Reference : Benfotiamine and cognitive decline in Alzheimer’s disease: Results of a randomized pl...
Scientific journals : Article
Human health sciences : Neurology
http://hdl.handle.net/2268/250937
Benfotiamine and cognitive decline in Alzheimer’s disease: Results of a randomized placebo-controlled phase IIa clinical trial.
English
Gibson, Gary E. [> >]
Luchsinger, José A. [> >]
Cirio, Rosanna [> >]
Chen, Huanlian [> >]
Franchino-Elder, Jessica [> >]
Hirsch, Joseph A. [> >]
Bettendorff, Lucien mailto [Université de Liège - ULiège > > Neurosciences-Neurophysiology >]
Chen, Zhengming [> >]
Flowers, S [> >]
Gerber, Linda [> >]
Grandville, Thomas [> >]
Schupf, Nicole [> >]
Xu, Hui [> >]
Stern, Yaakov [> >]
Habeck, Christian [> >]
Jordan, Barry [> >]
Fonzetti, Pasquale [> >]
2020
Journal of Alzheimer's Disease
IOS Press
78
989-1010
Yes (verified by ORBi)
International
1387-2877
1875-8908
Netherlands
[en] Benfotiamine ; Glucose ; Alzheimer’s disease ; Inflammation ; Oxidative stress ; Advanced 38 Glycation Endproducts ; Thiamine
[en] Background. In preclinical models, benfotiamine efficiently ameliorates the clinical and biological pathologies that define Alzheimer’s disease (AD) including impaired cognition, beta amyloid plaques, neurofibrillary tangles, diminished glucose metabolism, oxidative stress, increased advanced glycation end products (AGE) and inflammation.
Objective. To collect preliminary data on feasibility, safety and efficacy in individuals with amnestic mild cognitive impairment (aMCI) or mild dementia due to AD in a placebo-controlled trial of benfotiamine.
Methods. A twelve-month treatment with benfotiamine tested whether clinical decline would be delayed in the benfotiamine group compared to the placebo group. The primary clinical outcome was the AD-Assessment-Scale-Cognitive Subscale (ADAS-Cog). Secondary outcomes were the clinical dementia rating (CDR) score and fluorodeoxyglucose (FDG) uptake, measured with brain positron emission tomography (PET). Blood AGE were examined as an exploratory outcome.
Results. Participants were treated with benfotiamine (34) or placebo (36). Benfotiamine treatment was safe. The increase in ADAS-cog was 43% lower in the benfotiamine group than in the placebo group, indicating less cognitive decline, and this effect was nearly statistically significant (p=0.125). Worsening in CDR was 77% lower (p=0.034) in the benfotiamine group compared to the placebo group, and this effect was stronger in the APOE ε4 non-carriers. Benfotiamine significantly reduced increases in AGE (p=0.044), and this effect was stronger in the APOE ε4 non-carriers. Exploratory analysis derivation of an FDGPET pattern score showed a treatment effect at one year (p=0.002).
Conclusions Oral benfotiamine is safe and potentially efficacious in improving cognitive outcomes among persons with MCI and mild AD.
Brain and Mind Research Institute ; Giga-Neurosciences
F.R.S.-FNRS - Fonds de la Recherche Scientifique ; ADDF - Alzheimer's Drug Discovery Foundation ; Burke Rehabilitation Hospital ; BNI - Burke Neurological Institute
Researchers ; Professionals ; Students ; General public
http://hdl.handle.net/2268/250937
10.3233/JAD-200896

File(s) associated to this reference

Fulltext file(s):

FileCommentaryVersionSizeAccess
Restricted access
jad_2020_78-3_jad-78-3-jad200896_jad-78-jad200896.pdfPublisher postprint1.12 MBRequest copy

Bookmark and Share SFX Query

All documents in ORBi are protected by a user license.