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For effective therapies to prevent and slow progression to PD dementia (PDD), the key mechanisms that determine why some people with PD develop early dementia, while others remain cognitively unaffected, need to be understood. Neuroinflammation and tau protein accumulation have been demonstrated in post-mortem PD brains, and in many other neurodegenerative disorders leading to dementia. However, whether these processes mediate dementia risk early on in the PD disease course is not established. To this end, we used PET neuroimaging with 11C-PK11195 to index neuroinflammation and 18F-AV-1451 for misfolded tau in early PD patients, stratified according to dementia risk in our \u2018Neuroinflammation and Tau Accumulation in Parkinson\u2019s Disease Dementia\u2019 (NET-PDD) study. The NET-PDD study longitudinally assesses newly-diagnosed PD patients in two subgroups at low and high dementia risk (stratified based on pentagon copying, semantic fluency, MAPT genotype), with comparison to age- and sex-matched controls. Non-displaceable binding potential (BPND) in 43 brain regions (Hammers\u2019 parcellation) was compared between groups (pairwise t-tests), and associations between BPND of the tracers tested (linear-mixed-effect models). We hypothesized that people with higher dementia risk have greater inflammation and\/or tau accumulation in advance of significant cognitive decline. We found significantly elevated neuroinflammation (11C-PK11195 BPND) in multiple subcortical and restricted cortical regions in the high dementia risk group compared with controls, while in the low-risk group this was limited to two cortical areas. The high dementia risk group also showed significantly greater neuroinflammation than the low-risk group concentrated on subcortical and basal ganglia regions. Neuroinflammation in most of these regions was associated with worse cognitive performance (Addenbrooke\u2019s Cognitive Examination-III score). Overall neuroinflammation burden also correlated with serum levels of pro-inflammatory cytokines. In contrast, increases in 18F-AV-1451 (tau) BPND in PD versus controls were restricted to subcortical regions where off-target binding is typically seen, with no relationship to cognition found. Whole-brain 18F-AV-1451 burden correlated with serum phosphorylated tau181 levels. Although there was minimal regional tau accumulation in PD, regional neuroinflammation and tau burden correlated in PD participants, with the strongest association in the high dementia risk group, suggesting possible co-localization of these pathologies. In conclusion, our findings suggest that significant regional neuroinflammation in early PD might underpin higher risk for PDD development, indicating neuroinflammation as a putative early modifiable aetiopathological disease factor to prevent or slow dementia development using immunomodulatory strategies.<\/jats:p>","DOI":"10.1093\/brain\/awad322","type":"journal-article","created":{"date-parts":[[2023,9,25]],"date-time":"2023-09-25T12:56:10Z","timestamp":1695646570000},"page":"923-935","source":"Crossref","is-referenced-by-count":75,"title":["Neuroinflammation is linked to dementia risk in Parkinson\u2019s disease"],"prefix":"10.1093","volume":"147","author":[{"given":"Antonina","family":"Kouli","sequence":"first","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lennart R B","family":"Spindler","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tim D","family":"Fryer","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"},{"name":"Wolfson Brain Imaging Centre, University of Cambridge , Cambridge, CB2 0QQ , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young T","family":"Hong","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"},{"name":"Wolfson Brain Imaging Centre, University of Cambridge , Cambridge, CB2 0QQ , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8923-9656","authenticated-orcid":false,"given":"Maura","family":"Malpetti","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franklin I","family":"Aigbirhio","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"},{"name":"Wolfson Brain Imaging Centre, University of Cambridge , Cambridge, CB2 0QQ , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon R","family":"White","sequence":"additional","affiliation":[{"name":"Medical Research Council Biostatistics Unit, Cambridge Institute of Public Health , Cambridge, CB2 0SL , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1490-5703","authenticated-orcid":false,"given":"Marta","family":"Camacho","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0837-5080","authenticated-orcid":false,"given":"John T","family":"O\u2019Brien","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, University of Cambridge , Cambridge, CB2 0SZ , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2648-9743","authenticated-orcid":false,"given":"Caroline H","family":"Williams-Gray","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge , Cambridge, CB2 0PY , UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,9,27]]},"reference":[{"key":"2024030122265751700_awad322-B1","doi-asserted-by":"crossref","first-page":"1258","DOI":"10.1136\/jnnp-2013-305277","article-title":"The CamPaIGN study of Parkinson\u2019s disease: 10-year outlook in an incident population-based 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