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An investigation into the effects of background muscle activity on transcranial magnetic stimulation-induced muscle responses, in people with and without ALS

Alzheimer’s disease (AD) is the most common chronic neurodegenerative disease characterized by a progressive decline of cognition and memory, with no cure and effective treatment to manage symptoms. In AD the physiological balance between excitation and inhibition (E/I) in the brain is significantly affected. Glutamate is the main excitatory, while GABA is the main inhibitory neurotransmitter. This E/I imbalance if restored could halt the progression of AD. Caffeine’s functional capacities have been delineated from recent research which includes improved cognitive function, memory, and attention. In view of the general ability of caffeine to prevent memory and/or cognitive deterioration, it would be reasonable to expect its beneficial effects for AD patients. Indeed, many epidemiological studies demonstrated the neuroprotective role of caffeine in both reducing the risk of AD and improving cognition and/or memory as assessed by various neurological tests. Yet the conclusions from reviews and meta-analyses are not unequivocal. It should be emphasized that most experimental and observational studies from humans estimate the equivalent amount of caffeine from caffeinated drinks, but there is evidence for a critical caffeine plasma level that is required to promote the cognition-enhancing positive effects. I hypothesize that caffeine could have a positive effect on AD by increasing GABA release and this would compensate for or prevent glutamate-induced excitotoxicity, a major pathological hallmark of AD. My work will focus on examining the effect of caffeine on glutamate and GABA levels following beta-amyloid exposure using Liquid Chromatography Coupled to Tandem Mass Spectrometry (LC-MS/MS). We will determine at what concentrations caffeine will increase GABA release and if higher caffeine doses might have the opposite effect and lead to detrimental results by inducing neurotoxicity. This research aims to find a drug that will prevent or delay the progression of AD. Importantly, caffeine is used worldwide and thus offers easy access.