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. Author manuscript; available in PMC: 2022 Aug 9.
Published in final edited form as: J Alzheimers Dis. 2022;88(3):837–847. doi: 10.3233/JAD-210041

Fig.1.

Fig.1

Pathological behavior and increased seizure susceptibility in control and Tg2576 mice with partial or complete TREM2 loss of function mutations. A) Photographs showing large patches of missing hair caused by excessive self-grooming of individually housed TREM2 homozygous mutants crossed with transgenic AD mice (Tg2576(Hemi); upper panel) and their littermate wild-type controls (Tg2576(WT); lower panel). The same compulsive hair removal feature was found in TREM2 heterozygous mice of either genotype. B) Typical EEG recording of spontaneous epileptiform activity in the hippocampal CA1 region of TREM2 deficient mice under anesthesia. Trace shows aberrant large amplitude spiking discharges from Tg2576(WT)TREM2(Het) mouse lasting over 15 seconds. Enlarged segment of the trace (marked in red) is at the bottom. C) Distribution of susceptibility to epileptic seizures between different genotype groups of mice. In wild-type controls, seizures were detected in 44% of TREM2 heterozygous and 33% of TREM2 homozygous groups. In transgenic Tg2576 mice, they were present in 22% of mice from TREM2 heterozygous and homozygous groups. Scale bar: 0.02 mV, 1 s (upper trace); 0.02 mV, 0.2 s (lower trace).