Moreover, a mouse model of gracile axonal dystrophy (gad), which resulted in the lackof UCH-L1 because of the spontaneous deletions of exons 7 and 8, presents the aberrant accumulation of Aβ in the ascending gracile tract [44], strengthening the concept of UCH-L1 dysfunction in the onset of AD. This evidence concerns the gene UCHL1 and Alzheimer disease.