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Figure 5; supplement 4.

ID: ZDB-IMAGE-210208-78
Publication: Alyenbaawi et al., 2021 - Seizures are a druggable mechanistic link between TBI and subsequent tauopathy
All Figures: Figures for Alyenbaawi et al., 2021

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Figure Caption

Figure 5; supplement 4. Increasing intensity of traumatic brain injury (TBI) significantly increased Tau4R-GFP puncta abundance, but only modest insignificant increases in Tau puncta were observed with an increasing number of successive brain injuries.

(A) Following TBI of Tau4R-GFP larvae, the GFP+ aggregates in the brain tended to be fused. (B,C) Tau4R-GFP larvae were subjected to TBI via either one single hit or five consecutive hits. The number of GFP+ aggregates in the brain (B) and the spinal cord (C) were quantified at 3 and 4 days post-traumatic brain injury (dpi). The number of aggregates modestly increases with more hits but not consistently (not statistically significant). The symbols for treatment types are equivalent in panels B and C. (D) Performing TBI on Tau4R-GFP larvae on each of 3 consecutive days slightly increased the number of GFP+ Tau puncta in the spinal cord (relative to a single TBI treatment) but the increase was not statistically significant. (E) A nearly linear dose-response of TBI injury intensity varying with the abundance of GFP+ puncta in the spinal cord. TBI intensity was modulated by dropping weights of varying masses in the TBI method. Heavier weights induced more GFP+ puncta (*p<0.01 and **p<0.001). In each panel, raw data is plotted, along with mean ± standard error.

Acknowledgments

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