Search

Background: Post-stroke cognitive impairment (PSCI) represents a serious post-stroke complication with poor cognitive consequences. A vascular consequence after a stroke is that the occurrence and progression of PSCI may be closely related to blood pressure (BP). Thus, we systematically reviewed and performed a meta-analysis of the literature to examine the correlations between BP and PSCI., Methods: We systematically queried databases, including PubMed, the Cochrane Library, Embase, and Scopus, and conducted meta-analyses on studies reporting odds ratios (ORs) related to the association between BP and PSCI. Two authors autonomously assessed all titles, abstracts, and full texts and extracted data following the Meta-Analysis of Observational Studies in Epidemiology guidelines. The quality of the studies was evaluated using the modified Newcastle-Ottawa scale., Results: Meta-analyses incorporated 12 articles comprising a cumulative participant cohort of 21,732 individuals. The quality assessment indicated good in five studies, fair in one study, and poor in six. Through meta-analyses, we found that hypertension, systolic or diastolic BP (SBP or DBP) was significantly associated with PSCI (OR 1.53, 95% confidence interval (CI), 1.18-1.99; p = 0.001, I 2 = 66%; OR 1.13, 95% CI, 1.05-1.23; p = 0.002, I 2 = 52%; OR 1.38, 95% CI, 1.11-1.72; p = 0.004, I 2 = 90%, respectively). In the subgroup analysis, SBP < 120 mmHg, 120-139 mmHg, 140-159 mmHg, 160-179 mmHg, and DBP ≥ 100 mmHg highly predicted the occurrence of PSCI (OR 1.15, p = 0.0003; OR 1.26, p = 0.010; OR 1.15, p = 0.05; OR 1.02, p = 0.009; OR 1.96, p < 0.00001, respectively). However, the predictive effect of BP for PSCI declines when SBP ≥ 180 mmHg and DBP ≤ 99 mmHg ( p > 0.05). Statistical heterogeneity was moderate to high, and publication bias was detected in SBP for PSCI., Conclusions: Considering the multifactorial etiology of PSCI, it is difficult to conclude that BP is an independent risk factor for PSCI. Given the restricted inclusion of studies, caution is advised when interpreting the findings from this meta-analysis. Subsequent investigations with substantial sample sizes are essential to exploring BP as a prospective target for addressing PSCI., Trial Registration Number: CRD42023437783 from PROSPERO., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2024 The Author(s). Published by IMR Press.)

Background: In stroke patients with insulin resistance (IR), post-stroke cognitive impairment (PSCI) is associated with higher risk of recurrent stroke, but the effect of pioglitazone on that risk has not been explored. The goal of this study was to compare the secondary stroke prevention effect of pioglitazone against placebo in patients with versus without PSCI., Methods: We studied patients enrolled in the Insulin Resistance Intervention after Stroke (IRIS) trial with a post-stroke modified Mini-Mental State Examination (3MS) cognitive assessment (mean time of assessment: 79 days post-stroke). We considered a baseline score of ⩽ 88 on the 3MS to indicate global PSCI, and domain-specific summary scores in the lowest quartile to indicate attention, language, memory, orientation, and visuospatial impairments., Results: In n = 3338 patients with IR, the effect of pioglitazone versus placebo on secondary stroke significantly differed by initial post-stroke global (interaction p = 0.0127) and memory impairment status (interaction p = 0.0003). Hazard ratios (HRs) were time-dependent such that, among those with either global or memory impairment, pioglitazone has an increasingly stronger protective effect at later timepoints. There was no statistically significant effect of pioglitazone among those without either global or memory impairment. The effect of pioglitazone versus placebo on myocardial infarction (MI) also significantly differed by global impairment status (interaction p = 0.030). Pioglitazone was protective among those with global impairment (HR = 0.23 [95% CI: 0.08, 0.71]) but not among those without (HR = 0.88 [95% CI: 0.59, 1.31])., Conclusion: These data indicate that pioglitazone treatment may be more effective at reducing risk of recurrent stroke and MI in stroke patients with PSCI. Simple cognitive testing 2-3 months post-stroke may identify patients for whom treatment would be most beneficial., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

In recent years, the stroke incidence has been increasing year by year, and the related sequelae after stroke, such as cognitive impairment, motor dysfunction, and post-stroke depression, seriously affect the patient's rehabilitation and daily activities. Repetitive transcranial magnetic stimulation (rTMS), as a safe, non-invasive, and effective new rehabilitation method, has been widely recognized in clinical practice. This article reviews the application and research progress of rTMS in treating different functional impairments (cognitive impairment, motor dysfunction, unilateral spatial neglect, depression) after stroke in recent years, and preliminary summarized the possible mechanisms. It has been found that the key parameters that determine the effectiveness of rTMS in improving post-stroke functional impairments include pulse number, stimulated brain areas, stimulation intensity and frequency, as well as duration. Generally, high-frequency stimulation is used to excite the ipsilateral cerebral cortex, while low-frequency stimulation is used to inhibit the contralateral cerebral cortex, thus achieving a balance of excitability between the two hemispheres. However, the specific mechanisms and the optimal stimulation mode for different functional impairments have not yet reached a consistent conclusion, and more research is needed to explore and clarify the best way to use rTMS. Furthermore, we will identify the issues and challenges in the current research, explore possible mechanisms to deepen understanding of rTMS, propose future research directions, and offer insightful insights for better clinical applications., (© 2023. Fondazione Società Italiana di Neurologia.)

Objective: Although neurocognitive disorders (NCD) are common post-stroke, many populations do not have adapted cognitive screens and cut-offs. We therefore reviewed the appropriateness of the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and Oxford Cognitive Screen (OCS) for diagnosing NCD in culturally diverse stroke populations. Method: Using an extensive search string, diagnostic accuracy studies for MMSE, MoCA and OCS in the stroke population were retrieved from four databases. We compared translations and adaptations, adjustments in scores and cut-offs, and their diagnostic accuracy. Results: The search resulted in 28 MMSE, 39 MoCA and 5 OCS-studies in 13 western, educated, industrialized, rich and democratic (WEIRD) and 4 other countries. There was a lack of studies on South-American, African, and non-Chinese-Asian populations. All three tests needed adaptation for less WEIRD populations and populations with languages with non-Latin features. Optimal MMSE and OCS subtest cut-offs were similar across WEIRD and less WEIRD populations, whereas optimal MoCA cut-offs appeared lower for less WEIRD populations. The use of adjusted scores resulted in different optimal cut-offs or similar cut-offs with better accuracy. Conclusions: MoCA, MMSE and OCS are promising tools for diagnosing post-stroke-NCD. For culturally diverse populations, translation, adaptation and adjusted scores or cut-offs are necessary for diagnostic accuracy. Available studies report scarcely about their sample's cultural background and there is a lack of diagnostic accuracy studies in less WEIRD or culturally diverse populations. Future studies should report more cultural characteristics of their sample to provide better insight into the tests' accuracy in culturally diverse populations.

To investigate the effect of epimedium total flavone capsules on post-stroke cognitive impairment(PSCI) in rats. The transient middle cerebral artery occlusion(tMCAO) model was constructed on selected rats, and rats with impaired neurological function were randomly divided into the model group, low, middle, and high dose groups of epimedium total flavone capsules, and nimodipine tablet group. The cognitive function of rats was measured after administration. Pathological changes in brain tissue were observed after hematoxylin-eosin staining(HE). Neuronal nuclei(NeuN) and glial fibrillary acidic protein(GFAP) distribution in brain tissue were tested by immunofluorescent staining. The level of amyloid beta 1-42(Aβ&#95;(1-42)), neuron specific enolase(NSE), acetylcholine(ACH), dopamine(DA), 5-hydroxytryptamine(5-HT), norepinephrine(NE), interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α), and hypersensitive C-reactive protein(hs-CRP) in rat serum was tested. Moreover, Western blot was utilized to test the expression of nuclear factor-kappaB(NF-κB), p-NF-κB, alpha inhibitor of NF-κB(IκBα) protein, and p-IκBα protein in the hippocampus. The experimental results showed that epimedium total flavone capsules can improve the cognitive function of model rats, and the mechanism may be related to the regulation of the expression of p-IκBα and p-NF-κB proteins, so as to inhibit inflammatory response induced by ischemia-reperfusion.

Background: Stroke is highly prevalent globally and is an important cause of cognitive impairment and dementia.Aims: We determined the frequency of post-stroke cognitive impairment (PSCI) at 1, 3, and 6 months among patients with first clinical ischemic stroke compared to risk and age-matched controls.Methods: This study involved 32 cases and 32 controls, and was conducted over 6 months. Cases were inpatients aged >60 with first clinical ischemic stroke. Controls were age-matched subjects without prior stroke. Montreal Cognitive Assessment (MoCA) was performed in all patients at 1, 3, and 6 month post stroke. A MoCA score of

Background: Post-stroke cognitive impairment (PSCI) is common, but evidence of cognitive symptom profiles, course over time, and pathogenesis is scarce. We investigated the significance of time and etiologic stroke subtype for the probability of PSCI, severity, and cognitive profile.Methods: Stroke survivors (n = 617) underwent cognitive assessments of attention, executive function, memory, language, perceptual-motor function, and the Montreal Cognitive Assessment (MoCA) after 3 and/or 18 months. PSCI was classified according to DSM-5 criteria. Stroke severity was assessed with the National Institutes of Health Stroke Scale (NIHSS). Stroke subtype was categorized as intracerebral hemorrhage (ICH), large artery disease (LAD), cardioembolic stroke (CE), small vessel disease (SVD), or un-/other determined strokes (UD). Mixed-effects logistic or linear regression was applied with PSCI, MoCA, and z-scores of the cognitive domains as dependent variables. Independent variables were time as well as stroke subtype, time, and interaction between these. The analyses were adjusted for age, education, and sex. The effects of time and stroke subtype were analyzed by likelihood ratio tests (LR).Results: Mean age was 72 years (SD 12), 42% were females, and mean NIHSS score at admittance was 3.8 (SD 4.8). Probability (95% CI) for PSCI after 3 and 18 months was 0.59 (0.51–0.66) and 0.51 (0.52–0.60), respectively and remained constant over time. Global measures and most cognitive domains were assessed as impaired for the entire stroke population and for most stroke subtypes. Executive function and language improved for the entire stroke population (LR) = 9.05, p = 0.003, and LR = 10.38, p = 0.001, respectively). After dividing the sample according to stroke subtypes, language improved for ICH patients (LR = 18.02, p = 0.003). No significant differences were found in the severity of impairment between stroke subtypes except for attention, which was impaired for LAD and CE in contrast to no impairment for SVD (LR = 56.58, p < 0.001).Conclusions: In this study including mainly minor strokes, PSCI is common for all subtypes, both early and long-term after stroke, while executive function and language improve over time. The findings might contribute to personalizing follow-up and offer new insights into underlying mechanisms. Further research is needed on underlying mechanisms, PSCI prevention and treatment, and relevance for rehabilitation.

BackgroundThe mechanism of post-stroke cognitive impairment (PSCI) has not been explained. We aimed to investigate whether miR-let-7i participates in the PSCI and illuminates its underlying role in oxygen–glucose deprivation (OGD)-induced cell apoptosis.MethodsBlood samples from 36 subjects with PSCI and 38 with post-stroke cognitive normality (Non-PSCI) were collected to evaluate the differential expression of miR-let-7 family members, using qRT-PCT analysis. Spearman correlation was performed to estimate the correlation between the miR-1et-7i level and Montreal Cognitive Assessment (MoCA) score. Treatment of SH-SY5Y cells with OGD was used to induce cell apoptosis in vitro. Effects of miR-let-7i on OGD-induced cell apoptosis was estimated after transfection. The target gene of miR-let-7i was analyzed by dual luciferase reporter gene assay.ResultsThe expression of miR-let-7i was up-regulated in PSCI patients compared with Non-PSCI (p < 0.001) and negatively correlated with MoCA score (r = −0.643, p < 0.001). When exposed to OGD, SH-SY5Y cells showed significant apoptosis accompanied by miR-let-7i up-regulation. In OGD-treated cells, miR-let-7i up-regulation was accompanied by cell apoptosis, while down-regulation showed the opposite effect. Luciferase reporter assay showed that Bcl-2 was a target gene of miR-let-7i. Western blot showed that miR-let-7i up-regulation promoted Bcl-2 expression, while qRT-PCR showed that miR-let-7i had no effect on Bcl-2 expression.ConclusionmiR-let-7i was overexpressed in PSCI patients and it could be used as a diagnostic biomarker for PSCI. We illuminated the potential mechanism that miR-let-7i alleviated OGD-induced cell damage by targeting Bcl-2 at the post-transcriptional level.

Abstract Background Early and late onset post-stroke cognitive impairment (PCI) contributes substantially to disability following stroke, and is a high priority within stroke research. The aetiology for PCI is complex and related to the stroke itself, brain resilience, comorbid brain diseases, prestroke vulnerability and complications during the hospital stay. The aim of the Norwegian Cognitive Impairment After Stroke study (Nor-COAST) is to quantify and measure levels of cognitive impairments in a general Norwegian stroke population and to identify biological and clinical markers associated with prognosis for cognitive disorders following incident stroke. The study will be organised within five work packages: 1) Incidence and trajectories 2) Pathological mechanisms 3) Development of a risk score 4) Impact of physical activity and 5) Adherence to secondary prevention. Methods Nor-COAST is an ongoing multicentre (five participating hospitals), prospective, cohort study with consecutive inclusion during the acute phase and with follow-up at three and 18 months, and at three years. Inclusion criteria are stroke defined according to the WHO criteria. During the recruitment period from 18.05.2015 to 31.03.2017, 816 participants have been included. Cognitive impairment will be classified according to the DSM-5 criteria using a consensus group. Cognitive function is assessed by a standardised neuropsychological test battery, the Montreal Cognitive Assessment, Trail making A and B, ten-word immediate and delayed recall test, the Controlled Oral Word Association, Global Deterioration Scale and proxy based information by and the Ascertain Dementia 8 item informant questionnaire. Biomarkers include magnetic resonance imaging, routine blood samples and bio-banking. Clinical assessments include characteristics of the stroke, comorbidity, delirium, frailty and tests for cognitive and physical function, sensor based activity monitoring and adherence to secondary prophylaxis. Discussion Nor-COAST is the first Norwegian multicentre study to quantify burden of PCI that will provide reliable estimates in a general stroke population. A multidisciplinary approach aiming to identify biomarkers and clinical markers of overall prognosis will add new knowledge about risk profiles, including pre-stroke vulnerability and modifiable factors such as physical activity and secondary prophylaxis of relevance for clinical practice and later intervention studies. Trial registration ClinicalTrials.gov: NCT02650531. Retrospectively registered January 8, 2016. First participant included May 18, 2015.

Cognitive impairment (CI) is one of the causes of acquired disability in post-stroke patients. The article presents an analysis of the prevalence, pathogenesis, manifestations, diagnosis, treatment and prevention of post-stroke CI. It is noted that CI can be caused not only by focal vascular brain damage, but also by the presence of concomitant vascular and degenerative lesions in stroke patients. The authors present the results of their own study of CI in 350 patients after stroke within 5 years. The treatment and prevention of CI progression are based on stroke prevention, non-pharmaceutical and pharmaceutical methods for improving cognitive functions. The article discusses data on the use of Cerebrolysin in post-stroke patients, the results of the two latter meta-analyses of Cerebrolysin use.

目的 探讨青年卒中后认知障碍（post-stroke cognitive impairment，PSCI）的危险因素。 方法 连续收集2016年12月-2017年12月在天津市环湖医院神经内科住院的18～45岁的缺血性卒中 患者165例，记录患者人口学资料、血管危险因素、实验室检查资料，所有患者于发病14 d内行蒙特利 尔认知评估量表（Montreal cognitive assessment scale，MoCA）测评，根据MoCA评分

Abstract Many stroke survivors experience persisting episodic memory disturbances. Since hippocampal and para-hippocampal areas are usually spared from the infarcted area, alterations of memory processing networks remote from the ischemic brain region might be responsible for the observed clinical symptoms. To pinpoint changes in activity of hippocampal connections and their role in post-stroke cognitive impairment, we induced ischemic stroke by occlusion of the middle cerebral artery (MCAO) in adult rats and analyzed the functional and structural consequences using activity-dependent manganese (Mn2+) enhanced MRI (MEMRI) along with behavioral and histopathological analysis. MCAO caused stroke lesions of variable extent along with sensorimotor and cognitive deficits. Direct hippocampal injury occurred in some rats, but was no prerequisite for cognitive impairment. In healthy rats, injection of Mn2+ into the entorhinal cortex resulted in distribution of the tracer within the hippocampal subfields into the lateral septal nuclei. In MCAO rats, Mn2+ accumulated in the ipsilateral thalamus. Histopathological analysis revealed secondary thalamic degeneration 28 days after stroke. Our findings provide in vivo evidence that remote sensorimotor stroke modifies the activity of hippocampal-thalamic networks. In addition to potentially reversible alterations in signaling of these connections, structural damage of the thalamus likely reinforces dysfunction of hippocampal-thalamic circuitries.

Prior stroke plays an important role in the development of cognitive impairment (CI), the prevention of which requires detailed study.Patients and methods. A total of 350 patients (mean age, 65±17.7 years; 49% men) who had experienced a stroke with a small degree of neurological deficit were followed up. Cognitive functions were evaluated using the Mini-Mental State Examination (MMSE), Mattis dementia rating scale, the clock drawing test, the test on memorizing 12 words, and the Schulte table. During 5 years of follow-up, 61 (17.4%) patients died, including 45 (12.8%) from recurrent stroke; 89 recurrent strokes developed.Results. The first examination did not reveal CI in 59 (17%) patients; 73 (21%) were found to have marked CI (mild or moderate dementia). After 1, 3, and 5years of follow-up, the proportion of patients with marked CI increased up to 23.2, 29.5, and 34.5%, respectively. Within 5 years, there was an average decline of 2 MMSE scores. The maximum decrease in cognitive functions was seen in patients who had experienced a recurrent stroke, but this also occurred in the absence of a stroke. Cognitive functions were substantially better in a group of patients with blood pressure (BP) normalization.Conclusion. The 5-year follow-up has shown that post-stroke CI gradually progresses, which is associated with the progression of both vascular disease and a concomitant neurodegenerative process. BP normalization during antihypertensive therapy contributes to the prevention of progressive post-stroke CI.

Background: Post-stroke cognitive impairment (PSCI) is common, but evidence of cognitive symptom profiles, course over time, and pathogenesis is scarce. We investigated the significance of time and etiologic stroke subtype for the probability of PSCI, severity, and cognitive profile. Methods: Stroke survivors (n = 617) underwent cognitive assessments of attention, executive function, memory, language, perceptual-motor function, and the Montreal Cognitive Assessment (MoCA) after 3 and/or 18 months. PSCI was classified according to DSM-5 criteria. Stroke severity was assessed with the National Institutes of Health Stroke Scale (NIHSS). Stroke subtype was categorized as intracerebral hemorrhage (ICH), large artery disease (LAD), cardioembolic stroke (CE), small vessel disease (SVD), or un-/other determined strokes (UD). Mixed-effects logistic or linear regression was applied with PSCI, MoCA, and z-scores of the cognitive domains as dependent variables. Independent variables were time as well as stroke subtype, time, and interaction between these. The analyses were adjusted for age, education, and sex. The effects of time and stroke subtype were analyzed by likelihood ratio tests (LR). Results: Mean age was 72 years (SD 12), 42% were females, and mean NIHSS score at admittance was 3.8 (SD 4.8). Probability (95% CI) for PSCI after 3 and 18 months was 0.59 (0.51–0.66) and 0.51 (0.52–0.60), respectively and remained constant over time. Global measures and most cognitive domains were assessed as impaired for the entire stroke population and for most stroke subtypes. Executive function and language improved for the entire stroke population (LR) = 9.05, p = 0.003, and LR = 10.38, p = 0.001, respectively). After dividing the sample according to stroke subtypes, language improved for ICH patients (LR = 18.02, p = 0.003). No significant differences were found in the severity of impairment between stroke subtypes except for attention, which was impaired for LAD and CE in contrast to no impairment for SVD (LR = 56.58, p < 0.001). Conclusions: In this study including mainly minor strokes, PSCI is common for all subtypes, both early and long-term after stroke, while executive function and language improve over time. The findings might contribute to personalizing follow-up and offer new insights into underlying mechanisms. Further research is needed on underlying mechanisms, PSCI prevention and treatment, and relevance for rehabilitation. [ABSTRACT FROM AUTHOR]

• Ischemic brain injury impaired cognitive function at 28 days post-stroke in mice. • Ischemic brain injury triggered AIM2 inflammasome-mediated inflammation within 7 days post-stroke. • Microglia- or endothelial cell-induced AIM2 production mediated PSCI pathogenesis. • AIM2 inflammasome-induced pyroptosis may contribute to acute and chronic neuronal death after stroke. • AIM2 KO and administration of the caspase-1 inhibitor, Ac-YVAD-CMK, attenuated long-term cognitive deficits. Although over one-third of stroke patients may develop post-stroke cognitive impairment (PSCI), the mechanisms underlying PSCI remain unclear. We explored here, the involvement of post-stroke inflammasomes in long-term PSCI development, using a 45 min-middle cerebral artery occlusion (MCAO)/reperfusion-induced PSCI model. Immunohistological assessment on day 1, 3, and 7 was followed by cognitive function test 28 days post-stroke. Evaluation of inflammasome sensor gene expression in aged mouse brains showed dominant expression of absent in melanoma 2 (Aim2) in 6-, 12-, and 18-month-old mouse brains. AIM2 mRNA and protein increased until 7 days post-stroke. PSCI decreased anxiety in elevated plus maze test and impaired spatial learning and memory functions in Morris water maze test 28 days post-stroke. AIM2 and other inflammasome subunit immunoreactivities, including those for caspase-1, interleukin (IL)-1β, and IL-18, were higher in the hippocampus and cortex of the PSCI than in those of the sham group 7 days post-stroke. AIM2 immunoreactivity of the PSCI group was primarily co-localized with Iba-1 (microglial marker) and CD31 (endothelial cell marker) immunoreactivities but not NeuN (neuronal marker) and GFAP (astrocyte marker) immunoreactivities, suggesting that microglia or endothelial cell-induced AIM2 production mediated PSCI pathogenesis. Additionally, inflammasome-induced pyroptosis might contribute to acute and chronic neuronal death after stroke. AIM2 knockout (KO) and Ac-YVAD-CMK-induced caspase-1 inhibition in mice significantly improved cognitive function and reversed brain volume in the hippocampus relative to those in stroke mice. Conclusively, AIM2 inflammasome-mediated inflammation and pyroptosis likely aggravated PSCI; therefore, targeting and controlling AIM2 inflammasome could potentially treat PSCI. [ABSTRACT FROM AUTHOR]

Purpose of Review: In this review, we present the reader with the latest diagnostic and therapeutic approaches in the management of patients with post-stroke cognitive impairment (PSCI). We discuss the most commonly utilized and validated neuropsychological assessments and neuroimaging diagnostic assessment tools. We also provide a critical appraisal of the pharmacological treatment approaches of PSCI, in addition to highlighting the latest emerging non-pharmacological and technological advances in cognitive rehabilitation techniques. Recent Findings: Advanced MRI techniques and newer PET tracers are being utilized heavily in research into cognitive impairment. Non-invasive brain stimulation (NIBS), computer-based cognitive training (CBCT), and virtual reality (VR)–based rehabilitation are playing an increasing role in recent trials of cognitive rehabilitation techniques of PSCI patients. Summary: In approaching patients with PSCI, neuropsychological assessment and neuroimaging should be undertaken to aid in the diagnosis and classification of underlying pathological processes. Aggressive vascular risk factor modification, in addition to the use of cholinesterase inhibitors, is the recommended pharmacological treatment approach in these patients. This should be accompanied by encouraging exercise and prescribing conventional cognitive rehabilitation, while attempting to incorporate newer technological treatment modalities such as NIBS, CBCT, and VR. We identified a significant need for future research into treatment modalities aimed at PSCI and vascular dementia (VaD). [ABSTRACT FROM AUTHOR]

This pilot study designed to evaluate the efficacy and safety of MAO-B inhibitor in comparison with Donepezil (DNP) in elderly Chinese patients with Alzheimer disease (AD). In the present clinical trial, Chinese elderly patients aged ≥65 years with a confirmed diagnosis of AD were enrolled. The patients received MAO-B inhibitor (Selegiline 5 mg) or DNP 10 mg daily (reference) for 6 months. The efficacy and safety data were collected from 120 patients (60 patients in each group) every 3 weeks until 6 months. The primary endpoints were to assess the change in cognitive score from baseline in both the treatment group. The result of the present study showed that the patients treated with MAO-B inhibitor and DNP have similar efficacy and safety profile Considering the clinical benefit, mean (SD) improvement in sign and symptoms was numerically greater in DNP-treated patients as compared to MAO-B inhibitor at endpoint visit (SIB: 12.3 (3.7) vs 11.3 (4.2); AD severity: 14.2 (3.5); CIBIS+/CIBIC: 10.2 (2.7) vs 9.4 (3.2); ADCSADL: 14.3 (4.2) vs 13.2 (3.4); MMSE: 14.3 (3.7) vs 12.2 (3.2), P>0.05 respectively for each comparison). However, a statistical difference in terms of clinical benefit was similar between both the treatment groups (p>0.05). Overall, both the study drugs were found comparable in relieving the symptoms of AD (severity score after end of treatment: 14.2 vs 13.4 respectively; p >0.05). This indicates that MAO-B inhibitor is a potential target for the treatment of AD in China. The results of the present study may help to design a large clinical trial to evaluate the efficacy and safety of MAO-B inhibitor in comparison with DNP in AD patients. [ABSTRACT FROM AUTHOR]

Introduction: Unfortunately, over 40% of stroke victims have pre-existing diabetes which not only increases their risk of stroke up to 2-6 fold, but also worsens both functional recovery and the severity of cognitive impairment. Our lab has recently linked the chronic inflammation in diabetes to poor functional outcomes and exacerbated cognitive impairment, also known as post-stroke cognitive impairment (PSCI). Although we have shown that the development of PSCI in diabetes is associated with the upregulation and the activation of pro-inflammatory microglia, we have not established direct causation between the two. To this end, we evaluated the role of microglia in the development of PSCI.Methods: At 13 weeks of age, diabetic animals received bilateral intracerebroventricular (ICV) injections of short hairpin RNA (shRNA) lentiviral particles targeting the colony stimulating factor 1 receptor (CSF1R). After 14 days, animals were subjected to 60 min middle cerebral artery occlusion (MCAO) or sham surgery. Adhesive removal task (ART), novel object recognition (NOR), and 2-trial Y-maze were utilized to evaluate sensorimotor and cognitive function. Tissue from freshly harvested brains was analyzed by flow cytometry and immunohistochemistry.Results: CSF1R silencing resulted in a 94% knockdown of residential microglia to relieve inflammation and improve myelination of white matter in the brain. This prevented cognitive decline in diabetic animals.Conclusion: Microglial activation after stroke in diabetes may be causally related to the development of delayed neurodegeneration and PSCI. [ABSTRACT FROM AUTHOR]

Introduction: Stroke is one of the leading causes of morbidity and mortality and the second most common cause of cognitive impairment. Objectives: Therefore, this study is aimed at determining the prevalence and pattern of Post-Stroke Cognitive Impairment (PSCI) in Kano, Nigeria. Methods: A total number of 102 stroke survivors were contacted for the study but only seventy (70) of them participated and completed the study. Fifteen (15) patients declined to consent and 17 were excluded due to severe depression evaluated using the Beck Depression Inventory (BDI). The participants were assessed for levels of cognitive function and motor recovery using the MMSE and BRS scales, respectively Results: The results of this study showed that the overall prevalence of PSCI was 67.14% with mild PSCI accounting for 32.86% of cases, while moderate and severe for 27.14% and 7.14%, respectively. Most participants (71.43%) were at the chronic stage of stroke, while in terms of motor recovery, the majority of strokes survivors were at the Brunnstrom Recovery Stage (BRS) 3 (30%) and only 10% were at the final stage of recovery (BRS 6) Conclusion: Post-stroke cognitive impairment is high in Kano, especially among older stroke survivors with a low level of education and socio-economic status. It is very important to assess PSCI in the clinics to prevent subsequent complications. Future studies should evaluate other stroke outcomes, such as Activities of Daily Living (ADL), community participation and Quality of Life (QoL) as they are related to cognitive function. [ABSTRACT FROM AUTHOR]

Background and Aims: Post-stroke cognitive impairment (PSCI) is a clinical condition arising from stroke and causes significant changes to memory, thinking, and behavior. Trimethylamine-N-oxide (TMAO), the metabolite produced by gut microbiota, has mechanistic relevance to atherosclerotic diseases. This study aimed to investigate whether an association existed between elevated plasma TMAO levels and PSCI.Methods: Consecutive patients with acute ischemic stroke were prospectively enrolled during Jan. 2017 to Dec. 2017. TMAO concentration was measured within 24 h after admission. PSCI was assessed using the Mini-Mental State Examination (MMSE) score after 1 year and defined as MMSE score ≤ 26. Binary logistic regression analysis was used to determine the contribution of TMAO level in the prediction of PSCI.Results: Of the 256 patients studied (age, 67.1 ± 11.0 years; male, 54.3%), 86 (33.6%) patients were diagnosed as PSCI. The mean TMAO level was 5.6 ± 2.4 μM, with quartile level as follows: < 3.9 μM (first quartile), 3.9-5.1 μM (second quartile), 5.2-7.4 μM (third quartile), and > 7.4 μM (fourth quartile). After controlling for potential confounders, multivariable logistic analysis showed that higher level of plasma TMAO was an independent predictor for cognitive impairment in post-stroke patients (the quartile 1 was used as reference, the quartile 4 odds ratio, 3.304; 95% confidence intervals, 1.335-8.178; P = 0.010).Conclusions: This study demonstrated that increasing plasma level of TMAO may be associated with PSCI. [ABSTRACT FROM AUTHOR]

Copyright of Mezdunarodnyj Nevrologiceskij Zurnal is the property of Zaslavsky O.Yu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Post-stroke cognitive impairment (PSCI) is a common complication of stroke. Intermittent theta burst stimulation (iTBS) can inducing motor learning. We observed the effects of combination of iTBS with cognitive training on physical/cognitive dysfunctions in PSCI patients. PSCI patients treated with basic treatment & cognitive training (Control group)/iTBS & cognitive training (iTBS group) were enrolled, with Mini-mental State Examination (MMSE)/Montreal Cognitive Assessment (MoCA)/Frontal Assessment Battery (FAB)/barthel index (BI)/Upper Limb Fugl-Meyer Assessment (U-FMA)/Action Research Arm Test (ARAT) scores compared. Gait spatiotemporal parameters/dynamic parameters were analyzed by 3D gait analysis. Correlations between MMSE/MoCA scores and gait parameters in PSCI patients after iTBS & cognitive training were analyzed by Spearman analysis. Increased MMSE/MoCA/FAB/BI/U-FMA/ARAT scores, step speed, step frequency, stride length, step width, step length on the affected side, percentage of swing phase on the affected side, hip joint flexion angle on the affected side, knee joint flexion angle on the affected side, and ankle plantar flexion angle on the affected side and reduced gait period on the affected side and percentage of stance phase on the affected side were found in patients of both groups after treatment, with the effects in the iTBS group more profound. iTBS & cognitive training obviously improved the cognitive function scores/upper limb function scores/gait parameters in PSCI patients versus cognitive training treatment. After combination therapy, the MMSE/MoCA scores of PSCI patients were significantly correlated with gait parameters. This provided more data support for iTBS & cognitive training application in the rehabilitation treatment of PSCI patients. • iTBS&cognitive training improves MMSE, MoCA, FAB and BI scores in PSCI patients. • iTBS&cognitive training improves U-FMA and ARAT scores in PSCI patients. • iTBS&cognitive training improves gait spatiotemporal parameters in PSCI patients. • iTBS&cognitive training improves dynamic parameters on the affected side in PSCI. • MMSE/MoCA correlate with gait parameters after iTBS&cognitive training in PSCI. [ABSTRACT FROM AUTHOR]

• AU attenuates ischemic injury and inhibits the neuro-inflammatory response in MCAO mice. • AU downregulates the NF-κB and MAPK signaling pathways in ischemia–reperfusion injury. • AU alleviates post-stroke cognitive impairment and restores white matter integrity in MCAO mice. To study the role of Aucubin (AU) in cerebral ischemia–reperfusion injury and investigate the potential mechanisms. For the in vitro experiment, primary microglia were cultured and stimulated by Lipopolysaccharides (LPS) and treated with AU. Male C57/BL6J mice were used and middle cerebral artery occlusion (MCAO) model was performed to induce cerebral ischemia–reperfusion injury. For the short-term effects, mice administrated with AU (40 mg/kg) for 3 days after MCAO were evaluated for the infarct volume and neurological deficits. The neuroinflammatory factors and microglia activation were determined by Real-time PCR, western blot and immunofluorescence staining. For the long-term effects, MCAO mice were injected daily with AU (5 mg/kg or 10 mg/kg) for 28 days. Behavior tests were used to assess the neurological deficits of MCAO mice, and white matter integrity was determined by myelin basic protein (MBP) staining and black-gold staining. AU suppressed LPS‐induced activation of microglia and pro‐inflammatory cytokines release, and downregulated the NF‐κB and MAPK pathways in primary microglia. In addition, AU attenuated ischemic injury and inhibited the neuro-inflammatory response in MCAO mice. Moreover, AU induced prolonged improvements in sensorimotor function and memory function following MCAO, and preserved white matter integrity in the long-term experiments. AU protected against ischemic injury, which might be correlated with the downregulation of NF‐κB and MAPK signaling pathways. Furthermore, AU alleviated cognitive impairment after stroke and restored white matter integrity. Our data indicated that AU might be a potential compound for the treatment of stroke and post-stroke cognitive impairment. [ABSTRACT FROM AUTHOR]

To investigate the occurrence of post-stroke cognitive impairment (PSCI) and its influencing factors in convalescent young patients with first-ever stroke. A total of 300 first-ever young stroke patients (age ≤45 years) were collected. The Mini-Mental State Examination (MMSE) was used to assess the cognitive status. The sociodemographic data, clinical symptoms, social environment, and behavior-related information were collected and analyzed. The incidence of PSCI in young stroke patients was 62.33 %. Through univariate analysis, there were statistical differences in different levels of education, smoking status and hypertension (P < 0.05). With subsequently multivariate logistic regression analysis, it was found that junior high school (OR=8.58,95 %CI:2.25∼32.70) and high school (OR=10.50,95 %CI:2.69∼41.00) education levels, lesion volume >3.00 cm3 (OR=8.03,95 %CI:2.28∼28.36), stroke in the frontal-parietal-temporal region (OR=7.26,95 %CI:1.58∼33.40) and the basal ganglia area (OR=6.13,95 %CI:1.24∼30.43), high NIHSS score (OR=1.17,95 %CI: 1.06∼1.29), and high diastolic blood pressure variability coefficient (OR=1.43,95 %CI: 1.02∼2.01) were risk factors for PSCI. Meanwhile, 24≤BMI<28 (OR=0.06,95 %CI:0.02∼0.23) and BMI<24 (OR=0.18,95 %CI:0.06∼0.53), hospitalization cost >20,000/month (OR=0.22,95 %CI:0.09∼0.56), and stroke onset in spring and summer (OR=0.37,95 %CI:0.14∼0.96) were protective factors. The incidence of PSCI is relatively high in young stroke patients. Junior high and high school education, stroke lesions >3.00cm3, strokes in the frontal-parietal-temporal and basal ganglia regions, high NIHSS scores, and high DBPV are risk factors for PSCI in young stroke patients. Meanwhile, BMI<28, treatment cost >20,000/month, and stroke onset in spring and summer are protective factors for PSCI in young stroke patients. [ABSTRACT FROM AUTHOR]

• Many patients with ischemic stroke suffer from cognitive impairment which affects the quality of life. • No biomarkers have been widely recommended for identifying post-stoke cognitive impairment (PSCI) early. • The correlation between insulin resistance and PSCI remains unclear. • The triglyceride-glucose (TyG) index may be an easily available biomarker for identifying PSCI early. • This is the first study evaluating the predictive value of TyG for PSCI. Post-stroke cognitive impairment (PSCI) is a very common complication of ischemic stroke (IS). Triglyceride-glucose (TyG) index was an effective alternative marker of insulin resistance (IR). This prospective study was designed to explore the correlation between TyG index and PSCI. Between January 1 2021 to June 30 2022, consecutive patients with first onset IS were enrolled prospectively. Baseline information was collected at admission and fasting blood was drawn the next morning. Montreal Cognitive Assessment (MoCA) was used to evaluate cognitive function at three months after stroke. Multiple regression analysis was used to explore the correlation between PSCI and TyG. Receiver operating characteristic (ROC) was performed to evaluate the predictive ability. Ultimately, 313 patients were enrolled in this study. The TyG index was higher in patients with PSCI than those without PSCI (8.99 (8.55, 9.54) vs. 8.61(8.25, 8.87), P <0.001). The spearman correlation analysis indicated that TyG index was negatively correlated with MoCA score (r=-0.272, P< 0.001). The multivariate logistic regression analysis demonstrated that TyG index was correlated with PSCI independently (P< 0.001) regardless of whether the patients had diabetes or not. The area under curve (AUC) of the ROC was 0.684 (95%CI=0.635-0.768, P <0.001). The optimal cutoff value of TyG index for predicting PSCI was 8.81, with a sensitivity of 61.7% and a specificity of 73.6%. A higher TyG index level at admission was independently correlated with increased risk of PSCI three months later and could be used as a predictor. [ABSTRACT FROM AUTHOR]

After stroke, dynamic changes take place from necrotic-apoptotic continuum, inflammatory response to poststroke neurogenesis, and remodeling of the network. These changes and baseline brain pathology such as small vessel disease (SVD) and amyloid burden may be associated with the occurrence of early or late poststroke cognitive impairment (PSCI) or dementia (PSD), which affect not only stroke victims but also their families and even society. We reviewed the current concepts and understanding of the pathophysiology for PSCI/PSD and identified useful tools for the diagnosis and the prediction of PSCI in serological, CSF, and image characteristics. Then, we untangled their relationships with blood pressure (BP) and blood pressure variability (BPV), important but often overlooked risk factors for PSCI/PSD. Finally, we provided evidence for the modifying effects of BP and BPV on PSCI as well as pharmacological and non-pharmacological interventions and life style modification for PSCI/PSD prevention and treatment.

Objective: to evaluate the efficiency of using computer stimulation programs (CSPs) for acute ischemic stroke (IS) in patients with cognitive impairment (CI).Patients and methods. 81 patients aged 40 to 79 years with post-stroke CI (PSCI) were examined and randomized into two groups. A study group consisted of 45 people, including 31 and 14 patients with predementia CI and mild dementia, respectively; their median age was 61 [55; 68] years. A comparison group included 36 patients, including 21 and 15 patients with predementia CI and mild dementia; their median age was 64 [57; 70] years. In addition to standard stroke therapy, the study group received a ten-day correction cycle for CI, by using CSPs.Cognitive functions (CF) were evaluated before and after classes, by applying a short mental status questionnaire (SMSQ), a battery of frontal lobe dysfunction tests (BFLDT), a clock drawing test, and a speech activity test.Results. After 10 days of therapy (at 18–20 days of IS), the patients were observed to have statistically significant improvements of cognitive functions in all major neuropsychological scales: SMSQ, BFLDT, a clock drawing test, and a speech activity test (p>0.05).Assessing the total indicators of SMSQ subtests in both groups showed that the study group achieved statistically significant differences in memory, time and place orientation, and concentration. In the study group, the total values of BFTLD subtests were also statistically better in indicators, such as speech fluency (by 33.0%), dynamic praxis (by 23.3%), a simple choice reaction (by 30.0%), and a complicated choice reaction (by 26.7%). At the same time, not only trained functions (attention, memory), but also other cognitive indicators improved. Re-examination demonstrated that the achieved results persisted 6-8 months later.Conclusion. CSPs are a promising area of neurorehabilitation. The method is effective, easy-to-use; the patients can do lessons at hospital and at home after discharge in the presence of relatives or themselves. Further investigations will be able to evaluate the effectiveness of CSPs in patients with PSCI in the later periods of IS.

Abstract Background Vascular cognitive impairment (VCI) is a complex spectrum encompassing post-stroke cognitive impairment (PSCI) and small vessel disease-related cognitive impairment. Despite the growing health, social, and economic burden of VCI, to date, no specific treatment is available, prompting the introduction of the concept of a disease modifier. Consensus and suggestions Within this clinical spectrum, VCI and PSCI remain advancing conditions as neurodegenerative diseases with progression of both vascular and degenerative lesions accounting for cognitive decline. Disease-modifying strategies should integrate both pharmacological and non-pharmacological multimodal approaches, with pleiotropic effects targeting (1) endothelial and brain–blood barrier dysfunction; (2) neuronal death and axonal loss; (3) cerebral plasticity and compensatory mechanisms; and (4) degenerative-related protein misfolding. Moreover, pharmacological and non-pharmacological treatment in PSCI or VCI requires valid study designs clearly stating the definition of basic methodological issues, such as the instruments that should be used to measure eventual changes, the biomarker-based stratification of participants to be investigated, and statistical tests, as well as the inclusion and exclusion criteria that should be applied. Conclusion A consensus emerged to propose the development of a disease-modifying strategy in VCI and PSCI based on pleiotropic pharmacological and non-pharmacological approaches.

Abstract Introduction Studies have shown that high levels of the fibrinogen (FIB) are related to cognitive deficits. However, the relationship between fibrinogen and cognitive deficit after stroke remains unclear. Therefore, we explored the relationship between plasma fibrinogen and post‐stroke cognitive impairment (PSCI). Methods This study is carried out in the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China. A total of 210 patients with acute ischemic stroke were enrolled in this study. Ultimately, 134 patients completed 3‐month follow‐up. Blood samples were collected at hospital admission. Cognitive function was evaluated 3 months after stroke. All patients underwent the Mini‐Mental State Examination (MMSE) after 3 months. Results Higher levels of fibrinogen were observed in patients with post‐stroke cognitive impairment compared with the non‐PSCI group (p

Objectives: Post-stroke cognitive impairment (PSCI) is a common disease that may occur within 3 months after a stroke or even later. However, the mechanism of PSCI development is unclear. The present study investigated whether the levels of plasma amyloid beta-42 (Aβ42) and tau are associated with the onset of PSCI.Methods: Fifty-five patients admitted within 7 days of acute ischemic stroke were enrolled and followed up for 1 year. Montreal Cognitive Assessment (MoCA) was administered at 3 months and 1 year, and plasma Aβ42 and tau levels were determined using an ultrasensitive immunoassay (immunomagnetic reduction) within 7 days of the stroke event and 3 months later.Results: In this study, 13 of 55 patients developed PSCI (MoCA score

Competing Interests: No conflicts of interest.

In recent years, increasing evidence suggests that commensal microbiota may play an important role not only in health but also in disease including cerebrovascular disease. Gut microbes impact physiology, at least in part, by metabolizing dietary factors and host-derived substrates and then generating active compounds including toxins. The purpose of this current review is to highlight the complex interplay between microbiota, their metabolites. and essential functions for human health, ranging from regulation of the metabolism and the immune system to modulation of brain development and function. We discuss the role of gut dysbiosis in cerebrovascular disease, specifically in acute and chronic stroke phases, and the possible implication of intestinal microbiota in post-stroke cognitive impairment and dementia, and we identify potential therapeutic opportunities of targeting microbiota in this context. LINKED ARTICLES: This article is part of a themed issue From Alzheimer's Disease to Vascular Dementia: Different Roads Leading to Cognitive Decline. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc., (© 2023 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.)

Post-stroke depression (PSD) and post-stroke cognitive impairment (PSCI) are common complications following a stroke, significantly impacting the quality of life and survival time of survivors. Currently, the comorbidity of PSCI and PSD is receiving increasing attention, as they share some common clinical characteristics, mechanisms, risk factors, radiological features, and treatment strategies. They influence each other, with the clinical prevalence of PSD comorbid with PSCI reaching as high as 26.15 %. The prevention, screening, diagnosis, and treatment of PSD and PSCI require collaboration across clinical, radiological, and neuropsychological evaluations. This paper aims to summarize the common radiological features of both conditions from a radiological perspective, which may aid in identifying early screening and predictive imaging biomarkers., (© 2024 Walter de Gruyter GmbH, Berlin/Boston.)

Background: Psycho-cognitive consequences are a frequent cause of disability in stroke survivors but are often underdiagnosed also because of lack of services dedicated to these aspects. We started assessing systematically cognitive and behavioral functions in acute stroke patients and to follow them up. Here, we report a retrospective analysis of the organization of the Sacco VAS-COG stroke care pathway and the refinements implemented during 5 years of activity., Methods: The protocol includes baseline collection of clinical history, general and neurologic examinations, functional, neuropsychological, and neuroimaging assessment. At follow-up, a diagnosis of cognitive decline was made based on best clinical judgment in the first period (January 2018 to May 2019, namely VAS-COG protocol 1.0) and then based on an extensive neuropsychological battery (May 2019 to January 2023, namely VASCOG protocol 2.0); psychiatric and behavioral disturbances are investigated through suitable scales., Results: From January 2018 to December 2022, 834 patients (mean age 76±13.6 years; 46.6 % females) with acute cerebrovascular events were admitted to the stroke unit, mostly (80 %) for ischemic strokes. Pre-event cognitive impairment was not assessable in 78 patients (9.3 %) because no reliable informant was present and was reported in 327/756 (43 %) patients. During follow-up, post-stroke cognitive impairment was detected in 124/217 (57.1 %) patients in VAS-COG protocol 1.0 and in 137/201(68.2 %) patients in VAS-COG protocol 2.0, while 95/218 (43.2 %) patients were found to be depressed and patients presented on average 2.5 neuropsychiatric symptoms on Neuropsychiatric Inventory-questionnaire., Conclusions: The VAS-COG stroke care pathway represents a model for patients and for their families., Competing Interests: LP is member of the editorial boards of Neurology, Cerebrovascular Diseases, European Stroke Journal, Cerebral Circulation—Cognition and Behaviour and associate editor of Neurological Sciences., (© 2024 The Author(s).)

Neuroinflammation after intracerebral hemorrhage (ICH) is a crucial factor that determines the extent of the injury. Cofilin is a cytoskeleton-associated protein that drives neuroinflammation and microglia activation. A novel cofilin inhibitor (CI) synthesized and developed in our lab has turned out to be a potential therapeutic agent for targeting cofilin-mediated neuroinflammation in an in vitro model of ICH and traumatic brain injury. The current study aims to examine the therapeutic potential of CI in a mouse collagenase model of ICH and examine the neurobehavioral outcomes and its mechanism of action. Male mice were subjected to intrastriatal collagenase injection to induce ICH, and sham mice received needle insertion. Various concentrations (25, 50, and 100 mg/kg) of CI were administered to different cohorts of the animals as a single intravenous injection 3 h following ICH and intraperitoneally every 12 h for 3 days. The animals were tested for neurobehavioral parameters for up to 7 days and sacrificed to collect brains for hematoma volume measurement, Western blotting, and immunohistochemistry. Blood was collected for cofilin, TNF-α, and IL-1β assessments. The results indicated that 50 mg/kg CI improved neurological outcomes, reversed post-stroke cognitive impairment, accelerated hematoma resolution, mitigated cofilin rods/aggregates, and reduced microglial and astrocyte activation in mice with ICH. Microglia morphological analysis demonstrated that CI restored the homeostasis ramification pattern of microglia in mice treated with CI. CI suppressed endoplasmic reticulum stress-related neuroinflammation by inhibiting inflammasomes and cell death signaling pathways. We also showed that CI prevented synaptic loss by reviving the pre- and post-synaptic markers. Our results unveil a novel therapeutic approach to treating ICH and open a window for using CI in clinical practice.

Background: Post-stroke cognitive impairment (PSCI) is a prevalent complication among stroke survivors. It not only directly impacts patients' cognitive abilities but also hampers their capacity to regain independence in daily activities, consequently diminishing their quality of life. Among the various cognitive deficits following stroke, impaired attention is the most frequently observed, influencing not only daily functioning but also higher cognitive functions like working memory, executive functioning, and language.Emerging evidence indicates that Baduanjin, a traditional Chinese exercise, may have a positive impact on enhancing attention in older adults with mild cognitive impairment and stroke survivors. However, the precise mechanisms behind this effect remain unclear. In this study, we employed Baduanjin training as an intervention to address attention decline in post-stroke cognitive impairment patients and to delve into the potential mechanisms through which Baduanjin training may enhance attention in individuals with PSCI., Methods: In this prospective randomized controlled trial, we plan to recruit 72 participants diagnosed with post-stroke cognitive impairment (PSCI). These participants will be randomly assigned in a 1:1:1 ratio to one of three groups: Baduanjin training(left hemisphere stroke and right hemisphere stroke) and conventional treatment.The conventional treatment group will receive standard rehabilitation sessions. In addition to conventional treatment, participants in the octogenarian training groups will undergo octogenarian training sessions lasting 40 min, five times a week, over a total period of 12 weeks.The primary outcome measures will include the Montreal Cognitive Assessment (MoCA) scale and the Attentional Lateralization Index. These assessments will be conducted by a trained evaluator before the start of the intervention and at weeks 6 and 12 after the intervention begins.Secondary outcome measures will be assessed using the baseline Mandarin version of the Oxford Cognitive Screening (OCS-P) scale, the simplified Fugl-Meyer Motor Function Assessment (FMA) scale, the Pittsburgh Rehabilitation Participation (PRPS) scale, and the Activities of Daily Living (ADL) scale before and after the intervention, respectively., Discussion: This trial aims to examine the impact of Baduanjin training on attentional lateralization among patients with post-stroke cognitive impairment (PSCI). Functional brain imaging utilizing near-infrared spectroscopy will be employed to investigate how Baduanjin exercise influences the structural and functional connectivity of distinct brain regions or brain networks., Trial Registration: Chictr.org.cn, ID: ChiCTR2300076533 . Registered on 11 October 2023., (© 2024. The Author(s).)

Background: Post-stroke neurocognitive disorder, though common, is often overlooked by clinicians. Moreover, although the Montreal Cognitive Assessment (MoCA) has proven to be a valid screening test for neurocognitive disorder, even more time saving tests would be preferred. In our study, we aimed to determine the diagnostic accuracy of the Clock Drawing Test (CDT) for post-stroke neurocognitive disorder and the association between the CDT and MoCA., Methods: This study is part of the Norwegian Cognitive Impairment After Stroke study, a multicentre prospective cohort study following patients admitted with acute stroke. At the three-month follow-up, patients were classified with normal cognition, mild neurocognitive disorder, or major neurocognitive disorder according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition criteria. Any neurocognitive disorder compromised both mild- and major neurocognitive disorder. The CDT at the three-month assessment was given scores ranging from 0 to 5. Patients able to complete the CDT and whose cognitive status could be classified were included in analyses. The CDT diagnostic accuracy for post-stroke neurocognitive disorder was identified using receiver operating characteristic curves, sensitivity, specificity, positive predictive value, and negative predictive value. The association between the MoCA and CDT was analysed with Spearman's rho., Results: Of 554 participants, 238 (43.0%) were women. Mean (SD) age was 71.5 (11.8) years, while mean (SD) National Institutes of Health Stroke Scale score was 2.6 (3.7). The area under the receiver operating characteristic curve of the CDT for major neurocognitive disorder and any neurocognitive disorder was 0.73 (95% CI, 0.68-0.79) and 0.68 (95% CI, 0.63-0.72), respectively. A CDT cutoff of < 5 yielded 68% sensitivity and 60% specificity for any neurocognitive disorder and 78% sensitivity and 53% specificity for major neurocognitive disorder. Spearman's correlation coefficient between scores on the MoCA and CDT was 0.50 (95% CI, 0.44-0.57, p < .001)., Conclusions: The CDT is not accurate enough to diagnose post-stroke neurocognitive disorder but shows acceptable accuracy in identifying major neurocognitive disorder. Performance on the CDT was associated with performance on MoCA; however, the CDT is inferior to MoCA in identifying post-stroke neurocognitive disorder., Trial Registration: ClinicalTrials.gov (NCT02650531). Retrospectively registered January 8, 2016., (© 2024. The Author(s).)

A domain-specific perspective to cognitive functioning in stroke patients may predict their cognitive recovery over time and target stroke rehabilitation intervention. However, data about domain-specific cognitive impairment after stroke are still scarce. This study prospectively investigated the domain-specific pattern of cognitive impairments, using the classification proposed by the Montreal Cognitive Assessment (MoCA), in a cohort of 49 stroke patients at admission (T0), discharge (T1), and six-month follow-up (T2) from subacute intensive rehabilitation. The predictive value of T0 cognitive domains cognitive impairment at T1 and T2 was also investigated. Patients' cognitive functioning at T0, T1, and T2 was assessed through the MoCA domains for executive functioning, attention, language, visuospatial, orientation, and memory. Different evolutionary trends of cognitive domain impairments emerged across time-points. Patients' impairments in all domains decreased from T0 to T1. Attention and executive impairments decreased from T0 to T2 (42.9% and 26.5% to 10.2% and 18.4%, respectively). Conversely, altered visuospatial, language, and orientation increased between T1 and T2 (16.3%, 36.7%, and 40.8%, respectively). Additionally, patients' global cognitive functioning at T1 was predicted by the language and executive domains in a subacute phase ( p = 0.031 and p = 0.001, respectively), while in the long term, only attention ( p = 0.043) and executive ( p = 0.019) domains intervened. Overall, these results confirm the importance of a domain-specific approach to target cognitive recovery across time in stroke patients.

Background: Post-diagnostic care for people with vascular cognitive impairment (VCI) typically involves multiple professions and disjointed care pathways not specifically designed to aid VCI needs., Objective: Exploring perspectives of healthcare professionals on post-diagnostic care for people with VCI., Methods: We conducted a qualitative focus group study. We used purposive sampling to include healthcare professionals in different compositions of primary and secondary care professionals per focus group. Thematic saturation was reached after seven focus groups. Transcripts were iteratively coded and analyzed using inductive thematic analysis., Results: Forty participants were included in seven focus groups (4-8 participants). Results showed knowledge and awareness of VCI as prerequisites for adequate post-diagnostic care, and for pre-diagnostic detection of people with VCI (theme 1). In light of perceived lack of differentiation between cognitive disorders, participants shared specific advice regarding post-diagnostic care for people with VCI and informal caregivers (theme 2). Participants thought current care for VCI was fragmented and recommended further integration of care and collaboration across settings (theme 3)., Conclusions: People with VCI and their caregivers risk getting stuck in a "no man's land" between post-diagnostic care pathways; challenges lie in acknowledgement of VCI and associated symptoms, and alignment between healthcare professionals. Education about the symptoms and consequences of VCI, to healthcare professionals, people with VCI and caregivers, may increase awareness of VCI and thereby better target care. Specific attention for symptoms common in VCI could further tailor care and reduce caregiver burden. Integration could be enhanced by combining expertise of dementia and stroke/rehabilitation pathways.

Introduction: Stroke is common cerebrovascular disease in the elderly, which is characterized by neurological defects caused by cerebral vessels. Multiple studies have shown that miRNAs play important roles in stroke. In addition, a large number of evidence suggest that stroke increases the risk and severity of cognitive impairments., Methods: miR-511-3p expression levels were detected by real-time PCR. Receiver operating characteristic (ROC) curve analysis was used to evaluate the diagnostic value of miR-511-3p in distinguishing stroke patients from healthy controls and to assess risk of post-stroke cognitive impairment (PSCI) in stroke patients. Pearson correlation coefficient was used to determine the relationship between miR-511-3p expression level and Montreal Cognitive Assessment Scale (MoCA) scores., Results: Serum miR-511-3p expression levels were decreased in stroke patients, and the decrease was more significant in PSCI patients. ROC curve results showed that miR-511-3p had high diagnostic accuracy in distinguishing healthy controls from stroke patients. Moreover, the expression level of miR-511-3p can be used as an independent predictor for the occurrence of PSCI and is positively correlated with MoCA scores of PSCI patients., Conclusion: miR-511-3p may be involved in the occurrence and development of stroke. In addition, miR-511-3p may be a novel biomarker for predicting PSCI occurred in stroke patients. These results may help improve the quality of prognosis of stroke., (© 2023 S. Karger AG, Basel.)

The gut microbiome interacts with the brain bidirectionally through the microbiome-gutbrain axis, which plays a key role in regulating various nervous system pathophysiological processes. Trimethylamine N-oxide (TMAO) is produced by choline metabolism through intestinal microorganisms, which can cross the blood-brain barrier to act on the central nervous system. Previous studies have shown that elevated plasma TMAO concentrations increase the risk of major adverse cardiovascular events, but there are few studies on TMAO in cerebrovascular disease and vascular cognitive impairment. This review summarized a decade of research on the impact of TMAO on stroke and related cognitive impairment, with particular attention to the effects on vascular cognitive disorders. We demonstrated that TMAO has a marked impact on the occurrence, development, and prognosis of stroke by regulating cholesterol metabolism, foam cell formation, platelet hyperresponsiveness and thrombosis, and promoting inflammation and oxidative stress. TMAO can also influence the cognitive impairment caused by Alzheimer's disease and Parkinson's disease via inducing abnormal aggregation of key proteins, affecting inflammation and thrombosis. However, although clinical studies have confirmed the association between the microbiome-gut-brain axis and vascular cognitive impairment (cerebral small vessel disease and post-stroke cognitive impairment), the molecular mechanism of TMAO has not been clarified, and TMAO precursors seem to play the opposite role in the process of poststroke cognitive impairment. In addition, several studies have also reported the possible neuroprotective effects of TMAO. Existing therapies for these diseases targeted to regulate intestinal flora and its metabolites have shown good efficacy. TMAO is probably a new target for early prediction and treatment of stroke and vascular cognitive impairment., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Post-stroke depression and cognitive impairment are common conditions affecting patients after stroke. Serotonin is a neurotransmitter involved in modulating, among others, mood, cognition, learning, and memory. Sub-optimal serotonin activity may be in part responsible for cognitive deficits seen in depression. In this pilot study serotonin levels were evaluated in 29 patients with sub-acute stroke before and after a rehabilitation treatment (consisting of a program of upper limb robotic rehabilitation in addition to conventional physical therapy treatment). We employed the Back Depression Inventory scale to evaluate symptoms of depression, and specific tools to evaluate cognitive functions. We found a significant reduction of the serotonin levels after rehabilitation in the whole group (T0: 85.9 ± 92.4 ng/mL; T1: 61.9 ± 58.4 ng/mL; p = 0.0018), as well as in the subgroup of patients untreated with Selective Serotonin Reuptake Inhibitors (SRRI), (mean serotonin at T0: 154.0 ± 102.3 ng/mL; mean serotonin at T1: 92.9. ± 68.7 ng/mL at T1; p = 0.005). We also found a correlation with cognitive assessment: in particular, the change from baseline of the serotonin (ΔSerotonin) was correlated with the changes from baseline of the Rey’s Figure (ΔROCF) (r = 0.535; p < 0.05), the Tower of London (ΔToL) (subscore point: r = 0.621; p < 0.005; subscore time: r = −0.619; p < 0.005) meaning that a serotonin levels decrease is associated with a worsening of cognitive functions. Considering patients treated and untreated with SSRIs separately, in patients treated with SSRIs (n = 16) we found only a positive correlation between ∆Serotonin and ∆ToL (subscore point: r= 0.587; p = 0.045), whereas in patients untreated with SSRIs (n = 13) we found a positive correlations between ΔSerotonin and ΔROCF (r = 0.700; p = 0.036), ∆Stroop (subscore time: r = 0.750; p = 0.020) and ∆Tol (subscore point: r = 0.740; p = 0.023) and a negative correlation between ΔSerotonin and ∆Tol (subscore time: r= −0.833; p = 0.005). These results suggest that variation of serotonin levels should be monitored in patients during a rehabilitation program, not only for their relationship with depression symptoms, but also for the correlation with cognitive performance.

Objectives: Post-stroke cognitive impairment (PSCI) is a common disease that may occur within 3 months after a stroke or even later. However, the mechanism of PSCI development is unclear. The present study investigated whether the levels of plasma amyloid beta-42 (Aβ42) and tau are associated with the onset of PSCI. Methods: Fifty-five patients admitted within 7 days of acute ischemic stroke were enrolled and followed up for 1 year. Montreal Cognitive Assessment (MoCA) was administered at 3 months and 1 year, and plasma Aβ42 and tau levels were determined using an ultrasensitive immunoassay (immunomagnetic reduction) within 7 days of the stroke event and 3 months later. Results: In this study, 13 of 55 patients developed PSCI (MoCA score <23) at 3 months. Seven patients with PSCI at 3 months recovered to a cognitively normal state at 1 year, whereas seven cognitively normal patients developed PSCI at 1 year. The patients with PSCI at 1 year had a higher incidence of cognitive function deterioration between 3 months and 1 year compared with those without PSCI at 1 year. Plasma Aβ42 and tau levels at 3 months were lower in the patients with PSCI at 1 year than in those without PSCI (Aβ42: 15.1 vs. 17.2 pg/mL, P = 0.013; tau: 16.7 vs. 19.9 pg/mL, P = 0.018). Low education levels and pre-existing white matter disease were the most significant predictors of PSCI at 3 months, and poor cognitive performance at 3 months and low plasma Aβ42 and tau levels at 3 months were the most significant predictors of PSCI at 1 year. Conclusion: The pathogenesis of PSCI is complex and changes with time. Ischemia-induced Aβ42/tau pathology might be involved in PSCI development. [ABSTRACT FROM AUTHOR]

Highlights • C21 reduced weight loss and enhanced recovery in aged rats post-stroke. • C21 preserved non-spatial and short-term working memory in aged rats post-stroke. • C21 preserved reference memory and facilitated associative learning post-stroke. • C21 improved cognitive flexibility in aged rats post-stroke. • C21 prevented cortical accumulation of Aβ 1-42 in aged animals post-stroke. Abstract Post stroke cognitive impairment (PSCI) is an understudied, long-term complication of stroke, impacting nearly 30–40% of all stroke survivors. No cure is available once the cognitive deterioration manifests. To our knowledge, this is the first study to investigate the long-term effects of C21 treatment on the development of PSCI in aged animals. Treatments with C21 or vehicle were administered orally, 24 h post-stroke, and continued for 30 days. Outcome measures for sensorimotor and cognitive function were performed using a sequence of tests, all blindly conducted and assessed at baseline as well as at different time points post-stroke. Our findings demonstrate that the angiotensin receptor (AT2R) agonist C21 effectively prevents the development of PSCI in aged animals. [ABSTRACT FROM AUTHOR]

Post-stroke cognitive impairment (PSCI) adversely affects survivors' recovery trajectory and overall health outcomes. This study aimed to investigate the prevalence of PCSI and its associated risk factors. A cross-sectional study was conducted with stroke survivors recruited from the neurology units of three hospitals in Yunnan, China. Measures included the Frenchay Aphasia Screening Test (FAST), Apathy Evaluation Scale (AES), Fatigue Severity Scale (FSS), Informant Questionnaire for Cognitive Decline in the Elderly (IQCODE), Montreal Cognitive Assessment (MoCA), and Charlson Comorbidity Index (CCI). Logistic regression analysis was carried out to identify risk factors significantly and independently associated with PSCI. Of 389 stroke participants studied, 139 (36%) were found to have PSCI. Every 10-year increase in age [odds ratio (OR) =1.69, 95% confidence interval (CI): 1.27–2.24, p < 0.001], and 1-point increase in the AES (OR = 1.13, 95% CI: 1.07–1.18, p < 0.001) and FSS scores (OR = 1.06, 95% CI: 1.03–1.10, p < 0.001) were significantly associated with higher odds of PSCI. Conversely, a 1-point increase in the MoCA score (OR = 0.91, 95% CI: 0.87–0.95, p < 0.001) and having an undergraduate education (OR = 0.45, 95% CI: 0.24–0.84, p = 0.013) or postgraduate education (OR = 0.18, 95% CI: 0.06–0.50, p = 0.001) were associated with reduced odds of PSCI. PSCI is prevalent in the Chinese population, with advanced age, lower education levels, lower MoCA scores, and higher fatigue and apathy scores identified as strong risk factors. It is recommended that psychological and cognitive assessment be routinely incorporated into post-stroke rehabilitation pathways to mitigate cognitive decline. • Post-stroke cognitive impairment (PSCI) occurs in 36% of stroke survivors. • PSCI is associated with older age, lower education levels and higher fatigue and apathy scores. • Higher MoCA scores and post-secondary education were protective factors. [ABSTRACT FROM AUTHOR]

The kynurenine pathway is the main metabolic pathway of tryptophan degradation and has been associated with stroke and impaired cognitive functioning, but studies on its role in post-stroke cognitive impairment (PSCI) are scarce. We aimed to investigate associations between metabolites of the kynurenine pathway at baseline and post-stroke cognitive functioning over time. Baseline plasma kynurenines were quantified in 198 stroke patients aged 65.4 ± 10.8 years, 138 (69.7%) men, who were followed up over a period of three years after stroke. Baseline and longitudinal associations of kynurenines with PSCI and cognitive domain scores were investigated using linear mixed models, adjusted for several confounders. No evidence of associations between kynurenines and odds of PSCI were found. However, considering individual cognitive domains, higher plasma levels of anthranilic acid (AA) were associated with better episodic memory at baseline (β per SD 0.16 [0.05, 0.28]). Additionally, a linear-quadratic association was found for the kynurenic acid/ quinolinic acid ratio (KA/QA), a neuroprotective index, with episodic memory (Wald χ2 = 8.27, p =.016). Higher levels of KA were associated with better processing speed in women only (p interaction =.008; β per SD 0.15 [95% CI 0.02, 0.27]). These associations did not change over time. Higher levels of KA, AA and KA/QA were associated with better scores on some cognitive domains at baseline. These associations did not change over time. Given the exploratory nature and heterogeneity of findings, these results should be interpreted with caution, and verified in other prospective studies. • Higher levels of AA were associated with better episodic memory. • A linear-quadratic association was found of the KA/QA ratio with episodic memory. • Higher levels of KA were associated with better processing speed in women only. • These associations were present 3 months after stroke and did not change over time. • No evidence of associations between kynurenines and odds of PSCI was found. [ABSTRACT FROM AUTHOR]