Visual exploration disturbance has been examined in the elderly, mainly from the perspective of associations with cognitive function. However, it remains unknown whether this is a consequence of cognitive decline, age-related changes independent of cognitive decline, or both. In this study, 15 healthy elderly individuals were evaluated using two figure-matching tasks representing visual information processing (clock-matching and inverted clock-matching tasks). Cognitive functions were evaluated for each subject using the Mini-Mental State Examination (MMSE). Infrared eye-movement assessments were used to analyze eye movements during task performance. Behavioral analyses showed that age was associated with longer reaction time, while MMSE score was associated with higher accuracy on the inverted clock-matching task. Analyses of eye-movement parameters showed that MMSE score was negatively associated with a parameter indicating difficulty in the efficiency of visual exploration planning, while age was tended to be positively associated with the sum of saccade times in each trial, both predominantly on the inverted clock-matching task. Our approaches highlighted that age and cognitive decline are separately associated with eye-movement characteristics cognitive decline is associated with difficulty in visual exploration planning, particularly in situations that require substantial visual working memory resources, whereas aging may be associated with oculomotor dysfunction.Sleep loss leads to a spectrum of mood disorders such as anxiety disorders, bipolar disorder and depression in many individuals. However, the underlying mechanisms are largely unknown. In this study, sleep-disturbed animals were tested for anxiety and depressive behaviors. We then studied the effects of SD on hypothalamic-pituitary-adrenal (HPA) axis function by measuring serum and CSF levels of corticosterone (CORT), and at the end of the experiment, brains were collected to measure the circadian oscillations of clock genes expression in the hypothalamus, glial cell activation and inflammatory cytokine alterations. Our results indicated that SD for 3 days resulted in anxiety- and depressive-like behaviors. SD exaggerated cortisol response to HPA axis, significantly altered the circadian oscillations of clock genes, decreased the expression of tight junction protein ZO-1 and Claudin 5 and increased the number of GFAP-positive cells and Iba-1-positive cells and caused subsequent elevation of pro-inflammatory cytokines IL-6, IL-1β and TNFα. These findings demonstrated that SD for 3 days induced anxiety- and depression-like behaviors in rats in company with altering the circadian oscillations of clock genes and inducing neuroinflammation, indicating the underlying mechanism of sleep loss induced neuronal dysfunction.
Neuroimaging studies suggest that the inferior frontal operculum (IFO) is part of a neuronal network involved in facial expression processing, but the causal role of this region in emotional face discrimination remains elusive.
We used cathodal (inhibitory) tDCS to test whether right (r-IFO) and left (l-IFO) IFO play a role in discriminating basic facial emotions in healthy volunteers. Specifically, we tested if the two sites are selectively involved in the processing of facial expressions conveying high or low arousal emotions. BLU222 Based on the Arousal Hypothesis we expected to find a modulation of high and low arousal emotions by cathodal tDCS of the r-IFO and the l-IFO, respectively.
First, we validated an Emotional Faces Discrimination Task (EFDT). Then, we targeted the r-IFO and the l-IFO with cathodal tDCS (i.e. the cathode was placed over the right or left IFO, while the anode was placed over the contralateral supraorbital area) during facial emotions discrimination on the EFDT. Non-active (i.e. shamiscrimination of high arousal emotions but disrupting discrimination of low arousal emotions. These findings offer new insights for treating clinical population with deficits in processing facial expressions.
Post-traumatic Stress Disorder (PTSD) often does not respond to available treatments. Memories are vulnerable to disruption during reconsolidation, and electroconvulsive therapy (ECT) has amnestic effects OBJECTIVE/HYPOTHESIS To test the use of ECT to disrupt the reconsolidation of traumatic memories as a potential treatment for PTSD METHODS Participants were adults from the civilian population and were referred for ECT treatment for severe depression with comorbid PTSD symptoms. Twenty-eight participants were randomly assigned to reactivation of a traumatic or non-traumatic memory using audio script driven imagery prior to each ECT treatment. Primary outcomes were change in scores on the Modified PTSD Symptom Scale - Self Report (MPSS-SR) and the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5). Secondary outcomes included a comparison of the change in heart rate while listening to the script RESULTS Twenty-five female patients who completed a post-ECT assessment were included in the analysis. No significant group differences were found in the MPSS-SR or CAPS-5 scores from pre-ECT to post-ECT or 3-month follow-ups. However, both groups improved at post-ECT and 3-month follow up. Partial eta squared estimates of effect size showed large effect sizes for all outcomes (η
0.13). Changes in heart rate were not significantly different between groups or over time CONCLUSIONS ECT paired with pre-treatment traumatic memory reactivation was not more effective for treating PTSD symptoms than ECT with non-traumatic memory reactivation. While our primary hypothesis was not supported, our data provides further support for the efficacy of ECT for improving symptoms of PTSD with comorbid depression. ClinicalTrials.gov. https//clinicaltrials.gov/ct2/show/NCT04027452.
NCT04027452.
NCT04027452.
To compare the prevalence of psychopathology, particularly bipolar disorder (BD), between preschool offspring of parents with BD and community controls.
A total of 116 offspring of BD-I/II parents and 98 controls (53 parents with non-BD psychopathology and 45 healthy parents) were recruited at ages 2 to 5 years and followed on average 9.6 years (on average 2-5 1.6 times; after age 5 4 times) (average ages at intake/last follow-up 3.8/13.4, retention 98%). Participants were evaluated with standardized instruments blinded to parental diagnoses.
After adjusting for confounders, offspring of BD parents only showed more attention-deficit/hyperactivity disorder (ADHD) during ages 2 to 5 years than the other 2 groups. After age 5, offspring of BD parents did not differ from offspring of parents with non-BD psychopathology, but they had more anxiety, ADHD, and behavior problems than offspring of healthy parents. Only offspring of BD parents developed BD-I/II 3.4% (n = 4) and BD-not-otherwise-specified (BD-NOS) 11.BLU222
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