ArticleNeurobiology of disease2026
Aberrant medial ganglionic eminence (MGE) GABAergic neurogenesis contributes to Huntington's disease pathogenesis.
Article in Neurobiology of disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Although early telencephalic interneuron dysfunction in animal models and cortical interneuron deficits in Huntington's disease (HD) have been documented, their developmental origins and causal contributions to disease pathogenesis remain incompletely understood. Using the BACHD mouse model, we examined medial ganglionic eminence (MGE)-derived GABAergic lineage development across embryonic and early postnatal stages, integrated single-cell transcriptomic analyses of E12.5 MGE progenitors and assessed disease relevance through lineage-specific genetic rescue. At postnatal day (PND) 13, BACHD mice exhibited reduced numbers of cortical somatostatin-positive (SST
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