BRAIN: GABA and glutamate deficiency in frontal temporal lobe degeneration are associated with de-inhibition

Behavioral inhibition is a common feature of temporal lobe degeneration (FTLD)-related syndrome.
it is associated with high incidence and lacks a proven treatment strategy for the disease.
potential therapeutic strategy is to correct neurotransmitter defects associated with FLD, thereby improving behavior.
neurotransmitter glutamate and GABA in several neuropsychological disorders were associated with impulsive behavior, and there was posthumous evidence that they were defective in FLD.
here, we tested the hypothesis that FTLD lowers levels of glutamate and GABA in the body, and that their defects are associated with impaired reaction suppression.
included 33 participants with FLD-related syndromes (15 patients with behavioral variants of temporal dementia and 18 with carrying nuclear paralysis, including Richardson's syndrome and carrying nuclear paralytic-frontal subtypes) and 20 healthy control groups.
participants performed ultra-high magnetic field (7 T) magnetic resonance spectrum and response suppression stop signal tasks.
the levels of glutamate and GABA were measured using semi-LASER magnetic resonance spectrometry in the lower right forehead, as it is closely related to reaction inhibition and serves as a control area in the primary visual cortical layer.
stop signal reaction time is calculated using the pre-Gauss bayes model.
participants with frontal temporal lobe dementia and aggressive nuclear paralysis had weak reactive inhibition and longer signal response times than the control group.
the GABA concentration in patients with the disease decreased relative to the lower right forehead back (not the pillow leaf).
volume-corrected glutamate concentrations were not group-by-group between patients and control groups.
gabA and glutamate concentrations in the lower forehead are inversely proportional to the stop signal reaction time, indicating that impulsivity is proportional to the loss of each neurotransmitter.
studies have shown that glutamate and GABAergic defects in the frontal lobe are potential targets for drug treatment for frontal temporal lobe dementia and aggressive nuclear paralysis.
origins: Alexander G Murray, Matthew A Rouse, P Simon Jones, GABA and glutamate from the from frontotemporal lobar degeneration are associated with disinhibition. MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Original" are owned by Mets Medicine and are not authorized to be reproduced by any media, website or individual, and are authorized to be reproduced with the words "Source: Mets Medicine".
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