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Chronic Glutamate Toxicity in Neurodegenerative Diseases-What is the Evidence

doi: 10.1038/s12276-022-00725-z 192 WuTXieCHanJYeYWeielJLiQet al

In the attempts to study CAD and the causative agents for the disease, a metabolite circulating in the plasma termed trimethylamine-N-oxide (TMAO) has been found out to be an independent risk factor that increases CAD risk

The enzymes affected belong to one of three categories: Very long-chain acyl-CoA dehydrogenase (VLCAD): The symptoms that result from deficiencies in VLCAD were originally ascribed to loss of long-chain acyl-CoA dehydrogenase (LCAD) activity

Various molecular mechanisms, including cellular senescence, inflammation, mitochondrial function, changes to the sirtuin and Klotho signalling pathways, and the autophagylysosome system, are recognized as regulators of individual lifespan and are important factors that govern kidney ageing