Joseph T. Coyle

Several members of Coyle's family were physicians, including his maternal grandfather, who was a doctor in Iowa, and his father, who was an orthopedic surgeon.

Joseph grew up on the south side of Chicago, Illinois. As a child, Coyle showed a keen interest in how things worked. He attended a Jesuit high school and then went on to College of the Holy Cross in Worcester, Massachusetts. He spent a year at Sorbonne University in Paris, France, before his final year at College of the Holy Cross. The summer after college, Joseph was a psychiatric orderly at a local community hospital. While at the local community hospital, the brother of one of Joseph’s friends was admitted into the hospital with his first episode of schizophrenic psychosis which came to be of high interest to him.

Coyle attended Johns Hopkins University and received his MD in 1969. Subsequently he completed an internship in pediatrics, followed by a residency in psychiatry from 1973 until 1976. During this time period, Coyle worked with Julius Axelrod, a Nobel laureate, known for his research on catecholamines, which include epinephrine and norepinephrine.[2][3]

Coyle is the current Chair of Psychiatry and Neuroscience at Harvard Medical School. He became a member of the National Academy of Medicine in 1990, a fellow of Arts and Sciences, and of the American Psychiatric Association. From 1991 to 2001, he was the Chair of the Consolidated Department of Psychiatry, also at Harvard. Before beginning work for Harvard Medical School in 1991, Coyle was a professor of Child Psychiatry at Johns Hopkins, where he began in 1975, and was eventually named the Distinguished Service Professor of Child Psychiatry in 1985. During his clinical career Coyle established a basis combining neuroscience and clinical psychiatry studies, where he has contributed to the understanding of certain neuropsychiatric disorders such as schizophrenia and bipolar disorder. His studies of these disorders lead him to the discovery of neurological mechanisms underlying diseases such as Huntingtons and Alzheimers.[3]

Coyle was president of the Society for Neuroscience from 1991-1992 and the president of the American College of Neuropsychopharmacology in 2001. He was the Editor-in-Chief of the Archives of General Psychiatry from 2001-2014.[4]

Comparison between a non-schizophrenic brain and a schizophrenic brain

Joseph T. Coyle is the current Director of the Laboratory for Psychiatric and Molecular Neuroscience. Though he has earned recognition for work in numerous areas of neurobiology and psychopharmacology, an area of research that Coyle has earned distinction in is that of the neurotransmitter glutamate. Coyle has studied glutamate's excitatory effects on the brain along with the role this neurotransmitter plays in common mental illnesses, primarily in schizophrenia. A main focus of research for Coyle and his associates is the understanding of the neuromolecular mechanisms underlying psychiatric disorders, being able to understand how these mechanisms affect the brain and overall behavior, as well as aid in development of efficient and effective treatment methods. Coyle focused his attention specifically on schizophrenia and bipolar disorder, Huntington’s, and Alzheimer's disease. He was one of the first scientists to ever identify structural abnormalities in bipolar disorder, similar to schizophrenia. Coyle’s lab aims to mimic the neuromolecular mechanisms underlying these disorders in model organisms such as mice, who have similar nervous systems to humans. One way they do this is by targeting the N-methyl-D-aspartate receptor (NMDAR), which has a vital role in transmission of excitatory information within numerous brain pathways and structures. Results from these targeted experiments indicated that when genes encoding these NMDARs were altered, the resulting chemical pathways and behavioral traits in the model organisms mimicked those found/seen in schizophrenia patients. Such research can be beneficial to science/medical research because, In doing these experiments, they can target glutamatergic transmission pathways associated with mental illnesses like schizophrenia, and develop treatments that target and reverse/prevent the damage caused by such pathways, as well as provide a better overall understanding of a wide variety of mental conditions. For example, the work Coyle’s lab published regarding the role of NMDARs in schizophrenia led to testing of NMDAR-restoring medications, which resulted in reversal of damage to functional pathways, as well as overall improvement in behavior and cognitive abilities.[5][3]

His most cited papers are:

• Coyle JT, Puttfarcken P. Oxidative stress, glutamate, and neurodegenerative disorders. Science. 1993 Oct 29;262(5134):689-95. (Cited 4730 times, according to Google Scholar[9]
• Whitehouse PJ, Price DL, Struble RG, Clark AW, Coyle JT, Delon MR. Alzheimer's disease and senile dementia: loss of neurons in the basal forebrain. Science. 1982 Mar 5;215(4537):1237-9. (Cited 4210 times, according to Google Scholar.[9]
• Coyle JT, Price DL, Delong MR. Alzheimer's disease: a disorder of cortical cholinergic innervation. Science. 1983 Mar 11;219(4589):1184-90. (Cited 3710 times, according to Google Scholar.[9]
• Whitehouse PJ, Price DL, Clark AW, Coyle JT, DeLong MR. Alzheimer disease: evidence for selective loss of cholinergic neurons in the nucleus basalis. Annals of Neurology: 1981 Aug;10(2):122-6 (Cited 2084 times, according to Google Scholar.[9]
• Coyle JT, Schwarcz R. Lesion of striatal neurons with kainic acid provides a model for Huntington's chorea. Nature. 1976 Sep;263(5574):244-6.(Cited 1427 times, according to Google Scholar.[9]
• Murphy TH, Miyamoto M, Sastre A, Schnaar RL, Coyle JT. Glutamate toxicity in a neuronal cell line involves inhibition of cystine transport leading to oxidative stress. Neuron. 1989 Jun 1;2(6):1547-58. (Cited 1067 times, according to Google Scholar.[9]
• Goff DC, Coyle JT. The emerging role of glutamate in the pathophysiology and treatment of schizophrenia. American Journal of Psychiatry. 2001 Sep 1;158(9):1367-77. (Cited 1133 times, according to Google Scholar.[9]
• Lisman JE, Coyle JT, Green RW, Javitt DC, Benes FM, Heckers S, Grace AA. Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. Trends in neurosciences. 2008 May 1;31(5):234-42. (Cited 1078 times, according to Google Scholar.[9]
• Coyle JT. Glutamate and schizophrenia: beyond the dopamine hypothesis. Cellular and molecular neurobiology. 2006 Jul;26(4):363-82. (Cited 1021times, according to Google Scholar.[9]