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Mitochondrial fusion maintains the normal function of the tubular mitochondrial network (whose formation depends on mitochondrial fusion proteins and is commonly observed in cells with high energy demands) and also plays a crucial role in embryonic development [17, 18]

Prevents glycation this is when excess sugars in the body bond to proteins such as collagen and weakens them

Mitochondrial cascade hypothesis Mitochondrial dysfunction and the accumulation of reactive oxygen species lead to neuronal damage and ultimately contribute to the pathogenesis of neurodegenerative diseases, particularly AD

Whether this negative feedback is mediated directly by the GSL degradation product ITC, due to depletion of glutathione (GSH) [16] which is the sulphur donor in the biosynthesis of GSL [24] or through a sulphur starvation response (discussed later) would require further testing