alzheimer’s disease received oral benfotiamine (300mg daily) over 18 months.”
“All patients received oral benfotiamine (300mg/day; Doctor’s Best, Irvine, California) over 18 months.”
“All patients were examined by positron emission tomography with Pittsburgh compound B (PiB-PET) and exhibited positive imaging with β-amyloid deposition, and three received PiB-PET imaging at follow-up.”
“The five patients exhibited cognitive improvement as assayed by the Mini-Mental Status Examination with an average increase of 3.2 points at month 18 of benfotiamine administration.”
“The three patients who received follow-up PiB-PET had a 36.7% increase in the average standardized uptake value ratio in the brain compared with that in the first scan. Importantly, the MMSE scores of these three had an average increase of 3 points during the same period. Benfotiamine significantly improved the cognitive abilities of mild to moderate Alzheimer’s disease patients independently of brain amyloid accumulation.”
“These results indicate that brain dysfunction may be independent of amyloid deposition and that the disease progression can be halted in the dementia stage of Alzheimer’s disease.”
“Our study showed that Alzheimer’s disease patients with mild-to-moderate dementia manifested a long-term (over 18 months) improvement in cognitive ability after benfotiamine administration, despite the progressive exacerbation of brain amyloid accumulation as evaluated by PiB-PET scans.”
“These results reveal two important messages: (1) the progression of brain dysfunction in the dementia stage of Alzheimer’s disease can be halted and even improved
(2) the alteration of cognitive capability is independent of brain amyloid accumulation, which is consistent with previous results showing that the reduction of brain amyloid accumulation by vaccines, antibodies, or β- and γ-secretase inhibitors has little beneficial effect on the cognitive ability and disease progression….”
Xiaoli Pan, et al
Long-Term Cognitive Improvement After Benfotiamine Administration in Patients with Alzheimer’s Disease
Neuroscience Bulletin – Volume 32 #6 – December 2016 – page 591