Procyanidins, the oligomeric compounds formed from catechin and epicatechin molecules, are potentially effective targets as nutraceuticals or pharmaceuticals in the prevention and treatment of Alzheimer's disease (AD). Natural procyanidins can attenuate AD pathological features, extracellular amyloid deposits, and neurofibrillary tangles via reducing Aβ accumulation and tau pathology. The enhancement of cognition as well as modulation of synaptic plasticity by these compounds also participated in the alleviation of AD. Notably, procyanidins and some of their metabolites have been observed to upregulate SIRT1 (silent information regulator 1) which is essential for normal cognitive and synaptic plasticity, and stimulate CREB (cAMP response element binding) which acts as a molecular switch from short- to long-term memory. Based on the interplay of CREB-SIRT1 axis, it is therefore conceivable that the regulation of procyanidins by the means of CREB-SIRT1 could promote the cognitive function and is thus conducive for AD pathogenesis. This review focuses on the role of procyanidins, the main group of flavonoids, on AD and the potential mechanism involved CREB-SIRT1 axis.
Keywords: Alzheimer’s disease; CREB; Procyanidins; SIRT1; Synaptic plasticity.