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Fig. 2 | Acta Neuropathologica Communications

Fig. 2

From: Neuronal dysfunction caused by FUSR521G promotes ALS-associated phenotypes that are attenuated by NF-κB inhibition

Fig. 2

Neuronal expression of FUSR521G causes cell-autonomous defects in cognitive and motor function. a Schematic of the novel object recognition test. b hFUSR521G/Syn1 mice display significantly lower interaction time with the novel object (N) compared to the familiar object (F), and littermate control (CTL) mice spend more interaction time with the novel object. c Schematic of the passive avoidance test. d hFUSR521G/Syn1 mice display reduced latency time in entering the dark compartment compared to CTL mice. e hFUSR521G/Syn1 mice display motor impairments in hindlimb splay at 8 months of age compared to CTL mice. f Image shows impaired hindlimb splay of hFUSR521G/Syn1 mice. g hFUSR521G/Syn1 mice display grip weakness in the wire hanging test at 6 and 12 months of age compared to CTL mice. h hFUSR521G/Syn1 mice display signs of motor impairments in the rotarod test at 6 months and significant motor impairments at 12 months of age compared to CTL mice. Values from each group are expressed as mean ± SEM. Statistics uses an unpaired Student’s t-test for comparison between two groups (n = 12 hFUSR521G/Syn1 and n = 14 CTL mice/group). *p < 0.05, **p < 0.01, ***p < 0.005 ****p < 0.001, and not significant (ns)

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