Abstract
Dear Sirs,Heterozygous mutations in the gene encoding the lyso-somal enzyme beta-glucocerebrosidase (GBA) are associ-ated with an increased susceptibility to Parkinson’s disease(PD) and dementia with Lewy body disease [1, 2] and somecases with phenotypes similar to multiple system atrophywere reported [3]. GBA mutation carriers generally presentwith an earlier age at onset and particularly severe motor[2, 5] and non-motor [6] genotype-phenotype relationsprobably reflecting the more pronounced neocortical Lewybody-type pathology in GBA-associated PD [4]. Therefore,these were predicted to show an unfavorable therapeuticoutcome from Deep-brain stimulation of the subthalamicnucleus (STN-DBS). Here, we provide the first quantitativedata on the therapeutic outcomes of GBA-associated PD inresponse to
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