This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Alzheimer's Disease (AD) is a degenerative disorder associated with senile plaques and marked reactive microgliosis. Dementia is thought to arise from loss of neurons and decreased synaptic connections. A number of studies have implicated neurotoxins released by microglia activated by A (Beta)1-42 as one casue of neuronal and synaptic damage in AD brain. Moreover, it is now widely believed that anti-inflammatory drugs might reduce immune-mediated neuron injury occurring in AD. Based upon extensive pre-clinical testing from in vitro and in vivo models, we have selected 3 candidate drugs as immuno-suppressants for AD. Here, we will examine the ability of immuno-suppressing drugs to reduce production of microglia-derived neurotoxins detected within cerebrospinal fluid and to inhibit microglia responses to A (Beta)1-42.
In Aim 1, candidate anti-inflammatory agents will be examined for the ability to suppress immune responses in AD subjects. If successful, this proposed research will spur the development of new strategies to treat AD dementia.
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