{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T15:00:13Z","timestamp":1787065213161,"version":"build-2736575974"},"reference-count":93,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2021,8,19]],"date-time":"2021-08-19T00:00:00Z","timestamp":1629331200000},"content-version":"vor","delay-in-days":230,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Dementia in Lewy Body Diseases (Parkinson\u2019s disease and dementia with Lewy Bodies) affects progression of disabilities, quality of life and well-being. Understanding its pathogenetic mechanisms is critical to properly implement disease-modifying strategies. It has been hypothesized that synuclein- and amyloid-pathology act synergistically aggravating cognitive decline in elderly patients but their precise contribution to dementia is debated. In this study, we aimed at exploring if presence of amyloid deposits influences clinical, cognitive and neuroanatomical correlates of mental decline in a cohort of 40 Parkinson\u2019s disease patients with normal cognition (n = 5), mild cognitive impairment (n = 22), and dementia (n = 13) as well as in Dementia with Lewy Bodies (n = 10). Patients underwent simultaneous 3 T PET\/MRI with [18F]-flutemetamol and were assessed with an extensive baseline motor and neuropsychological examination, which allowed level II diagnosis of mild cognitive impairment and dementia. The role of amyloid positivity on each cognitive domain, and on the rate of conversion to dementia at 1-year follow-up was explored. A Kaplan Meier and the Log Rank (Mantel\u2013Cox) test were used to assess the pairwise differences in time-to-develop dementia in Parkinson\u2019s disease patients with and without significant amyloidosis. Furthermore, the presence of an Alzheimer\u2019s dementia-like morphological pattern was evaluated using visual and automated assessment of T1-weighted and T2-weighted MRI images. We observed similar percentage of amyloid deposits in Parkinson\u2019s disease dementia and dementia with Lewy Bodies cohorts (50% in each group) with an overall prevalence of 34% of significant amyloid depositions in Lewy Body Diseases. PET amyloid positivity was associated with worse global cognition (Montreal Cognitive Assessment and Mini Mental State Examination), executive and language difficulties. At 12-month follow-up, amyloid positive Parkinson\u2019s disease patients were more likely to have become demented than those without amyloidosis. Moreover, there was no difference in the presence of an Alzheimer\u2019s disease-like atrophy pattern and in vascular load (at Fazekas scale) between Lewy Body Diseases with and without significant amyloid deposits. Our findings suggest that in Lewy Body Diseases, amyloid deposition enhances cognitive deficits, particularly attention-executive and language dysfunctions. However, the large number of patients without significant amyloid deposits among our cognitively impaired patients indicates that synuclein pathology itself plays a critical role in the development of dementia in Lewy Body Diseases.<\/jats:p>","DOI":"10.1093\/braincomms\/fcab180","type":"journal-article","created":{"date-parts":[[2021,8,17]],"date-time":"2021-08-17T16:44:51Z","timestamp":1629218691000},"source":"Crossref","is-referenced-by-count":39,"title":["The contribution of beta-amyloid to dementia in Lewy body diseases: a 1-year follow-up study"],"prefix":"10.1093","volume":"3","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5846-755X","authenticated-orcid":false,"given":"Roberta","family":"Biundo","sequence":"first","affiliation":[{"name":"Department of General Psychology, University of Padua, Padua, Italy"},{"name":"Study Center for Neurodegeneration (CESNE), University of Padua, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luca","family":"Weis","sequence":"additional","affiliation":[{"name":"Parkinson and Movement Disorders Unit, Department of Neuroscience, University of Padua, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eleonora","family":"Fiorenzato","sequence":"additional","affiliation":[{"name":"Department of General Psychology, University of Padua, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francesca","family":"Pistonesi","sequence":"additional","affiliation":[{"name":"Parkinson and Movement Disorders Unit, Department of Neuroscience, University of Padua, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annachiara","family":"Cagnin","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, University of Padua, Padua, Italy"},{"name":"Padova Neuroscience Center, University of Padua, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alessandra","family":"Bertoldo","sequence":"additional","affiliation":[{"name":"Department of Information Engineering, University of Padua, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariagiulia","family":"Anglani","sequence":"additional","affiliation":[{"name":"Neuroradiology Unit, Padua University Hospital, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diego","family":"Cecchin","sequence":"additional","affiliation":[{"name":"Padova Neuroscience Center, University of Padua, Padua, Italy"},{"name":"Nuclear Medicine Unit, Department of Medicine\u2014DIMED, Padua University Hospital, Padua, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelo","family":"Antonini","sequence":"additional","affiliation":[{"name":"Parkinson and Movement Disorders Unit, Department of Neuroscience, University of Padua, Padua, Italy"},{"name":"Padova 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