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Figure 2 | Journal of Neuroinflammation

Figure 2

From: Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in mice

Figure 2

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.

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