Mark P. Mattson is the Head of the Neurosciences Laboratory at the National Institute on the Aging Research Program of the National Intramural Institute on Aging. He is also Professor of Neuroscience at Johns Hopkins University.
Video Mark Mattson
Early life and education
Mark P. Mattson was born in 1957 in Rochester, Minnesota. After receiving a PhD from the University of Iowa, Dr. Mattson completed a postdoctoral fellowship at Developmental Neuroscience at Colorado State University. He later joined Sanders-Brown Center on Aging and the Department of Anatomy and Neurobiology at the University of Kentucky College of Medicine as Assistant Professor. Dr. Mattson was promoted to the rank of Associate Professor with a tenure and then became a Full Professor. In 2000, Dr. Mattson took the position of Head of the Neurosciences Laboratory at the National Institute on Aging in Baltimore, where he led a multi-faceted research team that applied cutting-edge technology in research aimed at understanding the molecular and cellular mechanisms of brain aging and the pathogenesis of neurodegenerative disorders. He is also a Professor in the Department of Neurology at Johns Hopkins University School of Medicine.
Maps Mark Mattson
Careers
Dr Mattson is regarded as a leader in the field of cellular and molecular mechanisms underlying neuronal plasticity and neurodegenerative disorders, and has contributed greatly to understanding the pathogenesis of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and stroke, and for their prevention and treatment.. He has published over 900 peer-reviewed articles in leading journals and books, and has edited 10 books in the field of neural signal transduction, neurodegenerative disorders and aging mechanisms. Dr. Mattson is the most quoted neurologist in the world according to the ISI information database (http://www.in-cites.com/top/2006/second06-neu.html), and he has a h-index of over 200 (ie , 200 of the articles published each have been cited at least 200 times. Mattson has been published in various forums including: Science Watch (http://archive.sciencewatch.com/ana/st/alz2/11julSTAlz2Matt/). Natural Medicine (http://www.nature.com/nm/journal/v10/n4/full/nm0404-324.html).
Awards and acknowledgments
Dr. Mattson has received numerous awards including the Medical Research Award of the Metropolitan Life Foundation, the Alzheimer Association Zenith Award, Jordi Folch Pi Awards, Santiago Grisolia Chair Gifts, the Cov-Walerstein Science Tovi Award, and several Grass Lecture Awards. He was elected a Member of the American Association for the Advancement of Science. He is the Editor-in-Chief of NeuroMolecular Medicine and Aging Research Reviews, and has been a Managing or Associate Editor of the Journal of Neuroscience, Trends in Neurosciences, Journal of Neurochemistry, Neurobiology of Aging, and Journal of Neuroscience. Research. Dr. Mattson has served in several parts of the NIH research and in scientific advisory boards for many research foundations. He has trained over 70 postdoctoral and predoctoral scientists, and has contributed greatly to the education of undergraduate, graduate and medicine students.
Contribution to research
Dr. Mattson establishes a signal pathway in which neurons respond adaptively to bioenergetic and environmental challenges in a way that enhances neuroplasticity and resistance to neurodegenerative disorders. His discovery of the mechanisms by which intermittent fasting and exercise benefit the health of the brain and body is being translated into the prevention of disease and treatment in humans.
Research by Mattson in the field of molecular and cellular mechanisms that regulate neuronal plasticity and survival, in the context of brain development and aging, has established a new conceptual framework for understanding the pathogenesis of neurodegenerative disorders. He pointed out that the interference of cellular signaling mechanisms that regulate developmental neuroplasticity is responsible for the synaptic dysfunction and cell death in neurodegenerative disorders. In particular, he has been a leader in advancing the understanding of molecular events that destabilize cellular calcium homeostasis and ultimately lead to death of neurons in Alzheimer's disease, Parkinson's disease, ALS and stroke. Here are some specific examples of Dr.'s seminal findings. Mattson represents a major advance in the field of neuroscience and neurodegenerative disorders.
In a preliminary study, Dr. Mattson found that glutamate neurotransmitters, previously believed to function only in synapses, play a key role in regulating the growth of dendrites and synaptogenesis. He then pointed out that neurotropic factors can modify the effects of neurotransmitters on the growth of neurit, synaptogenesis and cell survival. Glutamate and neurotropic factors exert its effect on neuronal plasticity and survival by modulating cellular calcium homeostasis. These findings reveal the molecular basis for regulation depending on neuronal plasticity activity. Importantly, Dr. Mattson that neurotropic factors such as bFGF, BDNF and IGFs may protect neurons against dysfunction and degeneration in experimental models of stroke and Alzheimer's disease led to clinical trials of neurotrophic factor assignment in patients with stroke and neurodegenerative disorders.
A major contribution to the field of neuroscience and neurology is Dr. Mattson which explains the mechanism of synaptic dysfunction and degeneration in AD. He points out that amyloid peptides (Abeta) induce oxidative stress associated with membranes that interfere with calcium homeostasis and make neurons susceptible to excitotoxicity and apoptosis. His work shows that the 4-hydroxynonenal lipid peroxidation product mediates the Abeta toxicity by covalently modifying the ion-motive ATPase, and transporting glucose and glutamate. He also showed that presenilin mutations harm neurons by disrupting the calcium regulation of the endoplasmic reticulum. His work also reveals the physiological role for the secreted form of amyloid precursor proteins produced by alpha-secretase activity (sAPPalpha). He showed that sAPPalpha suppresses nerve stimulation and protects neurons against excitotoxicity by a mechanism involving receptor activation coupled with cyclic GMP production and potassium channel activation.
Dr. Mattson is the first to report that TNF and NF-B can promote neuronal survival, and he went on to point out that this mechanism involves the over-regulation of manganese superoxide dismutase and Bcl-2 expression, and cellular calcium stabilization. homeostasis. This provocative finding causes a 180-degree change in the view of proinflammatory cytokines and NF-B in nerve injury by establishing that NF-B activation in neurons is part of an adaptive response aimed at protecting neurons.
The discovery made in Dr. laboratory Mattson led to a new view of the apoptotic biochemical cascade in the physiological regulation of synaptic plasticity and structural remodeling, and introduced the field of neuroscience to the concept of "synaptic apoptosis". He showed that, by cleaving specific glutamate receptor subunits, caspases play an important role in regulating synaptic plasticity, an entirely new and unexpected function of apoptotic proteases.
A series of findings by Dr. Mattsons during the 1990s and 2000s linked diet and pathogenesis to neurodegenerative disorders. He has shown that intermittent fasts may increase neuronal resistance in the brain for dysfunction and degeneration in animal models of Alzheimer's, Parkinson's and Huntington's disease and stroke. The underlying mechanisms are shown to involve increased production of neurotrophic factors and complementary proteins, suggesting adaptive response of brain cells to stress associated with intermittent fasting. Collectively, these findings provide examples of how Dr. Mattson into the biochemistry and biology of neuronal plasticity and death has provided information that can be directly applied to improve the human condition.
Challenges of Bioenergy, Neuroplasticity and Neuroprotection: Research in Dr. Lab. Mattson has revealed the importance of intermittent energetic challenges such as strenuous exercise and fasting in promoting optimal brain function and brain resistance to age-related neurodegenerative disorders and disorders. The ability of neurons to respond adaptively to mild stress is an example of a hormesis, a process in which exposure of cells or organisms to mild stress/challenge produces beneficial effects on their function and stress resistance. Dr Mattson found that neurons can respond to energetic challenges by increasing their production: important neurotrophic factors for learning and memory, and neurogenesis (the production of new neurons from stem cells, DNA repairing enzymes that prevent accumulation of mutations, and antioxidant enzymes). which allows cells to quell free radicals. Laboratories also found that bioenergy challenges such as exercise can increase the number of mitochondria in neurons and can improve mitochondrial health. In related studies, some drugs that cause mild stress on mitochondria are found. useful in animal models of stroke.
Dr. Mattson has revealed a mechanism in which diabetes adversely affects the hippocampal plasticity and cognitive function. He showed that, in insulin-deficient and insulin-resistant mice, diabetes impaired hippocampus-dependent memory, synaptic plasticity perforation pathways and adult neurogenesis, and steroidal steroid corticosterone contributed to this adverse effect. The change in hippocampal plasticity and function in both models is reversed when normal physiologic corticosterone levels are maintained, suggesting that cognitive impairment in diabetes may occur due to glucocorticoid-mediated deficits in neurogenesis and synaptic plasticity. In a related study, Mattson showed that mice fed a high-fat, high-glucose diet supplemented with fructose corn syrup showed changes in energy and lipid metabolism similar to that of clinical diabetes, with increased fasting glucose and elevated cholesterol and triglycerides. Mice maintained on this diet for 8 months demonstrated impaired spatial learning ability, reduced hippocampal dendritic spine density, and reduced long-term potentiation of Schaffer's assurances - CA1 synapses. This change occurs along with a decrease in BDNF levels in the hippocampus. Dr. Mattson is also investigating whether manipulations that increase neurotropin levels will also restore nerve structure and function in diabetes. He found that wheelchair activity, caloric restriction, or a combination of two treatments increased BDNF levels in the diabetic hippocampus. Increased hippocampal BDNF is accompanied by increased dendritic spine density in secondary and tertiary dendrites of dentate granular neurons. These studies show that diabetes has a detrimental effect on the hippocampal structure, and that this state can be attenuated by increasing energy expenditure and reducing energy intake. The implications of these findings for cognitive senescence are obvious - moderation diets and regular exercise will improve cognitive function.
The role of key toll-like receptors (TLRs) as mediators of the detection and response of immune cells to attack pathogens is well known. However, Dr. Mattson recently found that neurons also express a subset of TLR and that their activation promotes neuronal degeneration in experimental models of stroke and AD He also provides evidence that toll-like receptors play a role in regulating neurogenesis and neurite growth processes. , suggest a role in neuronal plasticity. Levels of TLR2 and TLR4 increased in cerebral cortical neurons in response to ischemic/reperfusion injury, and the number of brain damage and neurological deficits caused by stroke was significantly less in mice lacking TLR2 or -4 compared with WT control mice. Mattson found that TLR4 expression increased in neurons when exposed to Abeta or the 4-hydroxynonenal lipid peroxidation product (HNE). Neuronal apoptosis induced by Abeta and HNE is mediated by N-terminal kinase (JNK); neurons from mutant-testing mice TLR4 reduce JNK and caspase-3 activation and are protected against apoptosis caused by Abeta and HNE. The TLR4 level decreases in the inferior cortical parietal tissue specimens of end-stage AD patients compared with the elderly control subjects, possibly as a result of loss of neurons expressing TLR4. These findings suggest that TLR4 signaling increases the susceptibility of neurons to Abeta and oxidative stress in AD, and identifies TLR4 as a potential therapeutic target for stroke and AD.
Glucagon-like peptide-1 (GLP-1) is an endogenous insulinotropic peptide secreted from the digestive tract in response to food intake. It increases the proliferation of pancreatic beta cells and glucose-dependent insulin secretion, and lowers blood glucose and food intake in patients with type 2 diabetes mellitus (T2DM). GLP-1 long-term receptor GLP-1 (GLP-1R), Exenatide, is the first of a new class of antihyperglycemia drugs approved by the FDA to treat T2DM. Mattson and his colleagues at the National Institute on Aging have shown that GLP-1R is expressed in neurons where they are paired with a second cAMP messenger pathway that results in neurotropic action. For example, he points out that Exenatide can protect neurons from being damaged and killed by Abeta. Administration of Exenatide reduces brain damage and improves functional outcome in stroke models of middle transient cerebral artery occlusion, and also protects dopaminergic neurons against degeneration, maintains dopamine levels, and improves motor function in 1-methyl-4-phenyl-1,2,3,6 -tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In addition, Exenatide treatments ameliorated abnormalities in peripheral glucose regulation and suppressed cellular pathology in both brain and pancreas in Huntington disease mouse model. Treatment also improves motor function and extends the survival time of Huntington disease rats. Because Exenatide improves glucose regulation and provides direct neuroprotective action on neurons in the brain, and related drugs are being tested in patients with mild cognitive impairment and Alzheimer's disease.
Intermittent Fasting
Dr. Mattson on animal models and human subjects has resulted in the adoption of intermittent fasting as an intervention to optimize health and reduce the risk of many major chronic diseases including obesity, diabetes, cancer, asthma and other inflammatory disorders, cardiovascular disease and neurodegenerative disorders.
Animal studies conducted at Dr. Mattson's Laboratory shows that intermittent fasting has a very beneficial effect on the body and brain including: 1) Increased glucose regulation; 2) loss of abdominal fat with maintenance of muscle mass; 3) Reduces blood pressure and heart rate, and increases heart rate variability (similar to what happens to trained endurance athletes; 4) Improved learning and memory and motor function; 5) Protection of neurons in the brain against dysfunction and degeneration in animal models of Alzheimer's disease, Parkinson's disease, stroke and Huntington's disease. He further found that intermittent fasting benefits health because it imposes a challenge on cells, and they respond adaptively by increasing their ability to cope with stress and fight disease.
After publishing the results of two studies documenting the beneficial effects of intermittent fasts on human subjects, one in asthma patients (in collaboration with Dr. James Johnson at LSU Medical Center) and others in women at risk for breast cancer (in collaboration with Dr. Michelle Harvie at the University of Manchester), media coverage research Dr. Mattson leads to a BBC documentary and a subsequent book by Dr. Michael Mosley has informed people around the world about the health benefits of intermittent fasting. In particular, the diet is called the 5: 2 diet, based on the study of Drs. Harvie and Mattson have become very popular. A person with a 5: 2 diet eats healthy foods in normal amounts 5 days per week and eats only one moderate serving (500-600 calories) eats 2 days each week. For many people, this diet proves to be easy to apply and maintain.
Phytochemical Hormesis: In 2006 Dr. Mattson proposes that the reason that vegetables, fruits, tea and coffee can improve brain health is that they contain harmful chemicals produced by plants to protect themselves from the eating of insects and other organisms. {Mattson, M. P. and A. Cheng (2006) Neurohormetic phytochemicals: Low-dose toxins that induce an adaptive neuronal stress response. Trend Neurosci. 29: 632-639} Such phytochemicals, classified as antifeedan or natural pesticides, trigger adaptive stress responses in brain cells that can improve brain function and can increase neuronal resistance to age-related neurodegenerative injuries and disorders such as Alzheimer's disease and Parkinson's disease. Dr. Mattson recently published an article in Scientific American that describes evolutionary grounds, molecular mechanisms and dietary implications of what he calls 'phytochemical hormones'
Mental Pattern Processing: The fundamental question in philosophy and neuroscience is why and how humans have transcended other species in their ability to think, communicate and engage in abstract thinking. In the year 2014. Mattson published an article entitled "Superior Pattern Processing is the Embryo of a Developing Brain Man" in which he proposes that superior mental processes of the pattern are the fundamental basis of all the advanced abilities of the human brain including intelligence, imagination, discovery. , language and beliefs in imaginary entities such as gods and ghosts. The expansion of the cerebral cortex during human evolution involves most areas of the brain such as the visual association cortex and the prefrontal cortex that serve to process visual images quickly and make appropriate decisions. Patterns, whether real or imagined, are reinforced by emotional and social experiences, indoctrination and even psychedelic drugs. Abnormal brain function and behavior that occurs in cognitive and psychiatric disorders occurs due to disturbed or distorted pattern processes. Dr. Theory Mattson has important implications for understanding human intelligence, creativity and imagination, and for developing new approaches to reduce irrational decisions and destructive behaviors that persist in radical individuals and groups around the world.
Personal life
Dr. Mattson lives with his wife, Joanne Mattson and is the father of two children, Elliot and Emma. In his spare time, he pursues running tracks, mountain bikes and off-road motorcycles. After being taught by DeWayne's father, Mark learned how to train and ride standard trotters and compete on race tracks in Minnesota, Wisconsin, Iowa and Michigan during the 1970s and 1980s. In the past, he also competed as a long-distance runner, and cross-country trainer at Patterson Mill High School in Bel Air, Maryland. In addition, he is a qualified Master Gardener and enjoys farming.
Quotes
"Superior pattern processing is the core of the evolving human brain."
"The human brain is very adept at the imagination, the ability that is responsible for understanding and escaping from reality."
"Nerve cells have innate ability to respond adaptively to intermittent challenges in ways that help them work optimally and fight aging adversity, thereby preventing Alzheimer's and Parkinson's disease."
"Imagination is an advanced form of mental pattern processing that allows formulation and testing of hypotheses, which are necessary to establish truth and predict future outcomes.
"The lack of understanding of the difference between possibility and possibility is a very consequential scientific illiteracy aspect."
"The unique ability of humans to interrogate and understand reality must be pursued diligently and with wisdom."
"The running trail is a classic human enjoyment."
References
External links
- Johns Hopkins Profile from Mark Mattson
- National Institute on Aging
- TED Talk
- cognitive performance optimization
Source of the article : Wikipedia
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