Parkinson’s disease II: longitudinal progression, development of dementia and new gene therapy

Abstract

As mentioned in last month’s Journal Club, a plethora of articles in various fields of Parkinson’s disease are published every month. In this edition of the Journal Club, another three of them will be presented. In the first, an 8-year follow-up study, the longitudinal progression of sporadic Parkinson’s disease was evaluated by multi-tracer positron emission tomography. This study confirms the previously described ‘‘caudate to putamen gradient’’ (with the caudate less affected than the putamen) and stresses that different factors might be involved in disease initiation and disease progression. The second study—also a longterm follow-up—focuses on cognitive impairment in Parkinson’s disease. It identifies three clinical factors and one genetic factor which have a highly predictive value for the risk of development of dementia in Parkinson’s disease: first, age above 72 years, second, impaired semantic fluency and third, inability to copy an intersecting pentagons figure; the major genetic predictor of dementia risk in Parkinson’s disease is evidently the so-called H1/H1 genotype of the gene coding for the microtubule-associated protein tau. In the third study, the safety, tolerability and efficacy of putaminal aromatic L-amino acid decarboxylase (AADC) gene therapy for Parkinson’s disease was evaluated in two small cohorts. This study shows on the one hand a clinical benefit and on the other a considerable risk of intracranial hemorrhage due to the surgical procedure. Longitudinal progression of sporadic Parkinson’s disease: a multi-tracer positron emission tomography study