Abstract
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are overlapping neurodegenerative disorders whose pathogenesis remains largely unknown. Using TDP-43 A315T mice, an ALS and FTD model with marked cortical pathology, we found that hyperactive somatostatin interneurons disinhibited layer 5 pyramidal neurons (L5-PNs) and contributed to their excitotoxicity. Focal ablation of somatostatin interneurons efficiently restored normal excitability of L5-PNs and alleviated neurodegeneration, suggesting a new therapeutic target for ALS and FTD.
Original language | English (US) |
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Pages (from-to) | 557-559 |
Number of pages | 3 |
Journal | Nature neuroscience |
Volume | 19 |
Issue number | 4 |
DOIs | |
State | Published - Mar 29 2016 |
ASJC Scopus subject areas
- Neuroscience(all)