Dataset Information

Decreased Glucose Utilization Contributes to Memory Impairment in Patients with Glufosinate Ammonium Intoxication.

ABSTRACT: The symptoms of glufosinate ammonium (GLA) intoxication include gastrointestinal and neurologic symptoms, respiratory failure, and cardiovascular instability. Among these, neurologic symptoms including loss of consciousness, memory impairment, and seizure are characteristic of GLA poisoning. However, the mechanism of brain injury by GLA poisoning is still poorly understood. We investigated nine patients who had performed an F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) scan because of memory impairment caused by GLA ingestion. FDG-PET images of patients with GLA intoxication were compared with 24 age- and sex-matched healthy controls to evaluate whether the patients had abnormal patterns of glucose metabolism in the brain. Decreased glucose metabolism was observed in the inferior frontal and temporal lobes of these patients with GLA intoxication when compared with 24 age- and sex-matched healthy controls. Three patients performed follow-up FDG-PET scans. However, it was shown that the results of the follow-up FDG-PET scans were determined to be inconclusive. Our study showed that memory impairment induced by GLA intoxication was associated with glucose hypometabolism in the inferior frontal and temporal lobes in the brain.

SUBMITTER: Park S

PROVIDER: S-EPMC7231126 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Decreased Glucose Utilization Contributes to Memory Impairment in Patients with Glufosinate Ammonium Intoxication.

Park Samel S Kim Joong Il JI Cho Nam-Jun NJ Oh Se Won SW Park Jongkyu J Yoo Ik Dong ID Gil Hyo-Wook HW Lee Sang Mi SM

Journal of clinical medicine 20200423 4

The symptoms of glufosinate ammonium (GLA) intoxication include gastrointestinal and neurologic symptoms, respiratory failure, and cardiovascular instability. Among these, neurologic symptoms including loss of consciousness, memory impairment, and seizure are characteristic of GLA poisoning. However, the mechanism of brain injury by GLA poisoning is still poorly understood. We investigated nine patients who had performed an F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) scan be ...[more]

PMID: 32340163

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Project description:Background: Poststroke cognitive impairments are common in stroke survivors, and pose a high risk of incident dementia. However, the cause of these cognitive impairments is obscure and required an investigation. Methods: Oxygen-glucose deprivation (OGD) model and middle cerebral artery occlusion (MCAO) model were used to imitate in vitro or in vivo acute cerebral ischemia, respectively. The differentially expressed synaptosome associated protein 29 (SNAP29)-interacting proteins upon ischemia and reperfusion were analyzed with bioinformatics analysis and the results indicated that the changes of SNAP29 after acute ischemia were mainly involved in the synaptic functions. The outcomes of SNAP29 reduction were assessed with SNAP29 knockdown, which mimicked the distribution of SNAP29 along neuronal processes after acute ischemia. Using the whole-cell patch clamp recording method and transmission electron microscope, the pre-synaptic function and readily releasable pool (RRP) were observed after SNAP29 knock down. Using photogenetic manipulations and behavioral tests, the neuronal projection and cognitive functions of mice with SNAP29 knock down in hippocampus CA1 region were evaluated. Results: It was found that SNAP29 protein levels decreased in both in vitro and in vivo ischemic models. Further, the SNAP29 reduction wasn't associated with impaired autophagy flux and neuronal survival. When SNAP29 was knocked down in primary cortical neurons, the frequency of AMPARs-mediated mEPSCs, but not the amplitude, significantly decreased. Meanwhile, the mice with SNAP29 knockdown at CA1 region of hippocampus developed an impairment in hippocampus-mPFC (middle prefrontal cortex) circuit and behavioral dysfunctions. Moreover, the size of RRP at presynaptic sites was diminished. Conclusion: Since SNAP29 protein levels didn't significantly influence the neuronal survival and its decrease was sufficient to disturb the neural circuit via a presynaptic manner, the SNAP29-associated strategies may be an efficient target against poststroke synaptic dysfunction and cognitive deficits.

Dataset Information

Decreased Glucose Utilization Contributes to Memory Impairment in Patients with Glufosinate Ammonium Intoxication.

Publications

Decreased Glucose Utilization Contributes to Memory Impairment in Patients with Glufosinate Ammonium Intoxication.

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