scholarly journals Theaflavins Improve Memory Impairment and Depression-Like Behavior by Regulating Microglial Activation

Molecules ◽  
2019 ◽  
Vol 24 (3) ◽  
pp. 467 ◽  
Author(s):  
Yasuhisa Ano ◽  
Rena Ohya ◽  
Masahiro Kita ◽  
Yoshimasa Taniguchi ◽  
Keiji Kondo
Keyword(s):  
Memory Impairment ◽  
Tail Suspension Test ◽  
Black Tea ◽  
Behavioral Changes ◽  
Y Maze ◽  
Research Gap ◽  
Dendritic Atrophy ◽  
The Brain ◽  
Anti Inflammation ◽  
Inflammatory Effect

Inflammation in the brain is associated with various disorders including Alzheimer’s disease and depression. Thus, inflammation has received increasing attention regarding preventive approaches to such disorders. Epidemiological investigations have reported that drinking tea reduces the risk of dementia and depression. Theaflavins, a polyphenol found in black tea, are known to have anti-oxidative and anti-inflammation effects, but the effects of theaflavins on cognitive decline and depression induced by inflammation have not been investigated. To address this research gap, the present study assessed whether theaflavins could protect synapses and dendrites damaged by inflammation and prevent concomitant memory impairment and depression-like behavior in mice. Intracerebroventricular injection with lipopolysaccharide (LPS) induces neural inflammation associated with reduced spontaneous alternations in the Y-maze test and increased immobility in the tail suspension test, indicating impaired spatial memory and depression-like behavior, respectively. Oral administration with theaflavins prevented these behavioral changes induced by LPS. Theaflavins also suppressed productions of inflammatory cytokines and prevented dendritic atrophy and spine loss in the brain. Notably, theaflavins have a stronger anti-inflammatory effect than other polyphenols such as catechin, chlorogenic acid, and caffeic acid. These results suggest that theaflavins can suppress neural inflammation and prevent the symptoms of inflammation-related brain disorders.

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 Modafinil Effects on Behavior and Oxidative Damage Parameters in Brain of Wistar Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Felipe Ornell ◽  
Samira S. Valvassori ◽  
Amanda V. Steckert ◽  
Pedro F. Deroza ◽  
Wilson R. Resende ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Open Field ◽  
Wistar Rats ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Behavioral Changes ◽  
Protein Damage ◽  
Behavioral Parameters ◽  
Carbonyl Formation ◽  
The Brain

The effects of modafinil (MD) on behavioral and oxidative damage to protein and lipid in the brain of rats were evaluated. Wistar rats were given a single administration by gavage of water or MD (75, 150, or 300 mg/kg). Behavioral parameters were evaluated in open-field apparatus 1, 2, and 3 h after drug administration. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation were measured in the brain. MD increased locomotor activity at the highest dose 1 and 3 h after administration. MD administration at the dose of 300 mg/kg increased visits to the center of open-field 1 h after administration; however, 3 h after administration, all administered doses of MD increased visits to the open-field center. MD 300 mg/kg increased lipid damage in the amygdala, hippocampus, and striatum. Besides, MD increased protein damage in the prefrontal cortex, amygdala, and hippocampus; however, this effect varies depending on the dose administered. In contrast, the administration of MD 75 and 300 mg/kg decreased the protein damage in the striatum. This study demonstrated that the MD administration induces behavioral changes, which was depending on the dose used. In addition, the effects of MD on oxidative damage parameters seemed to be in specific brain region and doses.

Multiple Memory Systems and Their Support of Language

2014 ◽  
Vol 24 (2) ◽  
pp. 64-73 ◽  
Author(s):  
Jake Kurczek ◽  
Natalie Vanderveen ◽  
Melissa C. Duff
Keyword(s):  
Memory Impairment ◽  
Language Use ◽  
Declarative Memory ◽  
Memory Systems ◽  
Memory And Learning ◽  
Multiple Memory Systems ◽  
History Of Research ◽  
Language And Communication ◽  
History Of ◽  
The Brain

There is a long history of research linking the various forms of memory to different aspects of language. Clinically, we see this memory-language connection in the prevalence of language and communication deficits in populations that have concomitant impairments in memory and learning. In this article, we provide an overview of how the demands of language use and processing are supported by multiple memory systems in the brain, including working memory, declarative memory and nondeclarative memory, and how disruptions in different forms of memory may affect language. While not an exhaustive review of the literature, special attention is paid to populations who speech-language pathologists (SLPs) routinely serve. The goal of this review is to provide a resource for clinicians working with clients with disorders in memory and learning in helping to understand and anticipate the range of disruptions in language and communication that can arise as a consequence of memory impairment. We also hope this is a catalyst for more research on the contribution of multiple memory systems to language and communication.

scholarly journals Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Alessio Molfino ◽  
Gianfranco Gioia ◽  
Filippo Rossi Fanelli ◽  
Alessandro Laviano
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Proinflammatory Cytokines ◽  
Adaptive Response ◽  
Energy Homeostasis ◽  
Cancer Cachexia ◽  
Behavioral Changes ◽  
Brain Areas ◽  
Functional Changes ◽  
The Brain

Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals.

scholarly journals Sport-related concussions

2014 ◽  
Vol 8 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Jéssica Natuline Ianof ◽  
Fabio Rios Freire ◽  
Vanessa Tomé Gonçalves Calado ◽  
Juliana Rhein Lacerda ◽  
Fernanda Coelho ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Behavioral Changes ◽  
American Football ◽  
Health Concern ◽  
Public Health Concern ◽  
Increased Risk ◽  
High Prevalence ◽  
Biomechanical Forces ◽  
The Brain

ABSTRACT Traumatic brain injury (TBI) is a major cause of lifelong disability and death worldwide. Sport-related traumatic brain injury is an important public health concern. The purpose of this review was to highlight the importance of sport-related concussions. Concussion refers to a transient alteration in consciousness induced by external biomechanical forces transmitted directly or indirectly to the brain. It is a common, although most likely underreported, condition. Contact sports such as American football, rugby, soccer, boxing, basketball and hockey are associated with a relatively high prevalence of concussion. Various factors may be associated with a greater risk of sport-related concussion, such as age, sex, sport played, level of sport played and equipment used. Physical complaints (headache, fatigue, dizziness), behavioral changes (depression, anxiety, irritability) and cognitive impairment are very common after a concussion. The risk of premature return to activities includes the prolongation of post-concussive symptoms and increased risk of concussion recurrence.

scholarly journals Effects of ozone on sickness and depressive-like behavioral and biochemical phenotypes and their relations to serum amyloid A and kynurenine in blood

2021 ◽  
Author(s):  
Kristen K Baumann ◽  
Wei-Shan Sandy Liang ◽  
Daniel V Quaranta ◽  
Miranda L Wilson ◽  
Helina S Asrat ◽  
...  
Keyword(s):  
Serum Amyloid A ◽  
Pulmonary Inflammation ◽  
Kynurenine Pathway ◽  
Air Pollutant ◽  
Behavioral Changes ◽  
Serum Amyloid ◽  
Present Evidence ◽  
Dose Time ◽  
Amyloid A ◽  
The Brain

Ozone (O3) is an air pollutant which primarily damages the lungs, but growing evidence supports that O3 exposure can also affect the brain. Serum amyloid A (SAA) and kynurenine have been identified as circulating factors that are upregulated by O3, and both can contribute to depressive-like behaviors in mice. However, little is known about the relations of O3 exposure to sickness and depressive-like behaviors in experimental settings. In this study, we evaluated O3 dose-, time- and sex- dependent changes in circulating SAA in context of pulmonary inflammation and damage, sickness and depressive-like behavioral changes, and systemic changes in kynurenine and indoleamine 2,3-dioxygenase (IDO), an enzyme that regulates kynurenine production and contributes to inflammation-induced depressive-like behaviors. Our results in Balb/c and CD-1 mice showed that 3ppm O3, but not 2 or 1ppm O3, caused elevations in serum SAA and pulmonary neutrophils, and these responses resolved by 48 hours. Sickness and depressive-like behaviors were observed at all O3 doses (1-3ppm), although the detection of certain behavioral changes varied by dose. We also found that Ido1 mRNA expression was increased in the brain and spleen 24 hours after 3ppm O3, and that kynurenine was increased in blood. Together, these findings indicate that acute O3 exposure induces transient symptoms of sickness and depressive-like behaviors which may occur in the presence or absence of overt pulmonary neutrophilia and systemic increases of SAA. We also present evidence that the IDO/kynurenine pathway is upregulated systemically following an acute exposure to O3 in mice.

scholarly journals Ebselen Prevents Cigarette Smoke-Induced Cognitive Dysfunction In Mice By Preserving Hippocampal Synaptophysin Expression

2021 ◽  
Author(s):  
Simone N. De Luca ◽  
Kurt Brassington ◽  
Stanley M. H. Chan ◽  
Aleksandar Dobric ◽  
Kevin Mou ◽  
...  
Keyword(s):  
Working Memory ◽  
Cognitive Dysfunction ◽  
Memory Impairment ◽  
Microglial Activation ◽  
Pulmonary Inflammation ◽  
Systemic Circulation ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Memory Impairments ◽  
The Brain

Abstract Background: Cigarette smoking (CS) is the leading cause of chronic obstructive pulmonary disease (COPD). The “spill-over” of pulmonary inflammation into the systemic circulation may damage the brain, leading to cognitive dysfunction. Cessation of CS can improve pulmonary and neurocognitive outcomes, however, its benefit on the neuroinflammatory profile remains uncertain. Here, we investigate how CS exposure impairs neurocognition and whether this can be reversed with CS cessation or an antioxidant treatment. Methods: Male BALB/c mice were exposed CS (9 cigarettes/day for 8 weeks) followed by 4 weeks of CS cessation. Another cohort of CS-exposed mice were co-administrated with a glutathione peroxidase (Gpx) mimetic, ebselen (10mg/kg) or vehicle (5% CM-cellulose). We assessed pulmonary inflammation, spatial and working memory, and the hippocampal microglial, oxidative and synaptic profiles. Results: CS exposure increased lung inflammation which was reduced following CS cessation. CS caused spatial and working memory impairments which were attributed to hippocampal microglial activation and suppression of synaptophysin. CS cessation did not improve memory deficits or alter microglial activation. Ebselen completely prevented the CS-induced working and spatial memory impairments, which was associated with restored synaptophysin expression without altering microglial activation.Conclusion: We were able to model the CS-induced memory impairment and microglial activation seen in human COPD. The preventative effects of ebselen on memory impairment is likely to be dependent on a preserved synaptogenic profile. Cessation alone also appears to be insufficient in correcting the memory impairment, suggesting the importance of incorporating antioxidant therapy to help maximizing the benefit of cessation.

scholarly journals Distinct Processing of Selection and Execution Errors in Neural Signatures of Outcome Monitoring

2019 ◽  
Author(s):  
Faisal Mushtaq ◽  
Samuel D. McDougle ◽  
Matt P. Craddock ◽  
Darius E. Parvin ◽  
Jack Brookes ◽  
...  
Keyword(s):  
Behavioral Adjustment ◽  
Behavioral Changes ◽  
Behavioral Correlates ◽  
Feedback Information ◽  
Future Action ◽  
Outcome Monitoring ◽  
Frontal Negativity ◽  
Neural Signature ◽  
The Brain ◽  
Insight Into

AbstractLosing a point playing tennis may result from poor shot selection or poor stroke execution. To explore how the brain responds to these different types of errors, we examined EEG signatures of feedback-related processing while participants performed a simple decision-making task. In Experiment 1, we used a task in which unrewarded outcomes were framed as selection errors, similar to how feedback information is treated in most studies. Consistent with previous work, EEG differences between rewarded and unrewarded trials in the medial frontal negativity (MFN) correlated with behavioral adjustment. In Experiment 2, the task was modified such that unrewarded outcomes could arise from either poor execution or selection. For selection errors, the results replicated that observed in Experiment 1. However, unrewarded outcomes attributed to poor execution produced larger amplitude MFN, alongside an attenuation in activity preceding this component and a subsequent enhanced error positivity (Pe) response in posterior sites. In terms of behavioral correlates, only the degree of the early attenuation and amplitude of the Pe correlated with behavioral adjustment following execution errors relative to reward; the amplitude of the MFN did not correlate with behavioral changes related to execution errors. These results indicate the existence of distinct neural correlates of selection and execution error processing and are consistent with the hypothesis that execution errors can modulate action selection evaluation. More generally, they provide insight into how the brain responds to different classes of error that determine future action.Significance StatementTo learn from mistakes, we must resolve whether decisions that fail to produce rewards are due to poorly selected action plans or badly executed movements. EEG data were obtained to identify and compare the physiological correlates of selection and execution errors, and how these are related to behavioral changes. A neural signature associated with reinforcement learning, a medial frontal negative (MFN) ERP deflection, correlated with behavioral adjustment after selection errors relative to reward outcomes, but not motor execution errors. In contrast, activity preceding and following the MFN response correlated with behavioral adjustment after execution errors relative to reward. These results provide novel insight into how the brain responds to different classes of error that determine future action.

scholarly journals Prevention of Memory Impairment and Neurotrophic Factors Increased by Lithium in Wistar Rats Submitted to Pneumococcal Meningitis Model

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Lutiana R. Simões ◽  
Roberta R. E. S. Abreu ◽  
Jaqueline S. Generoso ◽  
Jéssica A. Goularte ◽  
Allan Collodel ◽  
...  
Keyword(s):  
Group Treatment ◽  
Neurotrophic Factor ◽  
Memory Impairment ◽  
Pneumococcal Meningitis ◽  
Mood Stabilizer ◽  
Inhibitory Avoidance ◽  
Saline Control ◽  
Artificial Cerebrospinal Fluid ◽  
The Brain ◽  
Experimental Pneumococcal Meningitis

The aim of this study was to investigate the effects of lithium on brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and glial cell line-derived neurotrophic factor (GDNF) expression in the hippocampus and on memory in experimental pneumococcal meningitis. The mood-stabilizer lithium is known as a neuroprotective agent with many effects on the brain. In this study, animals received either artificial cerebrospinal fluid or Streptococcus pneumoniae suspension at a concentration of 5 × 109 CFU/mL. Eighteen hours after induction, all animals received ceftriaxone. The animals received saline or lithium (47.5 mg/kg) or tamoxifen (1 mg/kg) as adjuvant treatment, and they were separated into six groups: control/saline, control/lithium, control/tamoxifen, meningitis/saline, meningitis/lithium, and meningitis/tamoxifen. Ten days after meningitis induction, animals were subjected to open-field habituation and the step-down inhibitory avoidance tasks. Immediately after these tasks, the animals were killed and their hippocampus was removed to evaluate the expression of BDNF, NGF, and GDNF. In the meningitis group, treatment with lithium and tamoxifen resulted in improvement in memory. Meningitis group showed decreased expression of BDNF and GDNF in the hippocampus while lithium reestablished the neurotrophin expression. Lithium was able to prevent memory impairment and reestablishes hippocampal neurotrophin expression in experimental pneumococcal meningitis.

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