Understanding the protective effects of wine components and their metabolites in the brain function

They don't seem to have considered that only certain people can process alcohol healthily.

Moderate Drinking is Healthy Only for Some People

Understanding the protective effects of wine components and their metabolites in the brain function

¹ Instituto de Investigación en Ciencias de la Alimentación (CIAL), CSIC-UAM. Nicolás Cabrera, 9, 28049 Madrid, Spain
² Department of Food and Nutritional Sciences, School of Chemistry, Food and Pharmacy, University of Reading, Whiteknights Campus RG6 6AP, Reading, UK

^a e-mail: victoria.moreno@csic.es

Abstract

Moderate wine consumption has been suggested to exert a positive effect in prevention of neurodegenerative process and cognitive impairment. With the ultimate aim of achieving a better understanding of the molecular mechanisms behind this benefit, we have investigated the role of certain wine- derived phenolic metabolites and aroma compounds in the MAPK cascade (including ERK1/2, p38), one of the routes directly related to inflammation in neuronal cells. Some of the tested phenolic compounds, especially in the case of 3,4-dihydroxyphenylacetic acid, showed a significant neuroprotective effect against SIN-1-induced neuronal death. Regarding their effect over MAPK phosphorylation, inmunoblotting technique revealed a beneficial and significant decrease on the phosphorylation of p38 and ERK1/2 kinases after incubation with wine constituents. In addition, activity of caspase3-like protease, an executor of neuronal apoptosis and a downstream signal of MAPK, was significantly diminished by 3-(3-hydroxyphenyl) propionic acid and linalool, counterbalancing the increase produced by SIN-1. Altogether, these results suggest that wine aroma, phenolic compounds and their gut metabolites could exert neuroprotective actions by modulating MAPK signalling and caspase-3 proteases activation, which are known to play a key role in oxidative/ nitrosative stress-induced response.
© The Authors, published by EDP Sciences 2016

This is an Open Access article distributed under the terms of the Creative Commons Attribution License 4.0 (http://creativecommons.org/licenses/by/4.0/).

Neuroscientists discover key protein responsible for controlling nerve cell protection - SUMO

This one is hard to understand.
http://www.pharmiweb.com/pressreleases/pressrel.asp?ROW_ID=57779
A key protein, which may be activated to protect nerve cells from damage during heart failure or epileptic seizure, has been found to regulate the transfer of information between nerve cells in the brain. The discovery, made by neuroscientists at the University of Bristol and published in Nature Neuroscience and PNAS, could lead to novel new therapies for stroke and epilepsy.
A key protein, which may be activated to protect nerve cells from damage during heart failure or epileptic seizure, has been found to regulate the transfer of information between nerve cells in the brain. The discovery, made by neuroscientists at the University of Bristol and published in Nature Neuroscience and PNAS, could lead to novel new therapies for stroke and epilepsy.
The research team, led by Professor Jeremy Henley and Dr Jack Mellor from Bristol’s Medical School, has identified a protein, known as SUMO, responsible for controlling the chemical processes which reduce or enhance protection mechanisms for nerve cells in the brain.
These key proteins produce subtle responses to the brain’s activity levels to regulate the amount of information transmitted by kainate receptors - responsible for communication between nerve cells and whose activation can lead to epileptic seizures and nerve cell death.
Protein function is controlled by altering their structure in processes that can be independent or inter-related including phosphorylation, ubiquitination and SUMOylation. In the present work it is shown that phosphorylation of kainate receptors on its own promotes their activity. However, phosphorylation also facilitates SUMOylation of kainate receptors that reduces their activity. Thus there is a dynamic and delicate interplay between phosphorylation and SUMOylation that regulates kainate receptor function.
This fine balance between phosphorylation and SUMOylation is dependent on brain activity levels where damaging activity that occurs during stroke or epilepsy will enhance SUMOylation and therefore reduce kainate receptor function to protect nerve cells.
Dr Mellor, Senior Lecturer from the University’s School of Physiology and Pharmacology, said: “Kainate receptors are a somewhat mysterious but clearly very important group of proteins that are known to be involved in a number of diseases including epilepsy. However, we currently know little about what makes kainate receptors so important. Likewise, we also know that SUMO proteins play an important role in neuroprotection. These findings provide a link between SUMO and kainate receptors that increases our understanding of the processes that nerve cells use to protect themselves from excessive and abnormal activity.”
Professor Henley added: “This work is important because it gives a new perspective and a deeper understanding of how the flow of information between cells in the brain is regulated. The team has found that by increasing the amount of SUMO attached to kainate receptors – which would reduce communication between the cells – could be a way to treat epilepsy by preventing over-excitation of the brain’s nerve cells.”
The research follows on from previous findings published in Nature that discovered SUMO proteins target the brain’s kainate receptors altering their cellular location.
The research teams comprised academics from the University of Bristol’s MRC Centre for Synaptic Plasticity and the Division of Neuroscience in the School of Physiology & Pharmacology and the School of Biochemistry. This work was supported by the Wellcome Trust, Biotechnology and Biological Sciences Research Council (BBSRC), European Research Council (ERC), Medical Research Council (MRC) and EMBO