alexa Neurochemical Changes In Chronic Traumatic Encephalopathy | 61528
ISSN: 2329-6895

Journal of Neurological Disorders
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2nd International Conference on Neuroimmunology & Therapeutics

Lili-Naz Hazrati
Hospital for Sick Children-University of Toronto, Canada
Posters & Accepted Abstracts: J Neurol Disord
DOI: 10.4172/2329-6895.C1.015
Abstract
Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease associated with repetitive concussive and sub-concussive head injuries. This disease has become a popular topic due to its close association with sports involving repetitive and high impact collisions such as football and hockey. Post-mortem pathological analysis has defined CTE as a tauopathy with neurofibrillary tangles (NFTs) accumulating in both neurons and astrocytes. It is believed that these pathological abnormalities result in progressive deficits in cognition, behavioral, mood and motor function. CTE has been neuropathologically classified into four stages according to the location and spread of NFTs. As early as the stage II of the disease, NFTs are noted to involve deep-seated groups of neuro-chemically diverse brain structures (cholinergic, dopaminergic and serotoninergic). These deep and discrete neuronal groups often show few NFTs and there is no obvious evidence of neuronal death. However, the extent of the loss of their projections to their main targets is not known. Any loss of these biochemically varied projections to the cortex would seriously affect the function of cortical neurons in general and lead to neurological and psychiatric deficits. In this study we have examined the fiber densities of cholinergic (ChAT+), serotonergic (5HT+) and dopaminergic (Th+) fibers in the cortex of our cohort of young hockey players with neuropathologically proven CTE. Our results indicate significant deficits in all three systems in different cortical areas (with and without tau pathology). These findings indicate that multiple head traumas induce important brain biochemical imbalances that extend beyond the areas of tau deposits and can be suspected to cause more directly the behavioral and mood disorders associated with CTE.
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