{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T21:48:59Z","timestamp":1790804939831,"version":"4.1.0"},"reference-count":140,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2020,11,3]],"date-time":"2020-11-03T00:00:00Z","timestamp":1604361600000},"content-version":"vor","delay-in-days":2,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["103838"],"award-info":[{"award-number":["103838"]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000288","name":"Royal Society","doi-asserted-by":"publisher","award":["098436\/Z\/12\/B"],"award-info":[{"award-number":["098436\/Z\/12\/B"]}],"id":[{"id":"10.13039\/501100000288","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Cambridge Trust and Fitzwilliam College"},{"DOI":"10.13039\/501100000265","name":"Medical Research Council","doi-asserted-by":"publisher","award":["MR\/M008983\/1"],"award-info":[{"award-number":["MR\/M008983\/1"]}],"id":[{"id":"10.13039\/501100000265","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000265","name":"Medical Research Council","doi-asserted-by":"publisher","award":["SUAG\/051 G101400"],"award-info":[{"award-number":["SUAG\/051 G101400"]}],"id":[{"id":"10.13039\/501100000265","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Institute for Health Research Cambridge Biomedical Research Centre and Cambridge Brain Bank","award":["146281"],"award-info":[{"award-number":["146281"]}]},{"name":"Cambridge Centre for Parkinson Plus"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Behavioural disinhibition is a common feature of the syndromes associated with frontotemporal lobar degeneration (FTLD). It is associated with high morbidity and lacks proven symptomatic treatments. A potential therapeutic strategy is to correct the neurotransmitter deficits associated with FTLD, thereby improving behaviour. Reductions in the neurotransmitters glutamate and GABA correlate with impulsive behaviour in several neuropsychiatric diseases and there is post-mortem evidence of their deficit in FTLD. Here, we tested the hypothesis that prefrontal glutamate and GABA levels are reduced by FTLD in vivo, and that their deficit is associated with impaired response inhibition. Thirty-three participants with a syndrome associated with FTLD (15 patients with behavioural variant frontotemporal dementia and 18 with progressive supranuclear palsy, including both Richardson\u2019s syndrome and progressive supranuclear palsy-frontal subtypes) and 20 healthy control subjects were included. Participants undertook ultra-high field (7 T) magnetic resonance spectroscopy and a stop-signal task of response inhibition. We measured glutamate and GABA levels using semi-LASER magnetic resonance spectroscopy in the right inferior frontal gyrus, because of its strong association with response inhibition, and in the primary visual cortex, as a control region. The stop-signal reaction time was calculated using an ex-Gaussian Bayesian model. Participants with frontotemporal dementia and progressive supranuclear palsy had impaired response inhibition, with longer stop-signal reaction times compared with controls. GABA concentration was reduced in patients versus controls in the right inferior frontal gyrus, but not the occipital lobe. There was no group-wise difference in partial volume corrected glutamate concentration between patients and controls. Both GABA and glutamate concentrations in the inferior frontal gyrus correlated inversely with stop-signal reaction time, indicating greater impulsivity in proportion to the loss of each neurotransmitter. We conclude that the glutamatergic and GABAergic deficits in the frontal lobe are potential targets for symptomatic drug treatment of frontotemporal dementia and progressive supranuclear palsy.<\/jats:p>","DOI":"10.1093\/brain\/awaa305","type":"journal-article","created":{"date-parts":[[2020,8,28]],"date-time":"2020-08-28T15:13:32Z","timestamp":1598627612000},"page":"3449-3462","source":"Crossref","is-referenced-by-count":107,"title":["GABA and glutamate deficits from frontotemporal lobar degeneration are associated with disinhibition"],"prefix":"10.1093","volume":"143","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0813-0670","authenticated-orcid":false,"given":"Alexander G","family":"Murley","sequence":"first","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge, UK"},{"name":"Cambridge University Hospitals NHS Foundation Trust, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3157-4301","authenticated-orcid":false,"given":"Matthew A","family":"Rouse","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9695-0702","authenticated-orcid":false,"given":"P Simon","family":"Jones","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2529-7755","authenticated-orcid":false,"given":"Rong","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Clinical Neurosciences, University of Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0092-3289","authenticated-orcid":false,"given":"Frank 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of Psychology, University of Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catarina","family":"Rua","sequence":"additional","affiliation":[{"name":"Wolfson Brain Imaging Centre, University of Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2939-8222","authenticated-orcid":false,"given":"T Adrian","family":"Carpenter","sequence":"additional","affiliation":[{"name":"Wolfson Brain Imaging Centre, University of Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1275-1197","authenticated-orcid":false,"given":"Christopher T","family":"Rodgers","sequence":"additional","affiliation":[{"name":"Wolfson Brain Imaging Centre, University of Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7216-8679","authenticated-orcid":false,"given":"James 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