BENFOTIAMINE IMPROVES COGNITIVE ABILITY OF ALZHEIMER’S PATIENTS INDEPENDENT OF AMYLOID DEPOSITION

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Alzheimer’s disease (AD) is the most commonly neurodegenerative disease and lacks method to halt or delay the disease progression. The development of the disease-modifying therapies will produce remarkable impact on modern society. In this study, the effects of benfotiamine, a thiamine derivative, on cognitive ability of mild to moderate AD cases were investigated. A non-control and open clinical observation that benfotiamine treats mild to moderate AD was designed and performed at the outpatient clinic of the Department of Neurology at Zhongshan Hospital, Fudan University, Shanghai, China. AD patients continued the previous drug therapies during benfotiamine administration. Five AD patients with mild to moderate AD were voluntarily recruited from August, 2013 to December, 2015. Benfotiamine (300 mg/day) was orally taken by five cases over 18 months. Case I to IV continued donepezil administration (5 mg/day) during benfotiamine administration. Case V had no other drug administration for AD. The Mini-Mental Status Examination (MMSE), Activity of Daily Living (ADL), Clinical Dementia Rating (CDR), and Hamilton Depression Rating Scales were evaluated before and during the period of benfotiamine administration (more than 18 months). All the cases received the examination of positron emission tomography with Pittsburgh compound-B (PiB-PET). Case I, II, and V received a follow-up of PiB-PET scan after benfotiamine administration. The MMSE scores were increased by 2 to 6 points in four patients and did not significantly change in case IV, with the average of 3.2 ± 1.3 points (n = 5) at the 18th month of benfotiamine administration. In case I, II, and V, who had the second scan of PiB-PET, the average SUVR of the frontal, parietal, and temporal cortices at the second PiB-PET imaging was 2.42 ± 0.79, with a 36.7% increase from that at the first scan. Benfotiamine significantly improves cognitive decline and disease progression of the dementia stage of AD independent of amyloid accumulation. Our study provides new insight into AD disease-modifying therapy.