To ensure performance of everyday tasks, adherence to treatment regiments, appointments, and following dietary requirements, cognition is crucial.1 Cognitive impairment (CI) is a broad and inclusive term used to describe dysfunction of processes in various cognitive domains, such as attention, memory, judgment, reasoning, decision-making and problem solving, comprehension and production of language. Prevalence and Pathogenic MechanismsEvidence is mounting that impaired cardiac function may precipitate early-onset CI. Reported prevalence 2-8 of cognitive dysfunction in the heart failure (HF) population parallels the severity of HF, being the highest in the acute decompensation settings (see Table 1).Multiple factors contributing to cognitive decline in HF are presented in Figure 1. Hypertension is found to be independently associated with CI 9,10 through compromise in auto-regulation of cerebral blood flow and cerebral ischaemia (see Figure 2). Neuroimaging has revealed structural brain abnormalities (see Cognitive Domains and Assessment ToolsThe severity of CI may range from mild symptoms to advanced dementia. Mild CI is a commonly used definition for a clinical syndrome in which a patient has subjective complaints as well as objective symptoms of cognitive decline (measured by neuropsychological tests), though daily functioning of the patient is mostly intact.11 It is established that patients with mild cognitive impairment have an increased risk of progression to dementia. 12,13 Dementia is characterised by a progressive impairment in more than one cognitive domain, and compromised daily functioning is evident.Most of the HF patients suffer from mild impairment in cognition, but some of them may have moderate-to-severe CI.13 Heart failure adversely affects various cognitive domains, including attention, learning ability and working memory, executive functions, and information processing speed (see Figure 4). [13][14][15] Cognitive impairment in HF patients usually fulfils the criteria of vascular CI or vascular dementia. 16Being one of the most important cognitive functions, episodic memory of specific personal events and experiences was demonstrated to slowly decline in HF patients. 5,13,14,17 Furthermore, deficits in initial learning as well as delayed information recall were reported in the literature. 17 This suggests that CI in HF patients and CI in patients with vascular dementia could share pathophysiological mechanisms.18 Deficits in executive functioning (problem solving, planning, reasoning and flexibility) have a AbstractCognitive decline is a prevalent condition and independent prognostic marker of unfavourable outcomes in patients with heart failure. The highest prevalence, up to 80 %, is reported in patients hospitalised due to acute decompensation. Numerous factors contribute to cognitive dysfunction in heart failure patients, with hypertension, atrial fibrillation, stroke and impaired haemodynamics being the most relevant. Cerebral hypoperfusion, disruption of blood-brain barrier, oxidative da...

BackgroundLatency of P300 subcomponent of event-related potentials (ERPs) increases in Alzheimer disease (AD) patients, which correlate well with cognitive impairment. Cholinesterase inhibitors (ChEIs) reduce P300 latency in AD patients with parallel improvement in cognition. It is not known whether N200 response to ChEIs is similar to that of P300.The aim of this study was to evaluate and compare characteristics of P300 and N200 in AD patients, treatment-naïve and on stable donepezil treatment, matched by age, education, sex, and cognitive function.Material/MethodsWe recruited 22 consecutive treatment-naïve AD patients (AD-N group), 22 AD patients treated with a stable donepezil dose of 10 mg/day for at least 3 months (AD-T group), and 50 healthy controls were recruited. Neuropsychological testing (MMSE, ADAS-Cog, and additional tests) and ERP recording was performed and analyzed.ResultsAll groups did not differ according to age, duration of education, or sex (p>0.05). AD-N and AD-T groups did not differ according to cognitive function. The AD-T group had longer duration of disease than the AD-N group (p<0.001). The AD-T and AD-N groups did not differ in P300 latencies (p=0.49). N200 latency was longer in the AD-T group (p<0.001). The general linear model showed that significant predictors of P300 latency were age (p=0.019) and AD treatment status (p<0.001). Duration of AD was a significant predictor of N200 latency (p=0.004).ConclusionsThe response of N200 latency to donepezil treatment differs from the response of P300. P300 is a better marker of ChEI treatment-dependent cognitive functions. N200 is more dependent on the duration of AD.

Sex differences identified in the COVID-19 pandemic are necessary to study. It is essential to investigate the efficacy of the drugs in clinical trials for the treatment of COVID-19, and to analyse the sex-related beneficial and adverse effects. The histone deacetylase inhibitor valproic acid (VPA) is a potential drug that could be adapted to prevent the progression and complications of SARS-CoV-2 infection. VPA has a history of research in the treatment of various viral infections. This article reviews the preclinical data, showing that the pharmacological impact of VPA may apply to COVID-19 pathogenetic mechanisms. VPA inhibits SARS-CoV-2 virus entry, suppresses the pro-inflammatory immune cell and cytokine response to infection, and reduces inflammatory tissue and organ damage by mechanisms that may appear to be sex-related. The antithrombotic, antiplatelet, anti-inflammatory, immunomodulatory, glucose- and testosterone-lowering in blood serum effects of VPA suggest that the drug could be promising for therapy of COVID-19. Sex-related differences in the efficacy of VPA treatment may be significant in developing a personalised treatment strategy for COVID-19.

Background: The diuretic effect of valproates and its relation to urinary potassium (K + ) and chloride (Cl -) excretion have not yet been investigated, so the aim of this study was to evaluate the influence of a single dose of sodium valproate (NaVPA) on 24-h urinary K + and Cl -excretion in young adult Wistar rats of both genders. For measurement of K + in urine, the same animals and samples as in our earlier publication were used (Pharmacology 2005 Nov, 75:111-115). The authors propose a new approach to the pathophysiological mechanisms of NaVPA effect on K + and Cl -metabolism.

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