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As such, interventions aimed to reduce SOD1 G93A expression and/or SOD1 G93A protein accumulation are most likely to achieve large rescuing effects in this model, whereas interventions that do not directly target the SOD1 G93A mechanisms are less likely to achieve success in retarding motor neuron disease of this model 23,24,25

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456 Additionally, gene therapy approaches targeting defective genes associated with XLP1, FHL2, and FHL3 have shown encouraging results in preclinical mouse models, offering potential avenues for future curative treatments

Ren et al., 2022a, b

doi: 10.3389/fimmu.2025.1536020 140 ZhangPWangYMiaoQChenY