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000283058 0247_ $$2ISSN$$a1552-5279
000283058 037__ $$aDZNE-2025-01465
000283058 041__ $$aEnglish
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000283058 1001_ $$aRizzo, Marianna$$b0
000283058 1112_ $$aAlzheimer’s Association International Conference$$cToronto$$d2025-07-27 - 2025-07-31$$gAAIC 25$$wCanada
000283058 245__ $$aAssociations between CSF complement factors and biomarkers of amyloid, tau, neurofilament light chain, and α‐synuclein in AD, DLB, and PD
000283058 260__ $$c2025
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000283058 520__ $$aWhile evidence suggests complement system involvement in Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and Parkinson's disease (PD), its association with disease biomarkers remains unclear. We investigated the relationship of complement factors with amyloid, tau, NfL, and α-synuclein in CSF in AD, DLB, PD, and controls.We included 321 individuals with AD, DLB, PD, and controls from 6 centers of the EPND study. CSF Aβ42/40, p-tau181, NfL, and α-syn were centrally measured using NeuroToolKit (Roche Diagnostics), and 14 CSF complement factors using Milliplex (Merck KGaA). Controls were defined as normal cognition and normal Aβ42/40, whereas AD as abnormal Aβ42/40 without meeting clinical criteria of DLB or PD. Linear regression models adjusted for age and sex were used. Associations were post-hoc compared between individuals with low(≤23), intermediate(24-27), and high(≥28) MMSE scores.Sample characteristics are presented in Table 1. Lower Aβ42/40 levels were associated with lower levels of 7 complement factors in controls and with higher C1q and C2 levels specifically in AD (Figure 1, Figure 2). No associations of Aβ42/40 with complement were found in DLB and PD. Higher p-tau181 levels were associated with increased levels of 7 complement factors in controls and 6 in AD, and showed fewer associations in DLB and PD. The strength of p-tau181 associations with complement was similar across groups. Higher NfL levels were widely associated with higher complement factor levels in controls (13) and AD (12), and less in PD (6) and DLB (4). Higher α-syn levels were broadly associated with higher complement factor levels in AD (13), controls (12), and DLB (12), but only minimally in PD (1). The strength of these NfL and α-syn associations with complement was not disease-specific. Conversely, compared to all groups, in PD higher α-syn levels were associated with lower C5, C5a, C9, factor-I and properdin levels. Individuals with intermediate MMSE scores largely drove the associations of α-syn with complement in AD. MMSE level did not clearly impact other associations.CSF complement factors were associated with amyloid, tau, NfL, and α-synuclein, suggesting complement system involvement in several neurodegenerative diseases. Complement showed disease-specific associations with amyloid in AD and α-synuclein in PD.
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000283058 650_7 $$2NLM Chemicals$$aBiomarkers
000283058 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000283058 650_7 $$2NLM Chemicals$$atau Proteins
000283058 650_7 $$2NLM Chemicals$$aalpha-Synuclein
000283058 650_7 $$2NLM Chemicals$$aPeptide Fragments
000283058 650_7 $$2NLM Chemicals$$aNeurofilament Proteins
000283058 650_7 $$2NLM Chemicals$$aneurofilament protein L
000283058 650_7 $$2NLM Chemicals$$aamyloid beta-protein (1-42)
000283058 650_7 $$09007-36-7$$2NLM Chemicals$$aComplement System Proteins
000283058 650_2 $$2MeSH$$aHumans
000283058 650_2 $$2MeSH$$aFemale
000283058 650_2 $$2MeSH$$aMale
000283058 650_2 $$2MeSH$$aBiomarkers: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aAlzheimer Disease: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aAged
000283058 650_2 $$2MeSH$$aAmyloid beta-Peptides: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aParkinson Disease: cerebrospinal fluid
000283058 650_2 $$2MeSH$$atau Proteins: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aalpha-Synuclein: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aLewy Body Disease: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aPeptide Fragments: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aNeurofilament Proteins: cerebrospinal fluid
000283058 650_2 $$2MeSH$$aAged, 80 and over
000283058 650_2 $$2MeSH$$aMiddle Aged
000283058 650_2 $$2MeSH$$aComplement System Proteins: cerebrospinal fluid
000283058 7001_ $$aTeunissen, Charlotte E$$b1
000283058 7001_ $$0P:(DE-2719)2810593$$aBrosseron, Frederic$$b2$$udzne
000283058 7001_ $$0P:(DE-2719)2811186$$aKuhs, Sandra$$b3$$udzne
000283058 7001_ $$aKollmorgen, Gwendlyn$$b4
000283058 7001_ $$aZetterberg, Henrik$$b5
000283058 7001_ $$aBlennow, Kaj$$b6
000283058 7001_ $$aKrüger, Rejko$$b7
000283058 7001_ $$aFernandes, Sara B Gomes$$b8
000283058 7001_ $$aAarsland, Dag$$b9
000283058 7001_ $$aBorejko, Olga$$b10
000283058 7001_ $$aChokoshvili, Davit$$b11
000283058 7001_ $$avan der Flier, Wiesje M$$b12
000283058 7001_ $$aLemstra, Afina W$$b13
000283058 7001_ $$aTijms, Betty M$$b14
000283058 7001_ $$0P:(DE-2719)2810273$$aPetzold, Gabor C$$b15$$udzne
000283058 7001_ $$0P:(DE-2719)2811324$$aSpottke, Annika$$b16$$udzne
000283058 7001_ $$aFrisoni, Giovanni B$$b17
000283058 7001_ $$0P:(DE-2719)2811916$$aBrockmann, Kathrin$$b18$$udzne
000283058 7001_ $$0P:(DE-2719)2320009$$aGasser, Thomas$$b19$$udzne
000283058 7001_ $$aFladby, Tormod$$b20
000283058 7001_ $$aWettergreen, Marianne$$b21
000283058 7001_ $$0P:(DE-2719)2000032$$aJessen, Frank$$b22$$udzne
000283058 7001_ $$0P:(DE-2719)2000005$$aDüzel, Emrah$$b23$$udzne
000283058 7001_ $$0P:(DE-2719)2811373$$aHöglinger, Günter U$$b24$$udzne
000283058 7001_ $$aChevalier, Claire$$b25
000283058 7001_ $$aKrishnan, Rajaraman$$b26
000283058 7001_ $$aVisser, Pieter Jelle$$b27
000283058 7001_ $$aVos, Stephanie J B$$b28
000283058 7001_ $$aconsortium, IMI EPND$$b29$$eCollaboration Author
000283058 773__ $$0PERI:(DE-600)2201940-6$$a10.1002/alz70856_104363$$gVol. 21 Suppl 2, no. Suppl 2, p. e104363$$nSuppl 2$$pe104363$$tAlzheimer's and dementia$$v21$$x1552-5260$$y2025
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