In Alzheimer’s disease (AD) transgenic mice, overexpression of UCHL1 has been shown to reduce Aβ production, inhibit neuritic plaque formation and improve memory deficits [15], while in PD, suppression of UCHL1 activity in vitro has been shown in non-transgenic neurons to increase accumulation of presynaptic α-synuclein [16]. Here, SNCA is linked to Parkinson disease.