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Anti Ageing Conference London 2020
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AACL 2008 Speaker

Dr. Vittorio Calibrese MD PhD
Biochemistry & Mol. Biology Section, Department of Chemistry, Faculty of Medicine, University of Catania

Dr. Calibrese recived his medical degree (magna cum laude) from the University of Catania, Catania, Italy in 1984. He completed an advanced degree of Specialist in Neurobiology at New York University Medical School and Neuropharmacology at Thomas Jefferson University College in London, Northwick Park Institute for Medical Research at the University of London and University of Kentucky. He currently holds the academic position as Profesor of Clinical Biochemistry with the University of Catania, Catania, Italy. Dr. Calabrese's research interest has included the Role of Oxidative Stress and Mitochondrial Dysfunction in Aging and Neurodegenerative Disorderds, Nutritional Antioxidants and Modulcation of Cellular Redox State. Heat Shock Signal Pathway and Brain Cell Stress Response, Alcohol Metabolism and Alcohol Related Pathology and the Role of NO and CO in the regulation of gene expression.

2008 - Vitagenes Brain Function, and Food Factors: Functional Genomics and a Redox Proteomics Approaches

Calabrese V. MD, PhD
Dept. of Chemistry, University of Catania, Italy;

Reduced expression and/or activity of antioxidant proteins lead to oxidative stress, accelerated aging and neurodegeneration1-6 However, while excess reactive oxygen species (ROS) are toxic, regulated ROS play an important role in cell signaling. Perturbation of redox status, mutations favoring protein misfolding, altered glyc(osyl)ation, overloading of the product of polyunsaturated fatty acid peroxidation (hydroxynonenals, HNE) or cholesterol oxidation, can disrupt redox homeostasis. Collectively or individually these effects may impose stress and lead to accumulation of unfolded or misfolded proteins in brain cells. Alzheimer's (AD), Parkinson's and Huntington's disease, amyotrophic lateral sclerosis and Friedreich's ataxia are major neurological disorders associated with production of abnormally aggregated proteins and, as such, belong to the so-called "protein conformational diseases". The pathogenic aggregation of proteins in non-native conformation is generally associated with metabolic derangements and excessive production of ROS7-10. There is significant evidence that the pathogenesis of several neurodegenerative diseases, including Parkinson's disease (PD), Alzheimer's disease (AD), Friedreich's ataxia (FRDA), Multiple sclerosis (MS) and Amyotrophic lateral sclerosis (ALS), may involve the generation of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) associated with mitochondrial dysfunction. Mitochondrial genome may play an essential role in the pathogenesis of these diseases, and evidence for mitochondria being a site of damage in neurodegenerative disorders is based in part on observed decreases in the respiratory chain complex activities in PD, AD, and Huntington’s disease (HD). Such defects in respiratory complex activities, possibly associated with oxidant/antioxidant imbalance, are thought to underlie defects in energy metabolism and induce cellular degeneration4-8. The precise sequence of events in most of neurodegenerative disease pathogenesis is uncertain. The impaired intramitochondrial metabolism with increased free iron levels and a defective mitochondrial respiratory chain, associated with increased free radical generation and oxidative damage may be considered a possible mechanism that compromise brain cell survival.
In the central nervous system, heat shock protein (HSP) synthesis is induced not only after hyperthermia, but also following alterations in the intracellular redox environment. The major neurodegenerative diseases, AD, PD, ALS, MS, HD and FRDA are all associated with the presence of abnormal proteins9. The "unfolded protein response" has evolved to prevent accumulation of unfolded or misfolded proteins. Recent discoveries of the mechanisms of cellular stress signaling have led to new insights into the diverse processes that are regulated by cellular stress responses. The brain detects and overcomes oxidative stress by a complex network of "longevity assurance processes" integrated to the expression of genes termed vitagenes. Heat-shock proteins are highly conserved and facilitate correct protein folding. Heme oxygenase-1, an inducible and redox-regulated enzyme, has having an important role in cellular antioxidant defense. An emerging concept is neuroprotection afforded by heme oxygenase by its heme degrading activity and tissue-specific antioxidant effects, due to its products carbon monoxide and biliverdin, which is then reduced by biliverdin reductase in bilirubin. There is increasing interest in dietary compounds that can inhibit, retard or reverse the steps leading to neurodegeneration in AD. Specifically any dietary components that inhibit inappropriate inflammation, AbetaP oligomerization and consequent increased apoptosis are of particular interest, with respect to a chronic inflammatory response, brain injury and beta-amyloid associated pathology. Curcumin and ferulic acid, the first from the curry spice turmeric and the second a major constituent of fruit and vegetables, are candidates in this regard. Not only do these compounds serve as antioxidants but, in addition, they are strong inducers of the heat-shock response. Food supplementation with curcumin and ferulic acid are therefore being considered as a novel nutritional approach to reduce oxidative damage and amyloid pathology in AD.
We have recently focused our research on the role of acetylcarnitine (LAC) in the defense mechanisms against cellular stress and neurodegeneration3. In the present study we investigated mRNA expression and protein synthesis of Hsps and the oxidant status in adult (12 months) and senescent (28 months) rats, and the effect of LAC treatment in senescent rats. mRNA and protein synthesis of Hsps increased in senescent rats compared to adults in all brain regions examined; the maximum increase was observed in the hippocampus followed by cerebellum, cortex, and striatum. Hsps increase was associated with significant decrease in glutathione (GSH) redox state and decrease of carbonyls and HNE content. Interestingly, treatment with LAC resulted in a marked increase of heme oxygenase-1 (HO-1), Hsp70, and mtSOD expression, of GSH content, and a decrease of HNE and protein carbonyl contents in the hippocampus, striatum, cortex and cerebellum. These results were also confirmed by in situ hybridization experiments. We used also a parallel redox proteomic approach4-8 to identify the proteins that are oxidized in aged rat brain and those proteins that are protected by LAC treatment. Redox proteomics analysis in HP and CX, brain regions in which all indices of oxidative modification are elevated in brain aging showed that the specific carbonyl levels of three proteins, hemoglobin (HMG), cofilin 1 (COF 1) and beta-actin (ACT), are significantly increased in HP of senescent rats. Carbonyl levels of these proteins are reduced by LAC administration in old rats brains. In the CX of senescent rats, the specific carbonyl levels of eight proteins were increased. These proteins are heat shock protein 70 (Hsp70), glyoxylase 1 ( GOL 1), beta-actin (ACT), 3-mercaptopyruvate sulfurtransferase (MPST), peroxiredoxin 1 (PDX), phosphoribosyl pyrophosphate synthetase 1 (PPRPS1), and fumarase (FUM). LAC administration reduced the specific carbonyl levels of all these protein in the CX of senescent rats. The proteins identified in our study are involved in three processes which are impaired in aged brains: antioxidant defence, mitochondrial function and plasticity. LAC treatment might improve the decline of these functions. We posit that LAC should be considered as a potential therapeutic contributor for the treatment of cognitive decline in aging and age-related neurodegenerative disorders. I will outline here some of the emerging concepts of pathways to neurodegeneration and how these may be overcome by a nutritional approach. Moreover the emerging concept of vitagene modulation by redox active nutritional compounds will be discussed in the light of Antiaging medicine strategies and therapeutic interventions1-10.
Therapeutic strategies focussing on acetylcarnitine or food factors-derived modulation of redox homeostasis, by up-regulating vitagenes may represent a crucial mechanism of defence against free radical-induced damage of specific proteins occurring in aging brain and in neurodegenerative disorders. This findings are relevant to potential pharmacological strategy pointing to maximize cellular stress resistance in vulnerable tissues such as the brain and thus providing neuroprotection6-11.

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