Rajiv Ratan

Last updated
Rajiv Ratan
Rajiv Ratan.jpg
BornJuly 1960
Pittsburgh Pennsylvania
Occupation(s)Author, researcher, professor, administrator
SpouseRini Ratan

Rajiv Ratan is an Indian American academic, professor, administrator and scientist based in New York. He is the Burke Professor of Neurology and Neuroscience at Weill Cornell Medicine. [1] [2] Since 2003, he has served as the executive director of Burke Neurological Institute and as a member of the Council of Affiliated Deans of Weill Cornell Medicine. [3] [4]

Contents

Ratan's scientific efforts primarily focus on understanding how neurons respond to physiological stresses, particularly oxidative stress, adaptively and maladaptively at a transcriptional level, and how the balance of these activities leads to neuronal death and impairment, or cell survival and recovery or resistance. [5] [1] [6] He has published over 160 articles and has edited and contributed chapters to books. [7] Ratan's studies have identified novel transcriptional and epigenetic strategies for limiting neuronal ferroptosis which have identified novel small molecule approach which have been validated in numerous neurological disease models. [8] [1]

Early life and education

Ratan was born in July 1960 in Pittsburgh, Pennsylvania to immigrant parents from India. He attended the Webb School of California where he graduated with Honors in 1977. [9] He completed his BA in Neuroscience from Amherst College in 1981 graduating magna cum laude and received the John Woodruff Simpson Fellowship in Medicine. [4] At Amherst College, he completed an Honors thesis on the role of the cerebellum in regulating nuclei associated with emotion in the cerebrum. [10] He later completed his M.D. and Ph.D. from the New York University School of Medicine in 1988, where he was named to the medical honor society, Alpha Omega Alpha. [11] [12]

Ratan's Ph.D. work was done with Michael Shelanski and Fred Maxfield and focused on ways to monitor calcium dynamically in living cells. After the completion of his NIH funded Medical Scientist Training Program Fellowship at NYU in 1988, he completed an Internship in Medicine at the University of Chicago Hospitals and Clinics and later became the Chief Resident in Neurology at Johns Hopkins Hospital. [13] [14] At Johns Hopkins, he received the Jay Slotkin Award for excellence in research. From 1992 to 1994, he was a clinical fellow in Neurorehabilitation and a research fellow in the Department of Neuroscience at Johns Hopkins, where he developed data related to programmed cell death and disease with Jay Baraban and Tim Murphy. [15]

Career

After completing his fellowship at Johns Hopkins, Ratan became Assistant Professor in Physical Medicine, Rehabilitation and Neurology. He became the assistant professor in neurology in 1996 at the Harvard Medical School. The same year, he joined the Beth Israel Deaconess Medical Center as attending neurologist and Youville Hospital as consultant in neurorehabilitation. [16] He set up the Neuroprotection Laboratory at the Harvard Medical School in the Department of Neurology and he joined the Program in Neuroscience as well as the Center for NeuroDiscovery in Neurodegeneration. [17] He taught a course in the New Pathway and a seminar course on Transcriptional Mechanisms of Neuronal Death and Survival in Program in Biological and Biomedical Sciences at Harvard Medical School. He became an associate professor at Harvard Medical School in 1999 and taught there until 2004. [9] [18]

Ratan joined the Burke Neurological Institute in 2003 as its second director He has been on the advisory board of the Dana Brain Health Alliance since 2012.Ratan became a member of the Faculty of 1000, Neurorehabilitation in 2015, and cofounded a novel clinical trials platform called NeuroCuresNY in 2019. [11]

He has been on the editorial board of journals including serving as a Reviewing Editor at The Journal of Neuroscience for 6 years, Senior Associate Editor at Neurotherapeutics, Associate Editor at the Journal of Huntington's disease, and Editorial Boards for Antioxidants and Redox Signaling and Neurobiology of Disease in addition to several other journals. [8]

In 2020, Ratan was elected to the Johns Hopkins Society of Scholars. [19]

Research and Writing

The central focus of the Ratan laboratory's work is to understand adaptive programs that facilitate the brain's ability to combat injury and to foster repair. [20] His studies have tried to explain fundamental mechanisms by which oxidative stress triggers ferroptosis, the inappropriate demise of neurons, and accordingly his molecular and pharmacological studies have had an impact in a number of disease models including stroke, spinal cord injury, traumatic brain injury and Huntington's disease, Parkinson's disease, and Alzheimer's disease. [1] [21] His lab has developed strategies for manipulating reactive oxygen species, specifically peroxide in the nervous system. [22] [23]

In his research, he has worked with undergraduates, graduate students and post-doctoral fellows and has taught a seminar course at Harvard Medical School on the "Transcriptional regulation of survival and death in neurons". His studies have helped identify strategies for limiting neuronal apoptosis and potential markers for antioxidant treatment in the central nervous system. [23]

He co-edited the 1999 book Cell Death and Diseases of the Nervous System and wrote two chapters in it. [24] [25] [26] It was reviewed by Acta Neurologica Belgicathat that wrote "this volume broadly covers the field of neuronal death, and the large number of (mostly) up to date references make this a very useful textbook. Being written and edited by authorities in the field, it can be strongly recommended." [27] In a review of the book, Trends in Neurosciences wrote "overall, this is a sound book with well-recognized authors whose expertise spans the field of neurodegenerative disorders. [28]

In 2004, he co-edited Current Atherosclerosis Reports (Cardiovascular Disease and Stroke) with John Blass and in 2008, he co-edited Mitochondria and Oxidative Stress in Neurodegenerative Disorders with Gary Gibson and Flint Beal. [29]

Administration, committee work, and meetings

In 2003, Ratan was selected among a pool of applicants via a national search to Direct the Burke Medical Research Institute at Weill Cornell Medicine. [11] [30] From 2003-2016, Ratan lead a large-scale recruitment of repair focused scientists at Burke.[14] These recruitments were associated with significant renovation of facilities within the research institute. Accordingly, the focus of research at Burke expanded to include vision recovery, motor recovery, pain and sensory recovery and cognitive recovery and represent one of the largest benches to bedside efforts focused on spinal and brain repair in the world. [31] [8]

Ratan has been the Chair of the Scientific Advisory Board for the Partnership in Stroke Recovery in Canada; he has served on NIH Study Sections; and he Co-Chaired the Gordon Conference on Oxidative Stress in Ventura, California in March 2015. [13] In collaboration with Mark Noble and Marie Filbin, he was principal investigator of an eleven institution Center of Research Excellence in Spinal Cord Injury funded via a $15 million from the New York State Department of Health. [32]

Awards

Partial Bibliography

Books

Chapters

Related Research Articles

Neurotoxicity is a form of toxicity in which a biological, chemical, or physical agent produces an adverse effect on the structure or function of the central and/or peripheral nervous system. It occurs when exposure to a substance – specifically, a neurotoxin or neurotoxicant– alters the normal activity of the nervous system in such a way as to cause permanent or reversible damage to nervous tissue. This can eventually disrupt or even kill neurons, which are cells that transmit and process signals in the brain and other parts of the nervous system. Neurotoxicity can result from organ transplants, radiation treatment, certain drug therapies, recreational drug use, exposure to heavy metals, bites from certain species of venomous snakes, pesticides, certain industrial cleaning solvents, fuels and certain naturally occurring substances. Symptoms may appear immediately after exposure or be delayed. They may include limb weakness or numbness, loss of memory, vision, and/or intellect, uncontrollable obsessive and/or compulsive behaviors, delusions, headache, cognitive and behavioral problems and sexual dysfunction. Chronic mold exposure in homes can lead to neurotoxicity which may not appear for months to years of exposure. All symptoms listed above are consistent with mold mycotoxin accumulation.

<span class="mw-page-title-main">Neuroprotection</span> Relative preservation of neuronal structure and/or function

Neuroprotection refers to the relative preservation of neuronal structure and/or function. In the case of an ongoing insult the relative preservation of neuronal integrity implies a reduction in the rate of neuronal loss over time, which can be expressed as a differential equation. It is a widely explored treatment option for many central nervous system (CNS) disorders including neurodegenerative diseases, stroke, traumatic brain injury, spinal cord injury, and acute management of neurotoxin consumption. Neuroprotection aims to prevent or slow disease progression and secondary injuries by halting or at least slowing the loss of neurons. Despite differences in symptoms or injuries associated with CNS disorders, many of the mechanisms behind neurodegeneration are the same. Common mechanisms of neuronal injury include decreased delivery of oxygen and glucose to the brain, energy failure, increased levels in oxidative stress, mitochondrial dysfunction, excitotoxicity, inflammatory changes, iron accumulation, and protein aggregation. Of these mechanisms, neuroprotective treatments often target oxidative stress and excitotoxicity—both of which are highly associated with CNS disorders. Not only can oxidative stress and excitotoxicity trigger neuron cell death but when combined they have synergistic effects that cause even more degradation than on their own. Thus limiting excitotoxicity and oxidative stress is a very important aspect of neuroprotection. Common neuroprotective treatments are glutamate antagonists and antioxidants, which aim to limit excitotoxicity and oxidative stress respectively.

Neuroimmunology is a field combining neuroscience, the study of the nervous system, and immunology, the study of the immune system. Neuroimmunologists seek to better understand the interactions of these two complex systems during development, homeostasis, and response to injuries. A long-term goal of this rapidly developing research area is to further develop our understanding of the pathology of certain neurological diseases, some of which have no clear etiology. In doing so, neuroimmunology contributes to development of new pharmacological treatments for several neurological conditions. Many types of interactions involve both the nervous and immune systems including the physiological functioning of the two systems in health and disease, malfunction of either and or both systems that leads to disorders, and the physical, chemical, and environmental stressors that affect the two systems on a daily basis.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

<span class="mw-page-title-main">Max Planck Institute for Experimental Medicine</span>

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<span class="mw-page-title-main">Brain mitochondrial carrier protein 1</span> Protein-coding gene in the species Homo sapiens

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Anne Buckingham Young is an American physician and neuroscientist who has made major contributions to the study of neurodegenerative diseases, with a focus on movement disorders like Huntington's disease and Parkinson's disease. Young completed her undergraduate studies at Vassar College and earned a dual MD/PhD from Johns Hopkins Medical School. She has held faculty positions at University of Michigan and Harvard University. She became the first female chief of service at Massachusetts General Hospital when she was appointed Chief of Neurology in 1991. She retired from this role and from clinical service in 2012. She is a member of many academic societies and has won numerous awards. Young is also the only person to have been president of both the international Society for Neuroscience and the American Neurological Association.

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Benjamin Wolozin is an American pharmacologist and neurologist currently at Boston University School of Medicine and an Elected Fellow of the American Association for the Advancement of Science.

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References

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