Thiamine (Vitamin B1) and its perceived better alternative Benfotiamine are thought to be important in Glucose Metabolism, trials on Humans and Mice have backed this up, more trials are needed. Benfotiamine is available as a supplement. The link below discusses Thiamine and Dementia
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4846521/
From a trial involving mice the results suggested that, unlike many other thiamine-related drugs, Benfotiamine may be beneficial for clinical Alzheimer’s disease treatment
https://academic.oup.com/brain/article/133/5/1342/544302
The US department of health is running a 5 year clinical trial which will determine if Benfotiamine, a dietary supplement, can minimise cognitive decline in older adults with amnestic mild cognitive impairment (MCI) or mild Alzheimer’s disease.
https://www.nia.nih.gov/alzheimers/clinical-trials/benfotiamine-alzheimers-disease
https://www.clinicaltrials.gov/ct2/show/NCT02292238
Reduction of glucose metabolism in brain is one of the main features of Alzheimer’s disease. Thiamine (vitamin B1)-dependent processes are critical in glucose metabolism and have been found to be impaired in brains from patients with Alzheimer’s disease.
https://www.ncbi.nlm.nih.gov/pubmed/20385653/
A study by D Loew , Germany, on orally administered lipid-soluble Thiamine analogues like Benfotiamine showed the benefits of Benfotiamine over Thiamine Hydrochloride. It is quite clear that benfotiamine is absorbed much more better than water-soluble thiamine salts: maximum plasma levels of thiamine are about 5 times higher after benfotiamine, the bioavailability is at maximum about 3.6 times as high as that of thiamine hydrochloride and better than other lipophilic thiamine derivates. The physiological activity (alphaETK) increased only after benfotiamine was given. Due to its excellent pharmacokinetic profile benfotiamine should be preferred in treatment of relevant indications.
https://www.ncbi.nlm.nih.gov/pubmed/8929745
A small Long-Term Cognitive Improvement After Benfotiamine Administration in Patients with Alzheimer’s Disease. In summary, the results showed “that Benfotiamine can produce a long-term improvement (over 18 months) in the cognitive ability of AD patients during continued 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 AD. Our study provides new insights into understanding the mechanism of cognitive impairment in AD and suggests a new direction to develop disease-modifying therapies for the dementia stage. Further clinical trials in this direction are needed.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5567484/
VITforD contains 10mg of Vitamin B1, around 900% of NRV
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