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The comorbid mechanisms are complex, posing challenges for clinical treatment

Mitochondrial dysfunction as a trigger of programmed axon death

A particular point mutant of the protein, A53T, associated with familial PD is also known to fibrillate at a significantly higher rate than the normal protein (Coskuner and Wise-Scira, 2013) owing to its increased propensity to form beta fibrils as well as by partially negating the effect of long-range interactions between the N and C terminus

Dubler RE, Anderson BM: Simultaneous inactivation of the catalytic activities of yeast glutathione reductase by N-alkylmaleimides

When oocytes from the same healthy egg donor were used to create embryos which were then transferred to recipients with or without endometriosis, similar implantation rates were seen

Evidence of increased oxidative stress and DNA damages in women with recurrent abortions