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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Endogenous mouse huntingtin is highly abundant in cranial nerve nuclei, co-aggregates to Abeta plaques and is induced in reactive astrocytes in a transgenic mouse model of Alzheimer’s disease

Fig. 4

a Association of HTT with Abeta plaques and presence in reactive astrocytes in entorhinal cortex of an 18-month-old Tg2576 mouse. HTT immunoreactivity was found to be present in Abeta plaque-associated glia-like structures (Tg2576 left row, arrows) and aggregate-like structures in the periphery of ThS-positive Abeta plaques (Tg2576 left row, asterisk). This correlation can also be shown using the pan-Abeta-specific antibody 4G8 (Tg2576 middle row). Double fluorescence labelling of HTT and GFAP demonstrates the presence of HTT in reactive astrocytes (arrows) surrounding Abeta plaques (Tg2576 right row, asterisk). No glial HTT immunoreactivity or aggregate-like structures were detected in age-matched wild type mouse entorhinal cortex (wild type row). b Aggregation of 22.5 μM HTT (red dotted line) and its stimulation by addition of 1 μM Abeta (1–42) (yellow solid line) monitored by ThT fluorescence. Note the typical aggregation curve for 1 μM Abeta (1–42) aggregation alone (green broken line). Statistical analysis revealed an accelerated HTT aggregation rate (right diagram) without effects on the lag phase (middle diagram) after addition of small amounts of Abeta (1–42). c Electron microscopic demonstration of the co-occurrence of HTT (4 nm gold particles) and Abeta (1–42) (20 nm gold particles) after immunogold labelling of fibrils generated from 22.5 μM HTT in the presence of 1 μM Abeta (1–42)

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