This project will investigate the effect of chronic glial activation on brain structure and function, and test the efficacy of two cytokine-suppressive anti-inflammatory drugs (CSAIDs) against chronic glial activation and the resulting neuronal damage.
This project will not only create a new brain tumour model, but will also give us valuable information on mTOR’s involvement in the development of brain tumours.
Currently four out of the five pharmacological treatments used for Alzheimer’s disease (AD) are acetylcholinesterase inhibitors aimed at boosting the amount of acetylcholine in the brain, with the fifth being an N-methyl-D-aspartate (NMDA) receptor antagonist.
Microglia - brain-resident macrophages - carry out homeostatic surveillance functions in the brain, clearing dying cells, extracellular debris, and pruning synapses during development.
Mucopolysaccharidoses (MPS) are inherited metabolic disorders caused by the deficiency of specific lysosomal enzymes required for the catabolism of glycosaminoglycans (GAGs) where each MPS type lacks a specific enzyme resulting in the build-up of GAGs in all cells of the body.
Neurovascular dysfunction is a central process in the pathogenesis of Alzheimer’s disease and other dementias. In the brain, cerebrovasculature and neuronal structures are tightly integrated forming the multicellular neurovascular unit comprising endothelial cells, astrocytes, microglia and neurons.
