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*

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

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

BACKGROUND

Type 2 Diabetes Mellitus (T2DM) patients are predisposed to cognitive decline and dementia. The cooccurrence of the two diseases translate to a higher medical cost. Identification of factors contributing to cognitive impairment is warranted.

To determine the predictors of cognitive impairment among Filipino patients with Type 2 Diabetes Mellitus.

This is a cross-sectional analytical study involving Filipino patients diagnosed with T2DM in the outpatient clinic. A total of 171 patients were included and were screened using AD8-P tool.

A total of 171 adult patients were included and screened for cognitive impairment.19.3% were cognitively impaired, with mean age of 59.6 years old (vs. 55.5 years old, p < 0.029), and two-thirds were female. The mean duration of the patient’s diabetes was 11.2 years. After adjusting for confounders and multi-collinearity, the duration of diabetes was significantly associated with cognitive impairment with odds of developing cognitive impairment increasing as the duration reach 10 years above. Those with T2DM for at least ten years were 2.5 times more likely to develop cognitive impairment, holding the age constant. (OR = 2.5, 95% CI – 1.0 to 5.8, p < 0.043).

19.3% of Filipino patients with Type 2 Diabetes Mellitus in a tertiary government hospital are cognitively impaired and this can occur even in less than 65 years old. The ten years or longer duration of T2DM increases the risk of developing cognitive impairment by 2.5%.

BACKGROUND: Chronic illnesses such as Type 2 diabetes mellitus (T2DM) and obesity have been implicated as risk factors in the development of cognitive impairment (CI), but despite this, definite association between the two conditions in increasing cognitive impairment risk is not well defined. OBJECTIVE: This study aims to examine the association between body mass index (BMI) and cognitive impairment (CI) in elderly patients with Type 2 diabetes mellitus. METHODS: This is a cross-sectional study conducted in the outpatient clinics of a private hospital in Manila which included elderly patients with Type 2 diabetes. BMI categories of the subjects were determined using the Asia-Pacific criteria and the Montreal Cognitive Assessment – Philippines (MOCA-P) was administered to subjects who fulfilled the inclusion criteria. Descriptive statistics were used to determine the prevalence of impaired cognition among subjects while risk ratio analysis was used to determine the correlation between BMI and CI. Correlation analysis and linear regression analysis were used to determine the presence of association between cognition (measured by MOCA-P scores) and BMI. For all analysis, a 95% level of significance was used. RESULTS: A total of 109 subjects from the outpatient clinics were included in the study. A high percentage of the study population (90.83%) had CI based on MOCA-P scores. Subjects that belonged to the extremes of BMI- underweight and obese class 2 had higher incidence of CI compared to the other groups. Underweight subjects had 1.103 (95% CI: 1.038 to 1.172) times likelihood of having impaired cognition (p-value 0.0016), while obese 2 subjects had 1.110 (95% CI: 1.040 to 1.184) times likelihood of having impaired cognition (p-value 0.0016). Regression analysis revealed that in subjects with diabetes of less than 10 years, cognition scores were negatively correlated to BMI (p-value 0.0454). Correlation analysis revealed that at the general population level, regardless of the external factors, increasing or decreasing BMI did not have significant effect on cognition scores. CONCLUSION Subjects who belonged to the extremes of BMI-underweight and obese class 2 – had higher incidence of CI compared to the other BMI groups. Among subjects with T2DM duration of less than 10 years, cognition scores tend to be negatively correlated to BMI.
diabetes mellitus, Type 2 ; cognitive impairment ; cognitive dysfunction ; Body Mass Index

Humans ; Huntington Disease/diagnostic imaging* ; Brain/diagnostic imaging* ; Brain Mapping ; Magnetic Resonance Imaging