Journal club of the week: rapidly growing number of polyphenolic compounds with neuroprotective effects

Speaker: PhDs Faheem Maqbool 

Date: 22nd of February, 2016

Topic: rapidly growing number of polyphenolic compounds with neuroprotective effects

 In the today journal meeting on 22nd of February, 2016, first of all new Ph.Ds Fazlullah from Pakistan joined us with Prof. Dr. Mohammad Abdollahi. He briefly introduced himself in his first journal club meeting. After that all participants also induced themselves. After that Faheem Maqbool introduced the participants to polyphenols against neurodegenerative disorders. A rapidly growing number of polyphenolic compounds with neuroprotective effects were described. Many efforts have been made to explore the mechanisms behind the neuroprotective action of polyphenols. However, many pathways and mechanisms considered for mediating these effects are rather general than specific. Moreover, despite the beneficial effects of polyphenols in the experimental treatment of neurodegeneration, little has been achieved in bringing them into routine clinical applications. Neurodegenerative disorders such as Alzheimer’s disease (AD), stroke, and Parkinson’s disease (PD) represent a major clinical problem in the developed countries and are major economic burdens for health care systems. Dietary, genetic, and molecular factors are important determinants in the progression and intervention of neurodegenerative diseases. AD is a common cause of dementia and mortality in the United States. The total number of reported deaths due to AD has increased in the past years, and it is among the 10 leading causes of deaths in the United States. Amyloid-β (Aβ) peptides derived from amyloid precursor protein (APP) via γ-secretase and β-secretase cleavage are hallmarks of AD. Cellular prion protein (PrP(C)) and oxidative stress mediate Aβ neurotoxicity, and the latter contributes to neuronal death by lowering intracellular glutathione. Along with Aβ, tau protein alteration in neuronal microtubules also contributes to the pathology of AD. Abnormal phosphorylation and aggregation of tau protein leads to neural dysfunction and leads to pathological events which cause neuronal dysfunction in AD. Failed clearance of Aβ aggregates resulting from impaired autophagy may also contribute to AD. AD is also characterized by elevated peripheral blood cytokine concentrations for interleukin- (IL-) 6, tumor necrosis factor alpha (TNF-α), IL-1β, transforming growth factor beta (TGF-β), IL-12, and IL-18 suggestive of a pro-inflammatory response in AD pathology. He also described polyphenols and its pharmacological properties. He talked about some plants like green tea polyphenols that protect primary rat cortical neurons against Aβ-induced cytotoxicity. In the mouse model studies, polyphenols of grapes improved cognitive functions in AD. As well, epicatechin metabolite 3′-O-methyl-epicatechin-5-O-β-glucuronide improved synaptic transmission through cyclic adenosine monophosphate (cAMP) response element binding protein. Finally, he concluded that the future of polyphenol researches needs to aim towards clinical acceptance of health claims from preclinical in vitro and animal model studies. Therefore, future studies focusing on human clinical trials of several potent polyphenols and their combinations should be carried out. At the end all participants asked their valuable questions and he answered all the questions.