Figure 2From: Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in mice Lack of CD59a promotes abnormal tau phosphorylation, which is accompanied by neuronal and synaptic degeneration. A, Immunoreactivity of AT8 phosphorylated tau in the granular cell layer of the CA2/3 region of Cd59a−/− mice (n = 5) and wild-type (wt) littermate controls (n = 3) 5 months after intrahippocampal injection of adeno-associated virus (AAV2) encoding human P301L mutant tau (arrowheads indicates needle track). Contralateral hippocampus was injected with AAV2 encoding green fluorescent protein (AAV2-GFP), resulting in cytoplasmic and neuritic distribution of GFP. Occasionally, GFP-positive neuritis can also be observed in the AAV2-P301L tau-injected hemisphere. B, Number of AT8-positive cell bodies in the entire AAV2-P301L tau-injected hippocampus in Cd59a−/− mice and wild-type littermate controls. Each symbol indicates the mean number of 3 to 4 sections per mouse. Significance was calculated by Mann–Whitney U test; *P ≤ 0.05. Scale bar, 100 μm.Back to article page