scholarly journals Limbic Encephalitis Associated with COVID-19

Encyclopedia ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 26-35
Author(s):  
Natalia A. Shnayder ◽  
Timur K. Sirbiladze ◽  
Irina V. Demko ◽  
Marina M. Petrova ◽  
Regina F. Nasyrova

Limbic encephalitis (LE) is an inflammatory disease of the brain, in which lesion is anatomically limited in structures of the limbic system. In some cases, LE can start with symptoms of limbic dysfunction with further involvement of other regions of the brain. Classic LE syndrome includes such symptoms as the development of personality disorders, depression, sleep disorders, epileptic seizures, hallucinations and cognitive disorders (short-term and long-term memory impairment). The information of clinical examination, electroencephalogram (EEG), magnetic resonance imaging (MRI) and cerebrospinal fluid studies (CSF) suggest the diagnosis of LE in most patients with Coronavirus Disease 2019 (COVID-19).

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
LUNG-CHIH LI ◽  
WEI-YU CHEN ◽  
Jin Po Chen ◽  
Wen-Chin Lee ◽  
JENG-LIN YANG

Abstract Background and Aims Chronic kidney disease (CKD) is getting prevalent and causes big burden to the health care systems worldwide. CKD-associated cognitive impairment (CI) not only influences the behave function, but also results in longer hospitalization and higher risk of mortality. Inflammation is an important pathogenesis of CKD and plays a crucial role in progression of CKD. In this study, we hypothesized that accumulated uremic toxins, especially indoxyl sulfate (IS) and P-cresyl sulfate (PCS) induce neuroinflammation via activation of NLRP3 inflammasome in the brain tissue of CKD animals. This study aims to delineate the crosstalk between uremic toxins and inflammation in CKD-induced CI. Method Eight-week-old male C57B6 wildtype and NLRP3 knockout mice received sham and 5/6 nephrectomy to mimic CKD status. AST-120 (Kremezin), a spherical carbon adsorbent, was given orally to mice to neutralize the accumulated uremic toxins. The Y-maze and Morris water maze (MWM) testes were applied to evaluate cognitive function, including the spatial, short-term and long-term memory in shame, CKD, and AST-120 treated CKD mice. HPLC was used to examine the concentration of IS and PCS in the serum and brain tissues. Western blot and immunohistochemistry stain were used to identify the protein expression of target molecules in the brain tissue. Results CKD mice showed impaired spatial, short-term and long-term memory; however, 10% AST-120 attenuated CKD-induced memory impairment (Figure 1). IS, but not PCS, elevated in the brain tissues, especially in the frontal cortex and hippocampus. AST-120 reduced CKD-induced IS elevation in the brain tissue, and also ameliorated NLRP3 inflammasome activation in the astrocytes in the frontal and hippocampus. Finally, NLRP3 deficiency reversed the CKD-induced memory impairment (Figure 2). Conclusion IS is the major uremic toxin that causes CI in CKD mice via activating NLRP3 inflammasome pathway in the brain tissue. However, AST-120 effectively ameliorates CKD-induced CI.


SIMULATION ◽  
1964 ◽  
Vol 3 (6) ◽  
pp. 46-51
Author(s):  
W. Ross Adey ◽  
N.V. Findler

It is attempted in this paper to give a mathematical description of the short-term memory. Instead of using the microscopic properties of individual neu rons, such as the number of interconnections, neuron density, threshold value, etc., the cerebral cortex is regarded as a "neuron gas" that is a vast conglomer ate of neurons with statistically distributed charac teristics. Stimuli from the environment cause the receptor neurons to emit virtual electromagnetic waves into the brain. A self-optimizing process of the brain tis sue is here described by which the useful, informa tion-carrying energy reaching the long-term memory tends to maximum. It is emphasized that in the following a brain model is described and the physical processes in volved may have no direct equivalent in reality.


PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0250079
Author(s):  
Fernanda Ferreira Evangelista ◽  
Willian Costa-Ferreira ◽  
Francini Martini Mantelo ◽  
Lucimara Fátima Beletini ◽  
Amanda Hinobu de Souza ◽  
...  

The aim of this study was to investigate the effect of rosuvastatin treatment on memory impairment, and anxiogenic-like effects in mice chronically infected with Toxoplasma gondii. For this, Balb/c mice were infected orally with chronic ME-49 strain of Toxoplasma gondii. Oral treatment with rosuvastatin (40mg/kg/day) started on the 51st day post-infection and was performed daily for 21 days. After completion of treatment, anxiety-like effects and locomotion were investigated in the open field (OF) test, whereas novel object recognition (NOR) test was used for evaluation of short- and long-term memory. At the end of the experiments, the brain was collected for Toxoplasma gondii DNA quantification and histopathological analysis. Infection with ME-49 strain decreased the time spent in the center of OF, indicating an anxiogenic effect, without affecting total and peripheral locomotion. Rosuvastatin treatment inhibited the change in the center time. Besides, pharmacological treatment increased total and central locomotion in both non-infected and infected animals. Infection also impaired both short- and long-term memory in the NOR test, and these effects were reverted by rosuvastatin treatment. In addition to effects in behavioral changes, rosuvastatin also reduced parasite load in the brain and attenuated signs of brain inflammation such as perivascular cuffs, inflammatory cell infiltration and tissue damage. These findings indicate for the first time the efficacy of rosuvastatin in treatment of memory impairment and anxiogenic effect evoked by infection with Toxoplasma gondii. These effects might be mediated by reduced cyst load, which in turn decrease inflammation and damage in the brain.


2019 ◽  
Author(s):  
cika suteja

In daily life, humans can not be separated from the name of learning and remembering. Learning and remembering is the basis for someone to adapt their behavior to the environment. The brain is the organ that regulates learning and memory. The brain will store and bring back the information needed. Decline in memory usually occurs during old age but does not rule out the possibility of happening at a young age too. Decreasing memory recall at a young age is usually caused by a lack of physical activity. Sports is one of the factors that can improve memory. Exercise can improve blood circulation so that the brain can be well-nourished and will work optimally. To make our memories into long-term memories can be done by repeating the information obtained. Because repetition can accelerate and increase consolidation. Information entered in long-term memory will be grouped according to the type of information. This grouping serves to facilitate the search for the desired information. Short-term information will forever be forgotten, but long-term information can last up to a lifetime.


2021 ◽  
Vol 29 (3) ◽  
pp. 337-346
Author(s):  
Elena A. Muzyko ◽  
Valentina N. Perfilova ◽  
Ivan N. Tyurenkov ◽  
Olga S. Vasil'eva

BACKGROUND: Preeclampsia is a serious complication of pregnancy which augments the risk of cognitive disorders in the offspring at different stages of life. Presently, there are no methods with proven effectiveness for correction of post-hypoxic disorders in children of mothers with preeclampsia. AIM: To assess the cognitive functions of the offspring of rats with experimental preeclampsia (EP) through early (40th to 70th day of life) and late (24th to 25th month of life) pharmacological correction with gamma aminobutyric acid (GABA) derivatives: Succicard, Salifen, Phenibut, and the drug of comparisonPantogam. MATERIALS AND METHODS: EP was modeled by replacing drinking water with 1.8% sodium chloride solution in rats from the first day of pregnancy to delivery. In the offspring, short-term and long-term memory was studied at the age of 34, 1819, and 2526 months in the Novel object recognition test and Barnes Maze test. The functioning of the GABAergic and dopaminergic systems (which play an essential role in the development of memory) was evaluated by cases of convulsions after administering corazol at a dose of 20 mg/kg intraperitoneally (model of corazol kindling) and by haloperidol-induced catalepsy (haloperidol at a dose of 0.3 mg/kg intraperitoneally), respectively. RESULTS: Early and late pharmacological correction with GABA derivativessuccicard, Salifen, Phenibut, and comparison drug, Pantogamneutralized the negative effect of EP on the function of GABAergic and dopaminergic systems in the offspring of the experimental groups. Therapy with Succicard in puberty and long-term periods of life contributed to the improvement of short-term and long-term memory in the offspring of rats with EP. Thus, it could be reasonable enough to develop a drug against cognitive disorders in children of mothers with preeclampsia. CONCLUSION: In the offspring of rats with EP, short-term and long-term disorders of memory in the functioning of the GABAergic and dopaminergic systems were noted in the early and late stages of the individual development. Pharmacological correction with GABA derivatives improves cognitive processes and the functioning of neurotransmitter systems in the offspring of rats with complicated pregnancy. The highest effectiveness was demonstrated by succicard, and was comparable with or superior to the Pantogam (standard drug).


2017 ◽  
Vol 381 ◽  
pp. 126-127 ◽  
Author(s):  
Pedro Nascimento Alves ◽  
Carolina Maruta ◽  
Luísa Albuquerque ◽  
Isabel Pavão Martins

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Chuting Li ◽  
Yuan Liu ◽  
Dexiang Liu ◽  
Hong Jiang ◽  
Fang Pan

Several types of microRNA (miRNA) overexpression in the brain are associated with stress. One of the targets of miR-34c is the stress-related corticotrophin releasing factor receptor 1 mRNA (CRFR1 mRNA). Here we will probe into the short-term effect and long-term effect of early adolescent traumatic stress on the expression of miR-34c and CRFR1 mRNA. Traumatic stress was established by electric foot shock for six consecutive days using 28-day rats. The anxiety-like behaviors, memory damage, CRFR1 protein, CRFR1 mRNA, and miR-34c expression were detected in our study. The results of our study proved that exposure to acute traumatic stress in early adolescent can cause permanent changes in neural network, resulting in dysregulation of CRFR1 expression and CRFR1 mRNA and miR-34c expression in hypothalamus, anxiety-like behavior, and memory impairment, suggesting that the miR-34c expression in hypothalamus may be an important factor involved in susceptibility to PTSD.


2018 ◽  
Vol 155 ◽  
pp. 01026
Author(s):  
Vladimir Shumilov ◽  
Vladimir Syryamkin

In this paper, various types of memory are considered.Development of the nervous system and the brain of organisms ensures expansion of species with more developed brain. Different characteristics of the brain zones have created different conditions for forming traces of events. The various traces of trace events formed in different parts of the brain provided a wider range of functions and brain responses, which contributed to the survival and expansion of species. The work describes the appearance of memory varieties and the causes of these varieties.


2001 ◽  
Vol 88 (1) ◽  
pp. 102-110 ◽  
Author(s):  
L. N. Vaillancourt ◽  
M. A. Persinger

The concept of the neuromatrix assumes that all behaviours are associated with complex spatiotemporal electromagnetic fields within the brain. The same complex magnetic field can be supported potentially by different mosaics of neuronal associations and result in the same behaviours. In the present study the accuracy of long-term and short-term spatial memory for rats that had been treated with 100 mg/kg of ketamine immediately after the induction of seizures by lithium and pilocarpine did not differ from normal rats despite the conspicuous multifocal neuronal loss. A 30-min. delay of treatment with ketamine resulted in significant memory impairment. Whereas deficits in short-term memory were significantly correlated with cell loss within the CA field of the hippocampus, deficits in long-term memory were related to cell loss within specific thalamic-amygdaloid structures. Implications for the concept of the neuromatrix, if valid, are discussed.


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