THIS GRANT IS A CONTINUATION OF N000141410562 Glatiramer Acetate (Copaxone) Treatment of Noise-Induced Hearing Loss
Abstract
Funds are for research to determine if glatiramer acetate (GA), or a GA-antioxidant mixture, protects and/or rescues auditory function from pathology precipitated by noise induced trauma. Specific Aim 1: To test the hypothesis that treatment with the immunomodulator, glatiramer acetate (GA), prevents or reduces hearing loss following exposure to traumatizing acoustic stimulation. Two studies will be conducted to satisfy the goals of Specific Aim 1. In the first, guinea pigs will be treated with GA prior to noise exposure, the protection paradigm, and in the second study GA will be administered following noise exposure to determine if GA has the capacity to rescue hearing loss associated with traumatic noise exposure. The primary Phase I objective of this proposal (Specific Aims 1 and 2) is to determine if GA, or a GA-antioxidant mixture, protects and/or rescues auditory function from pathology precipitated by noise induced trauma. In studies supporting Aim 1, the goal is to determine if GA treatment alone reduces the amount of temporary and permanent hearing loss and/or accelerates the rate of recovery from temporary threshold shift (TTS). The investigators working hypothesis is that the protective character of GA is a product of the drugs known neuroprotective actions; i.e., it protects the cochlea, including sensory cells and spiral ganglion neurons (SGNs), from acoustic trauma. The a priori expectation based partially on preliminary findings is that recovery from NIHL will be significantly enhanced relative to control animals when animals are treated with the immune-modulator alone. In studies supporting Aim 2, the investigator will determine if antioxidant therapy augments the Neuro-protective properties of GA alone. The rationale underlying this treatment strategy is that antioxidant therapy has been shown in previous studies to protect sensory cells from metabolic defects resulting from acoustic trauma. The working global hypothesis is that GA triggers protection from noise-induced, inflammation-driven neurodegeneration of sensory cells/SGNs and the antioxidant actions of Nacetylcysteine and/or D-methionine protect sensory cells from metabolic trauma, and that the drug combination will act to promote recovery, perhaps synergistically, from NIHL. In Specific Aim 3, pro-inflammatory and anti-inflammatory cytokine profiles will be assayed to test the fundamental hypothesis that GA actions trigger anti-inflammatory, neuro-protective actions in the inner ear.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Nov 23, 2016
- Source ID
- N000141612396
Entities
People
- Edward Walsh
Organizations
- Office of Naval Research
- United States Navy