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Biomarkers associated with the pathways of these mutations, such as glucocerebrosidase enzyme (GCase) activity and amyloid\u2010beta 42 (A\u03b242) levels, may hold potential as predictive indicators, providing valuable insights into the likelihood of cognitive decline within these diagnoses. Our objective was to determine their association with cognitive decline in DLB and PD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A total of 121 DLB patients from the European\u2010DLB Consortium and 117 PD patients from the Norwegian ParkWest Study were included in this study. The four most commonly associated variants of <jats:italic>GBA1<\/jats:italic> mutations (E326K, T369M, N370S, L444P), <jats:italic>APOE\u03b54<\/jats:italic> status, and cerebrospinal fluid (CSF) A\u03b242 levels and GCase activity were assessed, as well as global cognition using the Mini\u2010Mental State Examination. Linear mixed\u2010effects regression models were used to evaluate the association of CSF biomarkers with cognitive decline in each diagnostic group, adjusted for age, sex, education, and genetic mutation profile.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Low CSF A\u03b242 levels were associated with accelerated cognitive decline in DLB, whereas reduced CSF GCase activity predicted faster cognitive decline in PD. These associations were independent of <jats:italic>GBA1<\/jats:italic> gene mutations or <jats:italic>APOE\u03b54<\/jats:italic> status.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>Our study provides important evidence on the relationship between brain A\u03b2 deposition and GCase activity in the Lewy body disease spectrum independent of their genetic mutation profile. This information could be relevant for designing future clinical trials targeting these pathways.<\/jats:p><\/jats:sec>","DOI":"10.1002\/acn3.52295","type":"journal-article","created":{"date-parts":[[2025,3,12]],"date-time":"2025-03-12T04:39:18Z","timestamp":1741754358000},"page":"915-924","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Relationship of cognitive decline with glucocerebrosidase activity and amyloid\u2010beta 42 in <scp>DLB<\/scp> and <scp>PD<\/scp>"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1061-4164","authenticated-orcid":false,"given":"Maria Camila","family":"Gonzalez","sequence":"first","affiliation":[{"name":"Department of Quality and Health Technology, Faculty of Health Sciences University of Stavanger  Stavanger Norway"},{"name":"Centre for Movement Disorders Stavanger University Hospital  Stavanger Norway"},{"name":"Centre for Age\u2010Related 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