Professor Giovanni Scapagnini MD PhD
Assistant Professor, Institute of Neurological
Sciences, Italian National Research Council, Catania, Italy
Assistant Professor, Blanchette Rockefeller
Neurosciences Institute, West Virginia University, Rockville (MD),
Visiting Professor, Institute of Human
Virology, University of Maryland, Baltimore (MD), USA
Professor Scapagnini attended the University of Catania School
of Medicine and Surgery in Catania, Italy and graduated in 1992 with
a medical degree. He continued his education by obtaining a Ph.D. in
Neurobiology also from the University of Catania in 2000. Since completing
his education, Dr. Scapagnini has conducted research with the Institute
of Pharmacology School of Medicine associated with the University of
Catania and has worked as a Visiting Scientist with Department of Surgical
Research, Northwick Park Institute for Medical Research, Harrow, UK
in 1999, and with Laboratory of Adaptive Systems, National Institute
of Neurological Disorders and Stroke, National Institute of Health
in Bethesda, MD, USA in 2000. Dr. Scapagnini currently holds two academic
positions as Assistant Professor with the Institute of Neurological
Sciences, Italian National Research Council and with Blanchette Rockefeller
Neurosciences Institute, West Virginia University. He has recently
obtained a visiting professorship with the Institute of Human Virology,
University of Maryland, where he is in charge of a research project
on HIV dementia. He is also the scientific director of the “Research & Progress” foundation,
founded by Dr Robert C. Gallo. He is author of 35 indexed scientific
papers and several book chapters. His fields of research regard gene
expression profiles of cellular stress response and biology and molecular
mechanisms of brain aging and nerurodegenerative disorders. In particular
he has studied the anti-aging activities of several nutraceuticals
present in the Mediterranean diet.
2013 - Brain Longevity Program: Use Mind to change your Age (Workshop)
This course will provide an overview about state of the art strategies to manage our brain fitness and preserve it from pathological aging. Brain is extremely susceptible to aging processes, mostly because its vulnerability to inflammation and oxidative stress. The potential loss of mental abilities, due to age related neurodegenerative process, may be the most worrisome of all ageing dysfunctions. Due to the progressive ageing of the population and to the age-associated increase in its incidence, Alzheimer disease (AD) will become in near future one of the major challenges that healthcare systems will have to face with in developed countries. Data from international AD associations suggest that AD patients will triple by year 2050, an epidemiologic trend that has elicited the definition of silent epidemic. Since the pathophysiological process of AD is thought to begin many years before the diagnosis of clinical dementia, in theory there is an opportunity for preventive therapeutic interventions. Therefore, new guidelines should incorporate a shared definition of the pathological continuum leading to clinical AD, as well as an agreement on risk factors for progression and on validated biomarkers for early identification of pre-clinical abnormalities. At the same time, there is urgent need for preventive approaches that prove to be safe, effective, and cost-efficient. Although absolute prevention of dementia is not possible, better dementia prevention and brain aging management is certainly achievable and of utmost importance. Research shows that the brain is highly responsive to the environment and displays impressive capacity to compensate for damage. Indeed, many studies have investigated the potential of nutritional protocols, technology-based software products and other approaches, like physical exercise, that may be useful in maintaining cognitive fitness. In the first part of the course we will look first at how to assess cognitive functions and brain health state, with major focus on the available selection of genetic and biochemical biomarkers for brain ageing and neurodegenerative diseases, particularly those linked to inflammation and oxidative stress. Then we’ll illustrate dietary interventions as a viable strategy for enhancing cognitive abilities and protecting the brain from damage, promoting repair and counteracting the effects of aging. Few dietary supplements have been also subjected to large randomized controlled trials that have been published in leading journals, and demonstrated useful activity against brain aging dysfunctions. Then we’ll look at Software-based cognitive training that have been shown to improve users’ performance on trained tasks, and their possible role for prevention of age related cognitive decline.
We’ll also illustrate beneficial effects of physical exercise programs on brain ageing. Physical exercise is not only a low-cost and effective way to improve your health but also an important key to improving brain fitness. Scientists have found that regular aerobic exercise increases blood flow to the brain, and helps to support formation of new neural and vascular connections. Physical exercise has been shown to improve attention, reasoning and components of memory.
Finally we will explore how the maintenance of brain fitness will improve the quality of our body aging. Several clues, indicates that many aspects of organism aging are directly controlled by the brain. What’s exciting is that it’s possible — at least in experimental models — to alter signaling within some parts of the brain to slow down the aging process and increase longevity. For example, recently, Dr. Cai and his team at the Albert Einstein College of Medicine in New York, demonstrated that activating the NF-κB pathway in the hypothalamus of mice significantly accelerated the development of aging, while blocking it significantly improved mice life span.
2013 - Antioxidants as Antidepressants: Fact or Fiction (Conference)
Depression is a condition with a complex biological pattern of etiology, that involve genetic and epigenetic contributors, along with different environmental stressors. Data showing immune activation in depressed patients were reported for the first time more than 20 years ago by Maes et al. Since then, the presence of an inflammatory response in depression has been described several times. Meta-analysis studies have revealed that increased peripheral blood levels of cytokines, interleukin (IL)-6, tumour necrosis factor (TNF)-α, the acute-phase reactant and C-reactive protein (CRP) are some of the most reliable biomarkers of increased inflammation in depressed patients. Inflammatory cytokines also interact with mitochondria to increase the reactive oxygen species (ROS) production, which in turn increases cytokine expression. Recent evidences suggest that oxidative stress processes might play a relevant role in the pathogenic mechanism underlying many major psychiatric disorders, included depression. Reactive oxygen and nitrogen species have been shown to modulate levels and activity of norepinephrine, serotonin, dopamine and glutamate, the principal transmitters involved in the neurobiology of depression. Major depression has been associated with a lower concentrations of several endogenous antioxidant compounds, such as vitamin E, zinc and coenzyme Q10, or enzymes, such as glutathione peroxidase, and with a decrease of the total antioxidant status. These data introduce new potential targets for the development of therapeutic interventions based on antioxidant compounds. Exogenous antioxidant are an heterogeneous class of compounds ranging from minerals to complex vegetable xenobiotics. N-acetyl cysteine has been shown to have a significant benefit on depressive symptoms in a randomized placebo-controlled trial. S-adenosyl methionine, a naturally occurring molecule that serves as a methyl donor in human cellular metabolism, endowed with potent antioxidant activity, has been demonstrated to be an effective and safe adjunctive treatment strategy for SRI non-responders with major depressive disorder. Curcumin, the yellow pigment of curry, has been shown to strongly interfere with neuronal redox homeostasis in the CNS and to possess antidepressant action in various animal models of depression, also due to its ability to inhibits monoamine oxidases. There is an urgent need to develop better tolerated and more effective treatments for depressive disorders, several antioxidant treatments appear promising and deserve further study.