Blast wave explosions are a major cause of hearing loss among military personnel, but blasts can also induce traumatic brain injury and impair memory. In preliminary experiments, we have shown that exposure to blast waves and continuous noise not only damaged the inner ear, but caused cell death in the hippocampus, suppressed neurogenesis and impaired memory function. The goals of this project are to: (1) Assess the amount of functional hearing impairment and cochlear damage (necrosis and apoptosis) that results from blast wave vs. continuous noise exposures. (2) Determine the extent to which D-methionine, an anti-antioxidant and apoptotic agent, can protect against blast wave induced hearing impairment and cochlear pathology. (3) Determine the extent to which blast wave exposure disrupts memory function and induces cell death and suppresses neurogenesis in the hippocampus. (4) Determine if D-methionine can protect against blast wave induced memory impairments, prevent hippocampal cell death and restore hippocampal neurogenesis. These studies will provide new mechanistic insights on the role of necrosis and apoptosis in blast and noise induced injury to the inner ear and hippocampus and whether antioxidant, anti-apoptotic drug therapy can prevent or ameliorate blast wave injury to the inner ear and hippocampus.
The goals of this project are to: (1) assess the effects of intense blast wave exposures on hearing loss, inner ear pathology, memory function and hippocampal damage and (2) determine if D-methionine, an anti- apoptotic agent, can protect against blast wave induced hearing loss, cochlear pathology, memory impairment and hippocampal damage. These studies will provide new insights on the mechanisms underlying blast wave- induced cell death in the inner ear and hippocampus and the degree to which an antioxidant, anti-apoptotic drug, can ameliorate injury to the inner ear and hippocampus thereby reducing the risk of blast-induced hearing loss and memory impairment.
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