Activated microglial cells and complement factors are unrelated to cortical Lewy bodies

Inflammatory mechanisms have been demonstrated in Alzheimer's disease (AD) but their presence in other neurodegenerative disorders is not well documen ted. Complement factors and activated microglia have been reported in the s ubstantia nigra of Parkinson's disease (PD). In the present study we invest igated the cingulate gyrus of 25 autopsied patients with clinically and neu ropathologically well-documented PD, with or without dementia, for the pres ence of (activated) microglial cells and their relation with Lewy body (LB) -bearing neurons. In addition, we studied the presence of complement factor s in LBs. Of the 25 patient, 15 were clinically demented, fulfilling criter ia for dementia with LBs (DLB); 7 also fulfilled CERAD morphological criter ia for probable or definite Alzheimer type of dementia. Microglia clusterin g was seen around congophilic plaques with or without tau pathology. Microg lial cells were not associated with LB-bearing neurons or noncongophilic pl aques. The cortex of DLB patients without AD plaques did not show more micr oglial cells than the cortex of non-demented controls. The number of microg lia was the lowest in young control patients who died immediately after tra uma. Complement factor C3d was occasionally seen in diffusely ubiquinated n eurons but late complement factors were not detected in these neurons. Doub le staining for complement and alpha -synuclein was negative, suggesting th e absence of complement in LBs. In contrast, AD plaques in the same section s 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.