Brain lesions, if any, have not been evidenced in TS. According to pharmacological and biochemical observations, and by analogy with the dopaminergic hypothesis of schizophrenia, TS may be associated to a hyperactivity of central dopaminergic systems. Alternatively, other hypotheses suggest an involvement of systems containing other neurotransmitters (chemical messengers) such as norepinephrine and/or acetycholine. One approach to the study of central neurological disorders is to search for specific neurotransmitter deficiencies. For example, this approach has demonstrated the existence of the selective degeneration of dopaminergic systems in the brains from subjects with Parkinson’s disease. Following this discovery, parkinsonian symptoms have been relieved or at least attenuated by the administration of levodopa, the precursor of the missing. neurotransmitter, dopamine. A detailed organization of neuronal symptoms in the human brain can now be investigated by combining biochemical and immunocytochemical methods. A careful comparison between normal pathological brains can be performed. The purpose of this research project is to study normal and TS brains with specific antibodies directed against messengers or specific marker neurotransmitters. It should then be possible to identify the biochemically defined neuronal systems which are damaged. We hope that a better knowledge of the neurochemical abnormalities found in TS brains will lead to more effective treatments. It might also be a first step to approach the cause of the disease. Etienne Hirsch, M.D. Massachusetts Institute of Technology, Dept. of Neuroanatomy Cambridge, MA Award: $15,000 Tourette Association of America Inc. – Research Grant Award 1986
Pathophysiology of TS: Biochemical and Immunocytochemical Analysis of the Human Brain with Reference to the Pathology of TS
Grant Type
Basic
Grant Year
1986
Institution Location
MA
Institution Organization Name
MIT
Investigators Name
Hirsch, Etienne, MD