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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Heparanase overexpression impedes perivascular clearance of amyloid-β from murine brain: relevance to Alzheimer’s disease

Fig. 1

Thalamic accumulation of Aβ in Hpa-tg mice. (a, b) Translocation of intracortically injected Aβ42 to the thalamus of Hpa-tg mouse. (a) Anti-Aβ42 immunostaining of a Hpa-tg mouse brain four weeks after intracortical injection (red arrow in a) of aggregated synthetic human Aβ42. (b) Enlarged view of a thalamic Aβ42 deposit with layered morphology. (c-e) Thalamic accumulation of endogenous murine Aβ in Hpa-tg (> 14-month-old) mice. (c) Anti-rodent Aβ immunostaining of 14-month-old Ctr (left panel) and Hpa-tg (middle panel) brains. Enlarged view of a layered thalamic Aβ deposit in Hpa-tg brain, is shown in the right panel. (d) Western blotting analyses of brain homogenates from AβPP knockout (AβPP KO), Ctr and Hpa-tg mice applying antibodies directed against rodent Aβ, AβPP (22C11), and the N-terminal domain of human Aβ (N’Aβ). Dot-blot assay of synthetic human and rodent Aβ40 detected with the anti-N’Aβ antibody, is presented in the right panel. (e) Immunostaining with anti-N’Aβ antibody detects a layered deposit of endogenous Aβ in the thalamus of Hpa-tg mouse

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