Hypotension is a leading cause of age-related cognitive impairment. The available literature evidences that vascular factors are associated with dementia and that hypotension alters cerebral perfusion flow and can aggravate the neurodegeneration of Alzheimer's disease (AD). Despite the discovery of biomarkers and the recent progress made in neurovascular biology, epidemiology, and brain imaging, some key issues remain largely unresolved: the potential mechanisms underlying the neural deterioration observed in AD, the effect of cerebrovascular alterations on cognitive deficits, and the positive effects of hypotension treatment on cognition. Therefore, further well-designed studies are needed to unravel the potential association between hypotension and cognitive dysfunction and reveal the potential benefits of hypotension treatment for AD patients. Here, we review the current epidemiological, pathobiological, and treatment-related literature on neurovascular changes and hypotension-related cognitive dysfunction and highlight the unsettled but imminent issues that warrant future research endeavors.
Humans ; Hypotension/complications* ; Cognitive Dysfunction/etiology* ; Alzheimer Disease/epidemiology* ; Cerebrovascular Circulation/physiology* ; Cognition Disorders/etiology*

OBJECTIVES: To explore the mechanisms of Qingre Lidan Jiedu Recipe (QLJR) for improving cognitive dysfunction in rats with high copper load. METHODS: Seventy-five male SD rats were randomized into normal control group, model group, QLJR group, penicillamine (PCA) group, and QLJR+ PCA group. Except for those in the control group, all the rats were fed a high-copper diet for 12 weeks. The effects of the treatments on cognitive function of the rats were assessed using the Barnes maze and passive avoidance tests. Hippocampal expressions of NIX, FUNDC1 and LC3 of the rats were detected using Western blotting and immunofluorescence staining, and changes in mitochondrial morphology were observed with transmission electron microscopy. RESULTS: Behavioral tests showed prolonged target hole latency, shortened latency to enter the dark chamber, and increased error counts of the rats in the model group, which were significantly improved in QLJR+PCA group; the error counts were significantly lower in QLJR+PCA group than in either QLJR or PCA group. Among all the groups, the hippocampal expressions of NIX and FUNDC1 were the lowest and LC3 I/II expression the highest in the model group; NIX and FUNDC1 expressions were significantly higher and LC3 I expression was lower in QLJR+PCA group than in QLJR group and PCA group. Immunofluorescence staining revealed weakened NIX and FUNDC1 expressions and enhanced LC3 expression in the hippocampus of the rats in the model group as compared with those in the normal control and QLJR+PCA groups, but their expressions did not differ significantly between QLJR and PCA groups. The rats in the model group showed obvious structural disarray of the mitochondria, which were improved in all the treatment groups. CONCLUSIONS QLJR improves cognitive dysfunction in rats with high copper load possibly by regulating mitophagy.
Animals ; Male ; Rats, Sprague-Dawley ; Rats ; Drugs, Chinese Herbal/therapeutic use* ; Copper/toxicity* ; Mitophagy/drug effects* ; Hippocampus/drug effects* ; Cognition Disorders/drug therapy* ; Cognitive Dysfunction/chemically induced*

Hemorrhagic shock is a common clinical emergency that can aggravate cell injury after resuscitation. Astrocytes are crucial for the survival of neurons because they regulate the surrounding ionic microenvironment of neurons. Although hemorrhagic shock and resuscitation (HSR) injury can impair cognition, it remains unclear how this insult directly affects astrocytes. In this study, we established an HSR model by bleeding and re-transfusion in mice. The social interaction test and new object recognition test were applied to evaluate post-operative cognitive changes, and the results suggest that mice experience cognitive impairment following exposure to HSR. In the HSR group, the power spectral density of β and γ oscillations decreased, and the coupling of the θ oscillation phase and γ oscillation amplitude was abnormal, which indicated abnormal neuronal oscillation and cognitive impairment after HSR exposure. In brief, cognitive impairment in mice is strongly correlated with Ca²⁺ signal strength in lateral septum astrocytes following HSR.
Animals ; Astrocytes/metabolism* ; Shock, Hemorrhagic/metabolism* ; Resuscitation/adverse effects* ; Male ; Mice ; Calcium Signaling/physiology* ; Mice, Inbred C57BL ; Septal Nuclei/metabolism* ; Cognitive Dysfunction/etiology* ; Disease Models, Animal ; Cognition Disorders/etiology*

Huntington's disease (HD) is an inherited neurodegenerative disorder caused by the abnormal expansion of CAG trinucleotide repeats in the Huntingtin gene (HTT) located on chromosome 4. It is transmitted in an autosomal dominant manner and is characterized by motor dysfunction, cognitive decline, and emotional disturbances. To date, there are no curative treatments for HD have been developed; current therapeutic approaches focus on symptom relief and comprehensive care through coordinated pharmacological and nonpharmacological methods to manage the diverse phenotypes of the disease. International clinical guidelines for the treatment of HD are continually being revised in an effort to enhance care within a multidisciplinary framework. Additionally, innovative gene and cell therapy strategies are being actively researched and developed to address the complexities of the disorder and improve treatment outcomes. This review endeavours to elucidate the current and emerging gene and cell therapy strategies for HD, offering a detailed insight into the complexities of the disorder and looking forward to future treatment paradigms. Considering the complexity of the underlying mechanisms driving HD, a synergistic treatment strategy that integrates various factors-such as distinct cell types, epigenetic patterns, genetic components, and methods to improve the cerebral microenvironment-may significantly enhance therapeutic outcomes. In the future, we eagerly anticipate ongoing innovations in interdisciplinary research that will bring profound advancements and refinements in the treatment of HD.
Huntington Disease/pathology* ; Humans ; Genetic Therapy/methods* ; Animals ; Huntingtin Protein/genetics* ; Cell- and Tissue-Based Therapy/methods*

Psychogenic non-epileptic seizures are accompanied by motor,behavioral,sensory,and/or cognitive changes,with the clinical manifestations similar to epileptic seizures.This disease is easy to be misdiagnosed and neglected in clinical work.At present,most intervention measures still depend on the experience of clinicians.This article reviews the comorbidities of psychogenic non-epileptic seizures,including mental and cognitive disorders,somatic syndrome,sleep disorders,and epilepsy.This review aims to strengthen the precision of clinical treatment and management of patients with psychogenic non-epileptic seizures and provide more efficient individualized diagnosis and treatment programs for patients.
Humans ; Seizures/diagnosis* ; Comorbidity ; Epilepsy ; Sleep Wake Disorders ; Mental Disorders ; Psychophysiologic Disorders ; Cognition Disorders

Chronic pain, a prevalent chronic disease, frequently manifests not only in physical symptoms but also in cognitive impairment, which seriously affects patients' quality of life. Interneurons are multipolar neurons, most of which are inhibitory, serving as crucial connectors within neural networks. They play key roles in signal transmission and fine-tuning of neural activity. In recent years, growing evidence has shown that interneurons are involved in the development of chronic pain and its associated cognitive dysfunction. Investigating the relationship between interneuron dysfunction and chronic pain-related cognitive impairment is of great significance, offering new potential targets and insights for the development of novel therapeutic approaches.
Interneurons/physiology* ; Humans ; Chronic Pain/complications* ; Cognitive Dysfunction/physiopathology* ; Cognition Disorders/physiopathology* ; Animals

Despite that sleep disturbance and poor neurocognitive performance are common complaints among coronavirus disease 2019 (COVID-19) survivors, few studies have focused on the effect of post-COVID-19 sleep disturbance (PCSD) on cognitive function. This study aimed to identify the impact of PCSD on neurocognitive function and explore the associated risk factors for the worsening of this condition. This cross-sectional study was conducted via the web-based assessment in Chinese mainland. Neurocognitive function was evaluated by the modified online Integrated Cognitive Assessment (ICA) and the Number Ordering Test (NOT). Propensity score matching (PSM) was utilized to match the confounding factors between individuals with and without PCSD. Univariate analyses were performed to evaluate the effect of PCSD on neurocognitive function. The risk factors associated with worsened neurocognitive performance in PCSD individuals were explored using binary logistic regression. A total of 8692 individuals with COVID-19 diagnosis were selected for this study. Nearly half (48.80%) of the COVID-19 survivors reported sleep disturbance. After matching by PSM, a total of 3977 pairs (7954 individuals in total) were obtained. Univariate analyses revealed that PCSD was related to worse ICA and NOT performance (P<0.05). Underlying disease, upper respiratory infection, loss of smell or taste, severe pneumonia, and self-reported cognitive complaints were associated with worsened neurocognitive performance among PCSD individuals (P<0.05). Furthermore, aging, ethnicity (minority), and lower education level were found to be independent risk factors for worsened neurocognitive performance in PCSD individuals (P<0.05). PCSD was related to impaired neurocognitive performance. Therefore, appropriate prevention and intervention measures should be taken to minimize or prevent PCSD and eliminate its potential adverse effect on neurocognitive function.
Humans ; COVID-19/epidemiology* ; Male ; Female ; Sleep Wake Disorders/epidemiology* ; Propensity Score ; Middle Aged ; Cross-Sectional Studies ; Adult ; SARS-CoV-2 ; Aged ; Risk Factors ; China/epidemiology* ; Cognition ; Cognitive Dysfunction/etiology* ; Neuropsychological Tests

As the most common chromosomal disorder compatible to life, Down syndrome (DS) is caused by an extra copy of chromosome 21. Almost all DS patients have cognitive dysfunction. Therefore, it is important to study the underlying pathogenetic mechanism to elucidate its molecular basis. This article has provided a review for the molecular mechanisms of NRIP1 and DYRK1A genes, which have been closely associated with the cognitive dysfunctions of DS patients. It has also summarized the research progress on the mechanism of DS and development of new therapeutic strategies based on such studies, with an aim to provide insights into the prevention and treatment for the cognitive dysfunctions in DS patients.
Down Syndrome/psychology* ; Humans ; Protein-Tyrosine Kinases/genetics* ; Dyrk Kinases ; Protein Serine-Threonine Kinases/genetics* ; Cognition Disorders/etiology*

Objective To explore the change of gait of middle-aged and elderly people with mild cognitive impairment in the community,the correlation between gait and cognitive domain,and the role of gait in early recognition of cognitive decline. Methods 140 people over 40 years old in Tongxing Village,Yancheng City,Jiangsu Province were enrolled.The subjects were divided into normal cognitive group (n=64) and mild cognitive impairment group(n=76)through the Montreal Cognitive Assessment and the Minimum Mental State Examination,and gait tests were conducted at the same time.The data were collected and statistically analyzed to explore the difference of gait indicators between the two groups,the relationship between gait indicators and cognitive domains,and the ability of gait indicators to recognize mild cognitive impairment. Results The gait of the mild cognitive impairment group was worse than that of the normal cognitive group in terms of space (stride length,step height,step width) and time (step speed,stride speed,swing speed).Partial correlation analysis showed that step width was negatively correlated with delayed recall;Step size,step width and delayed recall,step height and naming were positively correlated.The logistic regression model constructed by step speed,stride length,stride speed,swing speed,step height and step width can reliably identify the existence of MCI (AUC=0.761,95%CI 0.683-0.840,P<0.05). Conclusion In the middle-aged and elderly community,the spatial and temporal performance of gait of patients with mild cognitive impairment is worse than that of the normal cognitive population.There is a close relationship between spatial indicators and delayed recall and naming.The temporal and spatial characteristics of gait have the potential to identify cognitive decline at an early stage.
Mild cognitive impairment

Objective: To analyze the association between sleep duration and cognitive function of the elderly in six provinces of China. Methods: Based on the cross-sectional survey data of the elderly from the Healthy Ageing Assessment Cohort Study in 2019, 4 644 participants' sociodemographic and economic indicators, lifestyle, prevalence of major chronic diseases, and sleep status, including night-time sleep duration, daytime sleep duration and insomnia, were collected by questionnaires. Cognitive function was evaluated by the Mini-Mental State Examination. Multivariate logistic regression was used to analyze the association between night-time sleep duration, daytime sleep duration and cognitive function. Results: The mean age of 4 644 respondents was (72.3±5.7) years, and 2 111 of them were males (45.5%). The mean total daily sleep time of the elderly was (7.9±1.9) hours, and the proportion of those who slept less than 7.0, 7.0-8.9 and≥9.0 hours was 24.1% (1 119), 42.1% (1 954) and 33.8% (1 571), respectively. The mean sleep time at night was (6.9±1.7) hours. About 23.7% (1 102) of the elderly did not sleep during the day, and the mean duration of the elderly who slept during the day was (78±51) minutes. Among the elderly with insomnia, 47.9% were still satisfied with their sleep quality. The mean value of MMSE score of 4 644 respondents was (24.5±5.3), and the cognitive impairment rate was 28.3% (1 316). The results of multivariate logistic regression model analysis showed that the OR (95%CI) value of the risk of cognitive impairment in older people who did not sleep, slept for 31 to 60 minutes and slept more than one hour was 1.473 (1.139 to 1.904), 1.277 (1.001 to 1.629) and 1.496 (1.160 to 1.928), respectively, compared with those who slept for 1 to 30 minutes during the daytime. Compared with those who slept for 7.0‒8.9 hours at night, the OR (95%CI) value of the risk of cognitive impairment in older people who slept more than 9.0 hours was 1.239 (1.011 to 1.519). Conclusion: The cognitive function is related to sleep duration in the Chinese elderly.
Male ; Humans ; Aged ; Female ; Sleep Initiation and Maintenance Disorders/complications* ; Cross-Sectional Studies ; Cohort Studies ; Sleep ; Sleep Wake Disorders ; Cognition ; China/epidemiology*