Related Research Articles
An epileptic seizure, informally known as a seizure, is a period of symptoms due to abnormally excessive or synchronous neuronal activity in the brain. Outward effects vary from uncontrolled shaking movements involving much of the body with loss of consciousness, to shaking movements involving only part of the body with variable levels of consciousness, to a subtle momentary loss of awareness. Most of the time these episodes last less than two minutes and it takes some time to return to normal. Loss of bladder control may occur.
The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor is an ionotropic transmembrane receptor for glutamate (iGluR) that mediates fast synaptic transmission in the central nervous system (CNS). It has been traditionally classified as a non-NMDA-type receptor, along with the kainate receptor. Its name is derived from its ability to be activated by the artificial glutamate analog AMPA. The receptor was first named the "quisqualate receptor" by Watkins and colleagues after a naturally occurring agonist quisqualate and was only later given the label "AMPA receptor" after the selective agonist developed by Tage Honore and colleagues at the Royal Danish School of Pharmacy in Copenhagen. The GRIA2-encoded AMPA receptor ligand binding core was the first glutamate receptor ion channel domain to be crystallized.
Brain-derived neurotrophic factor (BDNF), or abrineurin, is a protein that, in humans, is encoded by the BDNF gene. BDNF is a member of the neurotrophin family of growth factors, which are related to the canonical nerve growth factor (NGF), a family which also includes NT-3 and NT-4/NT-5. Neurotrophic factors are found in the brain and the periphery. BDNF was first isolated from a pig brain in 1982 by Yves-Alain Barde and Hans Thoenen.
Tropomyosin receptor kinase A (TrkA), also known as high affinity nerve growth factor receptor, neurotrophic tyrosine kinase receptor type 1, or TRK1-transforming tyrosine kinase protein is a protein that in humans is encoded by the NTRK1 gene.
Tropomyosin receptor kinase B (TrkB), also known as tyrosine receptor kinase B, or BDNF/NT-3 growth factors receptor or neurotrophic tyrosine kinase, receptor, type 2 is a protein that in humans is encoded by the NTRK2 gene. TrkB is a receptor for brain-derived neurotrophic factor (BDNF). Standard pronunciation is "track bee".
The p75 neurotrophin receptor (p75NTR) was first identified in 1973 as the low-affinity nerve growth factor receptor (LNGFR) before discovery that p75NTR bound other neurotrophins equally well as nerve growth factor. p75NTR is a neurotrophic factor receptor. Neurotrophic factor receptors bind Neurotrophins including Nerve growth factor, Neurotrophin-3, Brain-derived neurotrophic factor, and Neurotrophin-4. All neurotrophins bind to p75NTR. This also includes the immature pro-neurotrophin forms. Neurotrophic factor receptors, including p75NTR, are responsible for ensuring a proper density to target ratio of developing neurons, refining broader maps in development into precise connections. p75NTR is involved in pathways that promote neuronal survival and neuronal death.
Tropomyosin receptor kinase C (TrkC), also known as NT-3 growth factor receptor, neurotrophic tyrosine kinase receptor type 3, or TrkC tyrosine kinase is a protein that in humans is encoded by the NTRK3 gene.
Neurotrophic factors (NTFs) are a family of biomolecules – nearly all of which are peptides or small proteins – that support the growth, survival, and differentiation of both developing and mature neurons. Most NTFs exert their trophic effects on neurons by signaling through tyrosine kinases, usually a receptor tyrosine kinase. In the mature nervous system, they promote neuronal survival, induce synaptic plasticity, and modulate the formation of long-term memories. Neurotrophic factors also promote the initial growth and development of neurons in the central nervous system and peripheral nervous system, and they are capable of regrowing damaged neurons in test tubes and animal models. Some neurotrophic factors are also released by the target tissue in order to guide the growth of developing axons. Most neurotrophic factors belong to one of three families: (1) neurotrophins, (2) glial cell-line derived neurotrophic factor family ligands (GFLs), and (3) neuropoietic cytokines. Each family has its own distinct cell signaling mechanisms, although the cellular responses elicited often do overlap.
Neurotrophin-3 is a protein that in humans is encoded by the NTF3 gene.
Short transient receptor potential channel 3 (TrpC3) also known as transient receptor protein 3 (TRP-3) is a protein that in humans is encoded by the TRPC3 gene. The TRPC3/6/7 subfamily are implicated in the regulation of vascular tone, cell growth, proliferation and pathological hypertrophy. These are diacylglycerol-sensitive cation channels known to regulate intracellular calcium via activation of the phospholipase C (PLC) pathway and/or by sensing Ca2+ store depletion. Together, their role in calcium homeostasis has made them potential therapeutic targets for a variety of central and peripheral pathologies.
Gamma-aminobutyric acid receptor subunit gamma-2 is a protein that in humans is encoded by the GABRG2 gene.
Epileptogenesis is the gradual process by which a typical brain develops epilepsy. Epilepsy is a chronic condition in which seizures occur. These changes to the brain occasionally cause neurons to fire in an abnormal, hypersynchronous manner, known as a seizure.
Neurotrophic factor receptors or neurotrophin receptors are a group of growth factor receptors which specifically bind to neurotrophins.
Daniel H. Lowenstein, M.D., is the Robert B. and Ellinor Aird Professor of Neurology and Executive Vice Chancellor and Provost at the University of California, San Francisco (UCSF). He is known internationally for his work in the field of epilepsy including laboratory-based and clinical research, the clinical care of patients with epilepsy, and advocacy for the needs of patients and family members living with epilepsy. He has had an active role in medical education and in efforts to advance social justice, has held many leadership positions at both UCSF and Harvard Medical School, was the originator of the “Academy of Medical Educators” concept, and is the recipient of numerous teaching awards both at UCSF and nationally. He has served as the Dean for Medical Education at Harvard Medical School, and as President of the American Epilepsy Society. In 2017, he was elected to the National Academy of Medicine in recognition of his many contributions to American medicine.
Gene therapy is being studied for some forms of epilepsy. It relies on viral or non-viral vectors to deliver DNA or RNA to target brain areas where seizures arise, in order to prevent the development of epilepsy or to reduce the frequency and/or severity of seizures. Gene therapy has delivered promising results in early stage clinical trials for other neurological disorders such as Parkinson's disease, raising the hope that it will become a treatment for intractable epilepsy.
D. James "Jim" Surmeier, an American neuroscientist and physiologist of note, is the Nathan Smith Davis Professor and Chair in the Department of Physiology at Northwestern University Feinberg School of Medicine. His research is focused on the cellular physiology and circuit properties of the basal ganglia in health and disease, primarily Parkinson's and Huntington's disease as well as pain.
Juan Lerma Gómez is a Spanish neuroscientist and research professor at the Instituto de Neurociencias in Alicante. Currently he is editor-in-chief of Neuroscience, the official journal of the International Brain Research Organization, and scientific director of the programme "Severo Ochoa Center of Excellence" (2014-2022).
Lorne Mendell is a neurobiologist currently employed as a distinguished professor in the department of neurobiology and behavior at Stony Brook University in New York. His research focuses primarily on neurotrophins in neonatal and adult mammals, and on the neuroplasticity of the mammalian spinal cord. His research interests lie in other areas including pain, nerve wind-up, and specifically the neurotrophin NT-3. He has contributed to the growing pool of knowledge of axonal development and regeneration of immature and mature neurons. He has been a part of the search for novel treatments for spinal cord injuries and continues to study neurotrophins to determine their effects on neuronal plasticity. He served a term as president of the Society of Neuroscience during 1997–1998.
Farah D. Lubin is an American neuroscientist and Professor of Neurobiology and Cell, Developmental, and Integrative Biology at the University of Alabama at Birmingham within the Heersink School of Medicine. Lubin is the Principal Investigator of the Lubin Lab which explores the epigenetic mechanisms underlying cognition and how these mechanisms are altered in disease states such as epilepsy and neurodegeneration. Lubin discovered the role of NF-κB in fear memory reconsolidation and also uncovered a novel role for epigenetic regulation of BDNF during long-term memory formation and in epilepsy leading to memory loss. Lubin is a champion for diversity at UAB as the Director of the Roadmap Scholar Program and as a faculty mentor for several institutional and national programs to increase retention of underrepresented minorities in STEM.
Raymond J Dingledine is an American pharmacologist and neurobiologist who has made considerable contributions to the field of epilepsy. He serves as Professor in the School of Medicine at Emory University, Atlanta GA, where he chaired the pharmacology department for 25 years and served as Executive Associate Dean of Research for 10 years.
References
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- ↑ Goodkin, Howard P. (January 2007). "The Founding of the American Epilepsy Society: 1936–1971". Epilepsia. 48 (1): 15–22. doi:10.1111/j.1528-1167.2007.00913.x. PMID 17241204.
- ↑ "Scientific Advisory Committee". Klingenstein Philanthropies. Retrieved 19 August 2022.
- ↑ Liu, Gumei; Gu, Bin; He, Xiao-Ping; Joshi, Rasesh B.; Wackerle, Harold D.; Rodriguiz, Ramona Marie; Wetsel, William C.; McNamara, James O. (2013-07-10). "Transient Inhibition of TrkB Kinase after Status Epilepticus Prevents Development of Temporal Lobe Epilepsy". Neuron. 79 (1): 31–38. doi:10.1016/j.neuron.2013.04.027. ISSN 0896-6273. PMC 3744583 . PMID 23790754.
- 1 2 Gu, Bin; Huang, Yang Zhong; He, Xiao-Ping; Joshi, Rasesh B.; Jang, Wonjo; McNamara, James O. (2015-11-04). "A Peptide Uncoupling BDNF Receptor TrkB from Phospholipase Cγ1 Prevents Epilepsy Induced by Status Epilepticus". Neuron. 88 (3): 484–491. doi:10.1016/j.neuron.2015.09.032. ISSN 0896-6273. PMC 4636438 . PMID 26481038.
- 1 2 "James O'Connell McNamara Sr. | Scholars@Duke". scholars.duke.edu. Retrieved 19 August 2022.
- ↑ "ASPET Award Archives". Default.
- ↑ "AES Research and Recognition Awardees". AES. Retrieved 19 August 2022.
- ↑ "Elected Fellows | American Association for the Advancement of Science". www.aaas.org.