title: Activated microglial cells and complement factors are unrelated to cortical Lewy bodies.
abstract: Inflammatory mechanisms have been demonstrated in Alzheimer's disease (AD) but their presence in other neurodegenerative disorders is not well documented. Complement factors and activated microglia have been reported in the substantia nigra of Parkinson's disease (PD). In the present study we investigated the cingulate gyrus of 25 autopsied patients with clinically and neuropathologically well-documented PD, with or without dementia, for the presence of (activated) microglial cells and their relation with Lewy body (LB)-bearing neurons. In addition, we studied the presence of complement factors in LBs. Of the 25 patient, 15 were clinically demented, fulfilling criteria for dementia with LBs (DLB); 7 also fulfilled CERAD morphological criteria for probable or definite Alzheimer type of dementia. Microglia clustering was seen around congophilic plaques with or without tau pathology. Microglial cells were not associated with LB-bearing neurons or noncongophilic plaques. The cortex of DLB patients without AD plaques did not show more microglial cells than the cortex of non-demented controls. The number of microglia was the lowest in young control patients who died immediately after trauma. Complement factor C3d was occasionally seen in diffusely ubiquinated neurons but late complement factors were not detected in these neurons. Double staining for complement and alpha-synuclein was negative, suggesting the absence of complement in LBs. In contrast, AD plaques in the same sections showed complement factors C3c, C3d, C1q and C5-9. In conclusion, we have found no evidence that inflammatory mechanism are involved in LB formation in cerebral cortex.
authors.affiliation: Department of Pathology, Free University Hospital Amsterdam, The Netherlands. j.m.rozemuller@amc.uva.nl
authors.forename: A J
authors.initials: AJ
authors.lastname: Rozemuller
authors.forename: P
authors.initials: P
authors.lastname: Eikelenboom
authors.forename: J W
authors.initials: JW
authors.lastname: Theeuwes
authors.forename: E N
authors.initials: EN
authors.lastname: Jansen Steur
authors.forename: R A
authors.initials: RA
authors.lastname: de Vos
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D003165:Complement System Proteins / Q000378:metabolism*; D004660:Encephalitis / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006179:Gyrus Cinguli / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D016631:Lewy Bodies / Q000378:metabolism / Q000473:pathology*; D020961:Lewy Body Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D017628:Microglia / Q000378:metabolism / Q000473:pathology*; D008875:Middle Aged; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology*; D010300:Parkinson Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D012276:Ricin / Q000494:pharmacology; D051843:Synucleins; D014452:Ubiquitins / Q000378:metabolism; D051844:alpha-Synuclein; D016875:tau Proteins / Q000378:metabolism
chemical_list: D009419:Nerve Tissue Proteins; C497604:SNCA protein, human; D051843:Synucleins; D014452:Ubiquitins; D051844:alpha-Synuclein; D016875:tau Proteins; D003165:Complement System Proteins; D012276:Ricin