Cocoa powder triggers neuroprotective and preventive effects in a human Alzheimer's disease model by modulating BDNF signaling pathway

Abstract

The molecular mechanisms linking Aβ to the onset of neurotoxicity are still largely unknown, but several lines of evidence point to reactive oxygen species, which are produced even under the effect of nanomolar concentrations of soluble Aβ-oligomers. The consequent oxidative stress is considered as the mediator of a cascade of degenerative events in many neurological disorders. Epidemiological studies indicate that dietary habits and antioxidants from diet can influence the incidence of neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. In the recent years, a number of reviews have reported on neuroprotective effects of polyphenols in cell and animal models. However, the majority of these studies have focused only on the anti-oxidant properties of these compounds and less on the mechanism/s of action at cellular level. In this work we investigated the effect of cocoa polyphenolic extract on a human AD in vitro model. The results obtained, other than confirming the anti-oxidant properties of cocoa, demonstrate that cocoa polyphenols triggers neuroprotection by activating BDNF survival pathway, both on Aβ plaque treated cells and on Aβ oligomers treated cells, resulting in the counteraction of neurite dystrophy. On the light of the results obtained the use of cocoa powder as preventive agent for neurodegeneration is further supported.

Role of intestinal microbiota in the generation of polyphenol‐derived phenolic acid mediated attenuation of Alzheimer's disease β‐amyloid oligomerization

“…Thus, GSPE phenolic acid metabolites derived from intestinal microbial fermentation, along with previously reported PACs and their conjugated metabolites should be further investigated as potential contributors to the observed health benefits associated with GSPE consumption. Moreover, outcomes from our studies support future preclinical and clinical investigations of the mechanisms behind PACs absorption, bioavailability, and potential preventative and therapeutic application targeting neuropathological features of age‐related disorders and other conditions .…”

Uric Acid Amplifies Aβ Amyloid Effects Involved in the Cognitive Dysfunction/Dementia: Evidences From an Experimental Model In Vitro

“…This effect of UA was observed starting from the dose of 40 µM while lower UA concentration did not significantly influence cell biology, this finding suggesting a dose‐dependent effect. Interestingly, UA was able to potentiate the reduction of cell viability induced by both oligomeric Aβ 1–42 and fibrillary Aβ 25–35, that is, two experimental conditions reproducing the earliest phase (Brouillette, ) or the late step (Cimini et al, ; Benedetti et al, ) of AD pathophysiology, respectively. In addition, UA was also able to enhance the detrimental effects of Aβ on neuronal cells interconnections by promoting synaptic disconnection of dystrophic neurites.…”

Cocoa and Dark Chocolate Polyphenols: From Biology to Clinical Applications

“…In an in vitro model of human AD, cocoa polyphenolic extracts have been shown to exert not only antioxidant effects but also to afford neuroprotection (116). This last effect has been attributed to the activation of BDNF survival pathway either on Aβ plaque-treated cells or on Aβ oligomer-treated cells, thus, ultimately, leading to reduction of neurite dystrophy.…”