Featured Paper of the Month – July 2016
Zhang, Wen; Zhang, Lifeng; Liang, Bo; Schroeder, David; Zhang, Zhong-Wei; Cox, Gregory A; Li, Yun; Lin, Da-Ting
Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders. Journal Article
In: Nat Neurosci, vol. 19, no. 4, pp. 557–559, 2016, ISSN: 1546-1726 (Electronic); 1097-6256 (Linking).
@article{Zhang2016,
title = {Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders.},
author = {Wen Zhang and Lifeng Zhang and Bo Liang and David Schroeder and Zhong-Wei Zhang and Gregory A Cox and Yun Li and Da-Ting Lin},
url = {https://www.ncbi.nlm.nih.gov/pubmed/26900927},
doi = {10.1038/nn.4257},
issn = {1546-1726 (Electronic); 1097-6256 (Linking)},
year = {2016},
date = {2016-04-01},
journal = {Nat Neurosci},
volume = {19},
number = {4},
pages = {557--559},
address = {Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 333 Cassell Drive, Baltimore, MD 21224, USA.},
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.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
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.
