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• What is the primary question addressed by this study? What are the clinical features of catatonia in patients with dementia? • What is the main finding of this study? Catatonia in dementia does not have a different syndromic presentation. However, the diagnosis of dementia leads to varying preferences regarding the choice of symptomatic therapy and seems to be a predictor of a poorer therapeutic response. • What is the meaning of the finding? Actively treating catatonia, particularly in patients with dementia, addressing the characteristics of these patients is of paramount importance and may contribute to a better overall prognosis. • Twitter This systematic review investigates catatonia in the elderly. Dementia influences treatment choices for catatonia and seems to be a predictor of a poorer therapeutic response. Catatonia is a neuropsychiatric syndrome characterized by motor, behavioral, and autonomic abnormalities. It is often underdiagnosed in geriatric patients with dementia despite established diagnostic criteria and treatment options. This systematic review investigates catatonia in the elderly, particularly those with dementia, to examine their clinical presentation, treatment response, and prognosis compared to elderly patients without dementia. We comprehensively searched MEDLINE and EMBASE, including case reports and series on catatonia in elderly patients. Reviewers independently performed data extraction and quality assessments. Statistical significance was set at a p value ≤0.05, and a multivariate logistic regression model was used to analyze differences between patients with and without dementia. Our review included 182 articles with 225 cases. We found no significant differences in the clinical presentation of catatonia between patients with and without dementia, with both groups commonly exhibiting the hypokinetic variant. However, patients with dementia were more frequently treated with NMDA receptor antagonists (OR: 3.27; CI: 1.05–10.11; p = 0.040) and had a lower complete response rate to treatment (OR: 0.37; CI: 0.19–0.75; p = 0.006). Patients with dementia also exhibited fewer acute medical conditions (OR: 0.17; CI: 0.05–0.65; p = 0.009). Catatonia in dementia does not have a different syndromic presentation. However, the diagnosis of dementia leads to varying preferences regarding the choice of symptomatic therapy and seems to be a predictor of a poorer therapeutic response. Actively treating catatonia, particularly in patients with dementia, addressing the characteristics of these patients is of paramount importance. [ABSTRACT FROM AUTHOR]

To identify triggers of acute mood episodes in bipolar disorder (BD). We performed a systematic review in the following databases: Pubmed, Embase, and PsycInfo following the preferred reporting items for systematic reviews and meta-analysis guidelines. The systematic search encompassed all relevant studies published until May 23rd, 2022. A total of 108 studies (case reports/case series, interventional, prospective and retrospective studies) were included in the systematic review. While several decompensation triggers were identified, pharmacotherapy was the one with the largest body of evidence, particularly the use of antidepressants as triggers of manic/hypomanic episodes. Other identified triggers for mania were brain stimulation, energy drinks, acetyl-l-carnitine, St. John's wort, seasonal changes, hormonal changes and viral infections. There is a relative paucity of evidence concerning triggers for depressive relapses in BD, with possible triggers including fasting, decreased sleep and stressful life events. This is the first systematic review about triggers/precipitants of relapse in BD. Despite the importance of identification and management of potential triggers for BD decompensation, there is a lack of large observational studies addressing this topic, with most of the included studies being case reports/case series. Notwithstanding these limitations, antidepressant use is the trigger with the strongest evidence for manic relapse. More studies are needed to identify and manage triggers for relapse in BD. [ABSTRACT FROM AUTHOR]

FOXP3+ regulatory T cells (Tregs) are central for peripheral tolerance, and their deregulation is associated with autoimmunity. Dysfunctional autoimmune Tregs display pro-inflammatory features and altered mitochondrial metabolism, but contributing factors remain elusive. High salt (HS) has been identified to alter immune function and to promote autoimmunity. By investigating longitudinal transcriptional changes of human Tregs, we identified that HS induces metabolic reprogramming, recapitulating features of autoimmune Tregs. Mechanistically, extracellular HS raises intracellular Na+, perturbing mitochondrial respiration by interfering with the electron transport chain (ETC). Metabolic disturbance by a temporary HS encounter or complex III blockade rapidly induces a pro-inflammatory signature and FOXP3 downregulation, leading to long-term dysfunction in vitro and in vivo. The HS-induced effect could be reversed by inhibition of mitochondrial Na+/Ca2+ exchanger (NCLX). Our results indicate that salt could contribute to metabolic reprogramming and that short-term HS encounter perturb metabolic fitness and long-term function of human Tregs with important implications for autoimmunity. [Display omitted] • High salt (HS) perturbs mitochondrial respiration of human Tregs • Salt-induced immunometabolic changes lead to dysfunctional, autoimmune-like Tregs • Short-term exposure to HS is sufficient to impair long-term fitness of Tregs • Inhibition of mitochondrial NCLX restores HS perturbed Treg function Herein, Côrte-Real et al. reveal that sodium directly interferes with mitochondrial respiration in Tregs on the level of the electron transport chain (ETC), leading to a dysfunctional autoimmune-like phenotype. Even a short-term high-salt (HS) encounter could perturb long-term metabolic fitness and function of Tregs, which may have important implications for autoimmunity. [ABSTRACT FROM AUTHOR]