scholarly journals Rosuvastatin revert memory impairment and anxiogenic-like effect in mice infected with the chronic ME-49 strain of Toxoplasma gondii

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 ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Memory Impairment ◽  
Brain Inflammation ◽  
Long Term Memory ◽  
Histopathological Analysis ◽  
Term Memory ◽  
Anxiogenic Effect ◽  
Short And Long Term ◽  
The Brain

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.

scholarly journals Daylight saving for the brain

2015 ◽  
pp. 60-64
Author(s):  
James Cully
Keyword(s):  
Functional Capacity ◽  
Modern Medicine ◽  
Long Term Memory ◽  
Healthy Human ◽  
Term Memory ◽  
Daylight Saving ◽  
Level Of Functioning ◽  
Short And Long Term ◽  
The Brain

Our lives are comprised of our doings. We love, we lose, we learn and we forget, and throughout we are dependent on our brains to maintain a level of cognitive functioning (such as short and long term memory, attention to specific sensations and speaking and understanding language) that allows us to live our lives in the manner we want. If we lose this level of functioning we are bereft and vulnerable. Growing old is something to which every healthy human aspires. More and more people are reaching old-age; the ageing of the world’s population is considered mankind’s greatest achievement of the 20th century. It has also become one of the main health challenges in modern medicine; diseases associated with ageing, such as Alzheimer’s disease (AD), have increased drastically in rate. One of the main consequences of developing AD is that your brain’s functional capacity decreases. You forget more and more ...

scholarly journals Paclitaxel Chemotherapy Induces Long-Term Memory Impairment and Neuroinflammation in a Mouse Model of Breast Cancer Survivorship

2021 ◽  
Author(s):  
Ni-Chun Chung ◽  
Aeson Chang ◽  
Ryan Gillis ◽  
Erica Sloan ◽  
Adam K Walker
Keyword(s):  
Cognitive Impairment ◽  
Memory Impairment ◽  
Cancer Surgery ◽  
Long Term Memory ◽  
Cumulative Impact ◽  
Term Memory ◽  
Maze Test ◽  
Y Maze ◽  
The Brain

Abstract BackgroundCancer-related cognitive impairment (CRCI) has been reported in cancer survivors 20 years or more after cancer treatment, and has been associated with sustained increases in circulating inflammatory biomarkers. One of the major risk factors for CRCI is chemotherapy, and preclinical studies typically examine the impact of chemotherapy in cancer naïve mice to evaluate potential mechanisms However, clinical evaluation of the long-term effects of chemotherapy cannot avoid the potential cumulative impact of preceding factors on the brain including the cancer itself and cancer surgery. MethodsTo evaluate the cumulative impact of cancer-related factors on cognitive impairment and hippocampal cytokine expression, we evaluated the effect of paclitaxel chemotherapy vs. placebo on a background of 67NR mammary carcinoma and surgical resection of the primary tumour in mice. Memory was assessed using the Y maze test and novel object/novel place recognition test. Changes in hippocampal pro-inflammatory and anti-inflammatory cytokines, microglia and neuron markers were assessed using qRT-PCR. Results Cancer and cancer surgery was sufficient to induce long-term memory impairment and sustained increases in hippocampal pro-inflammatory cytokines. Paclitaxel prolonged spatial memory impairment in the Y maze test and exacerbated hippocampal Il6 and Tnfa mRNA expression compared with placebo treatment. ConclusionsThese findings suggest that cancer and cancer surgery can sensitise the brain to an exaggerated neuroinflammatory response to chemotherapy, and may contribute to sustained chemotherapy-induced cognitive impairment observed in cancer survivors.

scholarly journals TO003CROSSTALK OF UREMIC TOXINS AND INFLAMMASOME IN CHRONIC KIDNEY DISEASE-RELATED COGNITIVE IMPAIRMENT

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
LUNG-CHIH LI ◽  
WEI-YU CHEN ◽  
Jin Po Chen ◽  
Wen-Chin Lee ◽  
JENG-LIN YANG
Keyword(s):  
Chronic Kidney Disease ◽  
Brain Tissue ◽  
Nlrp3 Inflammasome ◽  
Memory Impairment ◽  
Uremic Toxins ◽  
Long Term Memory ◽  
Short Term ◽  
Term Memory ◽  
The Brain

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.

The Acute Effect of Alcohol on Various Memory Processes

2010 ◽  
Vol 24 (4) ◽  
pp. 249-252 ◽  
Author(s):  
Márk Molnár ◽  
Roland Boha ◽  
Balázs Czigler ◽  
Zsófia Anna Gaál
Keyword(s):  
Low Dose ◽  
Short Term Memory ◽  
Acute Effect ◽  
Long Term Memory ◽  
Term Memory ◽  
Memory Processes ◽  
Different Types ◽  
The Brain ◽  
Legal Consequences

This review surveys relevant and recent data of the pertinent literature regarding the acute effect of alcohol on various kinds of memory processes with special emphasis on working memory. The characteristics of different types of long-term memory (LTM) and short-term memory (STM) processes are summarized with an attempt to relate these to various structures in the brain. LTM is typically impaired by chronic alcohol intake but according to some data a single dose of ethanol may have long lasting effects if administered at a critically important age. The most commonly seen deleterious acute effect of alcohol to STM appears following large doses of ethanol in conditions of “binge drinking” causing the “blackout” phenomenon. However, with the application of various techniques and well-structured behavioral paradigms it is possible to detect, albeit occasionally, subtle changes of cognitive processes even as a result of a low dose of alcohol. These data may be important for the consideration of legal consequences of low-dose ethanol intake in conditions such as driving, etc.

Short- and long-term memory tasks predict working memory performance, and vice versa.

2019 ◽  
Vol 73 (2) ◽  
pp. 79-93 ◽  
Author(s):  
Ian Neath ◽  
Jean Saint-Aubin ◽  
Tamra J. Bireta ◽  
Andrew J. Gabel ◽  
Chelsea G. Hudson ◽  
...  
Keyword(s):  
Working Memory ◽  
Memory Performance ◽  
Long Term Memory ◽  
Term Memory ◽  
Short And Long Term

The Improvement of Short- and Long-term Memory of Young Children by BF-7

2010 ◽  
Vol 39 (3) ◽  
pp. 376-382 ◽  
Author(s):  
Do-Hee Kim ◽  
Ok-Hyeon Kim ◽  
Joo-Hong Yeo ◽  
Kwang-Gill Lee ◽  
Geum-Duck Park ◽  
...  
Keyword(s):  
Young Children ◽  
Long Term Memory ◽  
Term Memory ◽  
Short And Long Term

scholarly journals Sotalol does not interfere with the antielectroshock action of selected second-generation antiepileptic drugs in mice

2021 ◽  
Author(s):  
Kinga K. Borowicz-Reutt ◽  
Monika Banach ◽  
Monika Rudkowska ◽  
Anna Stachniuk
Keyword(s):  
Antiepileptic Drugs ◽  
Second Generation ◽  
Antidepressant Drug ◽  
Experimental Models ◽  
Long Term Memory ◽  
Avoidance Task ◽  
Maximal Electroshock ◽  
Term Memory ◽  
The Brain

Abstract Background Due to blocking β-receptors, and potassium KCNH2 channels, sotalol may influence seizure phenomena. In the previous study, we have shown that sotalol potentiated the antielectroshock action of phenytoin and valproate in mice. Materials and methods As a continuation of previous experiments, we examined the effect of sotalol on the action of four chosen second-generation antiepileptic drugs (oxcarbazepine, lamotrigine, pregabalin, and topiramate) against the maximal electroshock in mice. Undesired effects were evaluated in the chimney test (motor impairment) and step-through passive-avoidance task (long-term memory deficits). Finally, brain concentrations of antiepileptics were determined by fluorescence polarization immunoassay, while those of sotalol by liquid chromatography–mass spectrometry. Results Sotalol at doses of up to 100 mg/kg did not affect the electroconvulsive threshold. Applied at doses of 80–100 mg/kg, sotalol did not affect the antielectroshock action of oxcarbazepine, lamotrigine, pregabalin, or topiramate. Sotalol alone and in combinations with antiepileptics impaired neither motor performance nor long-term memory. Finally, sotalol significantly decreased the brain concentrations of lamotrigine and increased those of oxcarbazepine and topiramate. Pharmacokinetic interactions, however, did not influence the final antielectroshock effects of above-mentioned drug combinations. On the other hand, the brain concentrations of sotalol were not changed by second-generation antiepileptics used in this study. Conclusion Sotalol did not reduce the antielectroshock action of four second-generation antiepileptic drugs examined in this study. Therefore, this antidepressant drug should not interfere with antiseizure effects of lamotrigine, oxcarbazepine, pregabalin, and topiramate in patients with epilepsy. To draw final conclusions, our preclinical data should still be confirmed in other experimental models and clinical conditions.

The Relationship Between Brain Fog and Medication Adherence for Individuals With Hypothyroidism

2021 ◽  
pp. 105477382110381
Author(s):  
Kelly Haskard-Zolnierek ◽  
Courtney Wilson ◽  
Julia Pruin ◽  
Rebecca Deason ◽  
Krista Howard
Keyword(s):  
Memory Impairment ◽  
Hormone Replacement ◽  
Long Term Memory ◽  
Adherence Level ◽  
Thyroid Hormone Replacement ◽  
Memory Impairments ◽  
Cognitive Failures ◽  
Short And Long Term ◽  
The Relationship

Individuals with hypothyroidism suffer from symptoms including impairments to cognition (i.e., “brain fog”). Medication can help reduce symptoms of hypothyroidism; however, brain fog may hinder adherence. The aim of this study was to determine if memory impairment and cognitive failures are related to treatment nonadherence in 441 individuals with hypothyroidism. Participants with a diagnosis of hypothyroidism and currently prescribed a thyroid hormone replacement medication were placed in two groups according to adherence level and compared on validated scales assessing impairments to memory and cognition. Results indicated a significant association between treatment nonadherence and self-reported brain fog, represented by greater cognitive and memory impairments. Nonadherent individuals indicated impairments with prospective, retrospective, and short- and long-term memory; and more cognitive failures, compared to adherent individuals. Findings suggest the importance of interventions to enhance adherence for individuals with brain fog, such as encouraging the use of reminders.

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