LAUSR

Recent evidence from histopathologic, CSF, and amyloid PET studies show that β-amyloid (Aβ) pathology is also involved in the pathophysiology of Parkinson disease (PD), correlating with a more rapid cognitive decline and predicting progression in levodopa-resistant gait impairment.1 The pathophysiology as well as the neural networks involved, however, are not fully understood, especially the intriguing interaction between α-synuclein and Aβ pathology. Decreased clearance rates, in contrast to increased production rates, for both Aβ1-42 and Aβ1-40 may be the main trigger in Alzheimer disease.2 Whether this is also true in patients with PD awaits future research. Thus, Brockmann and colleagues3 investigated genetic variants in proteins (loss of function alleles) involved in the clearance of Aβ (APOE, membrane metalloproteinase, and cystatin C [CST]). They identified a large group of patients with PD (n=456) with a subgroup of 103 patients with dementia and evaluated single nucleotide polymorphisms (SNP) in the respective genes in relation to a number of clinical variables and CSF Aβ1-42 levels.