Microglial voltage-gated proton channel 1 ablation in diabetic mice mitigates diabetes-driven demyelination and cognitive decline

Table 1 Key strengths and innovations

Aspect	Summary	Supporting data
Multimodal approach	In vivo (HFD + STZ, Hv1 KO) and in vitro (high-glucose + siHv1) models converge on Hv1’s role	Behavioral (Figure 1 in the study of Li et al[1]), IF (Figures 2 and 6 in the study of Li et al[1]), TEM (Figure 5 in the study of Li et al[1]), ferroptosis markers (Figure 7 in the study of Li et al[1])
Functional rescue	Hv1 KO restores working/spatial memory deficits	40% fewer errors; 30% more entries (Figure 1C and D in the study of Li et al[1])
White matter protection	TEM shows normalization of g-ratio from 0.81 (diabetic) to 0.78 (KO)	Figure 5A-F in the study of Li et al[1]

HFD: High-fat diet; STZ: Streptozotocin; Hv1: Voltage-gated proton channel 1; KO: Knockout; siHv1: Small interfering RNA-mediated voltage-gated proton channel 1; IF: Immunofluorescence; TEM: Transmission electron microscope.