Schizophrenia is a debilitation mental illness characterized by positive symptoms (mania and hallucinations), negative symptoms (flat affect), and cognitive impairments (learning and memory deficits). These symptoms arise from dysfunction of several neurotransmitter systems including the dopaminergic, seratonergic, cholinergic, and glutamatergic pathways. As such, treatment of this disease has been difficult due to the number of systems involved. Various theories dealing with maternal infection, chemical imbalance, genetics, and epigenetics have emerged postulating the origin of the disease. To date, there is no one unifying hypothesis that encompasses all of the behavioral and biological deficits manifested in schizophrenia. A review of the current research suggests a central role of kynurenic acid (KYNA) in all of these theories. As an endogenous antagonist of cholinergic and glutamatergic receptors, KYNA has been shown to mimic the disease when administered exogenously. Additionally, KYNA levels appear to be elevated in the brains of schizophrenics. Understanding how this chemical works and how it becomes elevated in the first place will be key to understanding the pathology of schizophrenia and developing effective treatments.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/21264 |
| Date | January 2013 |
| Creators | Trecartin, Katelyn V. |
| Publisher | Boston University |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
| Rights | This work is being made available in OpenBU by permission of its author, and is available for research purposes only. All rights are reserved to the author. |
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