Cognitive Impairment Research Articles

Modulating the cholinergic system—Novel targets for deep brain stimulation in Parkinson's disease

AbstractParkinson's disease (PD) is the second‐fastest growing neurodegenerative disease in the world. The major clinical symptoms rigor, tremor, and bradykinesia derive from the degeneration of the nigrostriatal pathway. However, PD is a multi‐system disease, and neurodegeneration extends beyond the degradation of the dopaminergic pathway. Symptoms such as postural instability, freezing of gait, falls, and cognitive decline are predominantly caused by alterations of transmitter systems outside the classical dopaminergic axis. While levodopa and deep brain stimulation (DBS) of the subthalamic nucleus or globus pallidus internus effectively address PD primary motor symptoms, they often fall short in mitigating axial symptoms and cognitive impairment. Along these lines, the cholinergic system is increasingly recognized to play a crucial role in governing locomotion, postural stability, and cognitive function. Thus, there is a growing interest in bolstering the cholinergic tone by DBS of cholinergic targets such as the pedunculopontine nucleus (PPN) and nucleus basalis of Meynert (NBM), aiming to alleviate these debilitating symptoms resistant to traditional treatment strategies targeting the dopaminergic network. This review offers a comprehensive overview of the role of cholinergic dysfunction in PD. We discuss the impact of PPN and NBM DBS on the management of symptoms not readily accessible to established DBS targets and pharmacotherapy in PD and seek to provide guidance on patient selection, surgical approach, and stimulation paradigms.image

Cognitive reorganization in patients with Parkinson’s Disease and Mild Cognitive Impairment: a neuropsychological network approach

Cognitive reorganization in patients with Parkinson’s Disease and Mild Cognitive Impairment: a neuropsychological network approach

Rehabilitation With Exergames in Individuals With Moderate to Severe Cognitive Impairment: A Case Report

Rehabilitation With Exergames in Individuals With Moderate to Severe Cognitive Impairment: A Case Report

Cognitive impact and brain structural changes in long COVID patients: a cross-sectional MRI study two years post infection in a cohort from Argentina

Abstract Objective Long COVID is a condition characterised by persistent symptoms after a SARS-CoV-2 infection, with neurological manifestations being particularly frequent. Existing research suggests that long COVID patients not only report cognitive symptoms but also exhibit measurable cognitive impairment. Neuroimaging studies have identified structural alterations in brain regions linked to cognitive functions. However, most of these studies have focused on patients within months of their initial infection. This study aims to explore the longer-term cognitive effects and brain structural changes in long COVID patients, approximately two years post-infection, in a cohort from San Martín, Buenos Aires, Argentina. Methods We conducted a cross-sectional study involving 137 participants: 109 with long COVID symptoms and 28 healthy controls. The participants underwent an initial clinical assessment, completed a structured questionnaire and standardised scales, underwent a cognitive assessment, and had a brain MRI scan. Structural MRI images were processed via FreeSurfer and FSL to obtain volumetric measures for subcortical and cortical regions, along with regional cortical thickness. Differences between groups for these variables were analysed using ANCOVA, with permutation tests applied to correct for multiple comparisons. Results Long COVID patients reported persistent cognitive symptoms such as memory problems and brain fog, with higher levels of fatigue and reduced quality of life compared to controls. Despite subjective cognitive complaints, cognitive tests did not reveal significant differences between groups, except for the TMT-A (p = 0.05). MRI analysis revealed decreased volume in the cerebellum (p = 0.03), lingual gyrus (p = 0.04), and inferior parietal regions (p = 0.03), and reduced cortical thickness in several areas, including the left and right postcentral gyri (p = 0.02, p = 0.03) and precuneus (p = 0.01, p = 0.02). Conclusions This study highlights the enduring impact of long COVID on quality of life and physical activity, with specific brain structural changes identified two years post-infection. Although cognitive tests did not show clear impairment, the observed brain atrophy and significant reduction in quality of life emphasize the need for comprehensive interventions and further longitudinal studies to understand the long-term effects of long COVID on cognition and brain health.

Compromised CD8+ T cell immunity in the aged brain increases severity of neurotropic coronavirus infection and postinfectious cognitive impairment.

Advanced age increases the risk of severe disease from SARS-CoV-2 infection, as well as incidence of long COVID and SARS-CoV-2 reinfection. We hypothesized that perturbations in the aged antiviral CD8+ T cell response predisposes elderly individuals to severe coronavirus infection, re-infection, and postinfectious cognitive sequelae. Using MHV-A59 as a murine model of respiratory coronavirus, we found that aging increased CNS infection and lethality to MHV infection. This was coupled with increased CD8+ T cells within the aged CNS but reduced antigen specificity. Aged animals also displayed a decreased proportion of CD103+ resident memory cells (TRM), which correlated with increased severity of secondary viral challenge. Using a reciprocal adoptive transfer paradigm, data show that not only were fewer aged CD8+ T cells retained within the adult brain post-infection, but also that adult CD8+ cells expressed lower levels of TRM marker CD103 when in the aged microenvironment. Furthermore, aged animals demonstrated spatial learning impairment following MHV infection, which worsened in both aged and adult animals following secondary viral challenge. Spatial learning impairment was accompanied by increased TUNEL positivity in hippocampal neurons, suggestive of neuronal apoptosis. Additionally, primary cell coculture showed that activated CD8+ T cells induced TUNEL positivity in neurons, independent of antigen-specificity. Altogether, these results show that non-antigen specific CD8+ T cells are recruited to the aged brain and cause broad neuronal death without establishing a TRM phenotype that confers lasting protection against a secondary infection.

Understanding the Best Nutritional Management for Creutzfeldt–Jakob Disease Patients: A Comparison Between East Asian and Western Experiences

(1) Background: Creutzfeldt–Jakob disease (CJD) is a rare and fatal neurodegenerative disorder caused by the accumulation of an altered prion protein, which usually leads to death within one year after clinical onset. CJD patients usually present with rapid cognitive impairment associated with declines in cerebellar, motor, visual, behavioral, and swallowing functions. Moreover, CJD patients lose their ability to eat and take medications orally very early on in treatment; nevertheless, there are no specific nutritional guidelines for this disease shared worldwide. (2) Methods: This review aims to describe the nutritional outcomes of CJD patients in Western countries to compare them with those described in East Asian countries and then aims to explore the most recent trends in the nutritional management of CJD patients, including some dietary compounds that present neuroprotective effects. (3) Results: In Japan’s, Taiwan’s, and China’s healthcare systems, CJD patients receive intensive life-sustaining treatment that prolongs their survival (i.e., artificial feeding); conversely, in Western countries, intensive life-sustaining treatments like tube feeding are not commonly provided to CJD patients. (4) Conclusions: It is difficult to pinpoint the reasons for these discrepancies around CJD palliative care supply, but it is clear that specific nutritional guidelines may directly improve the nutritional management of CJD patients and thus allow their families and caregivers to ensure the best end-of-life care for these patients.

Changes in choroidal thickness quantified by Optical Coherence Tomography across cognitive impairment: data from the NORFACE cohort.

Optical coherence tomography (OCT) enables high-resolution imaging of ocular structures in health and disease. Choroid thickness (CT) is a key vascular retinal parameter that can be assessed by OCT and might be relevant in the evaluation of the vascular component of cognitive decline. We aimed to investigate CT changes in a large cohort of individuals cognitive unimpaired (CU), with mild cognitive impairment due to Alzheimer's (MCI-AD), mild cognitive impairment due to cerebrovascular disease (MCI-Va), Alzheimer's disease dementia (ADD), and vascular dementia (VaD). Clinical, demographical, ophthalmological and OCT data from the Neuro-ophthalmological Research at Fundació ACE (NORFACE) project were analyzed. CT was assessed in the macula across nine Early Treatment Diabetic Retinopathy Study (ETDRS) quadrants, average thickness, total volume, and subfoveal choroidal thickness. Differences of CT among the five diagnostic groups were assessed in a multivariate regression model, adjusting for demographic and cardiovascular risk factors and OCT image quality. A comparison between manual and automatic CT measurements in a subset of participants was also performed. The study cohort comprised 1,280 participants: 301 CU, 196 MCI-AD, 112 MCI-Va, 578 ADD, and 93 VaD. CT was significantly increased in individuals with cognitive impairment compared to those CU, particularly in the VaD and MCI-Va groups and in the peripheral ETDRS regions. No significant differences were found in inner superior, center and subfoveal choroidal thickness. The interaction of sex and diagnosis had no effect in differentiating CT. Mini-Mental State Examination (MMSE) scores were not correlated to CT. Manual and automated CT measurements showed good reliability. Our findings indicated that peripheral choroidal thickening, especially in patients with cerebrovascular disease, may serve as a potential choroidal biomarker for cognitive decline and suggest different pathogenic pathways in AD and VaD. Further research is required to explore CT as a reliable ocular biomarker for cognitive impairment.

Higher socioeconomic deprivation in areas predicts cognitive decline in New Zealanders without cognitive impairment.

Previous studies identified individual-level socioeconomic factors as key determinants of cognitive health. This study investigated the effect of area-based socioeconomic deprivation on cognitive outcomes in midlife to early late-life New Zealanders without cognitive impairment at baseline. Data stemmed from a subsample of the New Zealand Health, Work and Retirement Study, a cohort study on ageing, who completed face-to-face interviews and were reassessed two years later. Cognitive functioning was measured using Addenbrooke's Cognitive Examination-Revised, adapted for culturally acceptable use in Aotearoa New Zealand. Area-based socioeconomic deprivation was assessed using the New Zealand Deprivation Index (NZDep2006). Linear mixed-effects models analysed the association between area-based socioeconomic deprivation and cognitive outcomes. The analysis included 783 participants without cognitive impairment at baseline (54.7% female, mean age 62.7 years, 25.0% Māori, the Indigenous people of Aotearoa New Zealand). There was an association between higher area-based socioeconomic deprivation and lower cognitive functioning (B = -0.08, 95%CI: -0.15;-0.01; p = .050) and cognitive decline (B = -0.12, 95%CI: -0.20;-0.04, p = .013) over two years, while controlling for covariates. The findings emphasise the importance of considering neighbourhood characteristics and broader socioeconomic factors in strategies aimed at mitigating cognitive health disparities and reducing the impact of dementia in disadvantaged communities.

Morin Ameliorates Lipopolysaccharides-Induced Sepsis-Associated Encephalopathy and Cognitive Impairment in Albino Mice.

Sepsis-associated encephalopathy is a common neurological complication of sepsis that is characterized by neuroinflammation, oxidative stress and apoptosis, which results in cognitive impairments in septic survivors. Despite numerous treatment options for this condition, none of them are definite. Therefore, this study aimed to investigate the impact of morin, a flavone known for its neuroprotective and anti-inflammatory effects, against lipopolysaccharides-induced sepsis-associated encephalopathy in albino mice for 7 days. Mice were divided into 4 groups: Negative control, morin, septic, and septic morin-treated mice. Sepsis was induced by a single injection of lipopolysaccharides (5mg/kg, intraperitoneally), morin (50mg/kg b. wt.) was given orally, starting from 5h after sepsis induction, then daily for 4 other days. Morin ameliorated septic structural and functional alternations as manifested by improving the survival rate, the behavioral functions, in addition to preserving and protecting the brain tissue. This was accompanied with the augmentation of the total antioxidant capacity, as well as the suppression of tissue levels of the lipid peroxidation marker malondialdehyde, apoptosis (cleaved-caspase-3), glial fibrillary acidic protein, and the proinflammatory cytokine tumor necrosis factor. In conclusion, morin has a promising ameliorative effect to counteract the sepsis-associated encephalopathy via its anti-inflammatory and antioxidant effects and to prevent the associated cognitive impairments.

In-Depth Proteome Profiling of the Hippocampus of LDLR Knockout Mice Reveals Alternation in Synaptic Signaling Pathway.

The low-density lipoprotein receptor (LDLR) is a major apolipoprotein receptor that regulates cholesterol homeostasis. LDLR deficiency is associated with cognitive impairment by the induction of synaptopathy in the hippocampus. Despite the close relationship between LDLR and neurodegenerative disorders, proteomics research for protein profiling in the LDLR knockout (KO) model remains insufficient. Therefore, understanding LDLR KO-mediated differential protein expression within the hippocampus is crucial for elucidating a role of LDLR in neurodegenerative disorders. In this study, we conducted first-time proteomic profiling of hippocampus tissue from LDLR KO mice using tandem mass tag (TMT)-based MS analysis. LDLR deficiency induces changes in proteins associated with the transport of diverse molecules, and activity of kinase and catalyst within the hippocampus. Additionally, significant alterations in the expression of components in the major synaptic pathways were found. Furthermore, these synaptic effects were verified using a data-independent acquisition (DIA)-based proteomic method. Our data will serve as a valuable resource for further studies to discover the molecular function of LDLR in neurodegenerative disorders.

Investigating the Comparative Effectiveness of Yoga and Relaxation Therapy on Restlessness, Fatigue and Difficulty Concentrating in Multiple Sclerosis Patients

Background: Multiple sclerosis (MS) is a long-term autoimmune disorder affecting the central nervous system, leading to reduced quality of life and impaired physical and psychological functions. Objectives: This study aims to examine the relative efficacy of yoga and relaxation therapy in improving sleep disturbances, fatigue, and cognitive impairment among individuals diagnosed with MS. Methods: This study employed a semi-experimental research design, including a pre-test, post-test, and follow-up over three months. The target population comprised all MS patients referred to the Iranian MS Association in Tehran between July and November 2023. Sixty participants were selected using purposive sampling and randomly assigned to research groups: Two yoga therapy groups with 17 participants each, a relaxation therapy group with 16 participants, and a control group with 18 participants. The yoga therapy group participated in twelve 90-minute sessions twice a week, while the control group received no intervention and was placed on a waiting list. Various tools, including the Multidimensional Fatigue Inventory (MFI), Cohen-Mansfield Agitation Inventory (CMAI-O), and a concentration skills questionnaire, were used to collect data. The data were analyzed using ANOVA, Bonferroni post hoc test, MANCOVA, and Kruskal-Wallis H tests with a significance level of 0.05, utilizing SPSS 27 software. Results: The study found a significant difference (P < 0.001) in the restlessness factor in both the post-test and follow-up phases. Additionally, there was a significant difference (P < 0.001) in the levels of physical fatigue, mental fatigue, decreased activity, and decreased motivation in both the post-test and follow-up phases, indicating significant changes in the fatigue factor among the research groups. However, there was no significant difference in the general fatigue component between the research groups. A significant difference (P < 0.001) was also found in the concentration factor, particularly in the components of voluntary and involuntary concentration, during both the post-test and follow-up stages. Conclusions: The results of this study indicate that both yoga and relaxation therapy techniques significantly reduce restlessness, physical tiredness, mental fatigue, decreased activity, and decreased motivation. Furthermore, the findings validate that both yoga and relaxation therapy techniques effectively enhance voluntary and involuntary concentration.

EFFICACY OF CANNABIDIOL (CBD) IN THE TREATMENT OF ALZHEIMER'S DISEASE: A CRITICAL REVIEW OF EVIDENCE AND CLINICAL IMPLICATIONS

Introduction: This study investigates the therapeutic potential of cannabidiol (CBD) in treating Alzheimer's disease (AD), which is characterized by progressive cognitive decline, memory impairment, and behavioral changes. As traditional treatment options are limited, the exploration of alternative therapies, including CBD, has gained prominence in recent years. Objective: The aim of this research is to evaluate the efficacy of CBD in modulating neuroinflammation and oxidative stress, as well as its potential impact on slowing the progression of Alzheimer's disease. Method: A literature review was conducted using ten articles published between 2019 and 2024. Databases such as the Virtual Health Library, LILACS Plus, and Medline were utilized, applying descriptors related to CBD and Alzheimer's disease. The articles were filtered based on specific inclusion criteria, focusing on studies published in Portuguese, Spanish, and English that are freely accessible online. Results: The reviewed literature indicates that CBD may inhibit the formation of beta-amyloid plaques, a hallmark of Alzheimer's pathology, suggesting its potential for both symptom relief and slowing disease progression. Additionally, the interaction between CBD and the endocannabinoid system (ECS) highlights its role in managing cognitive decline and memory issues associated with AD. Conclusion: While the findings are promising, there is a pressing need for more rigorous clinical studies to validate the efficacy and safety of CBD in Alzheimer's treatment. This research underscores the potential of cannabinoids as a therapeutic option in managing neurodegenerative diseases.

Inhibition of PCSK9 Protects against Cerebral Ischemia‒Reperfusion Injury via Attenuating Microcirculatory Dysfunction.

Proprotein convertase substilin/kexin type 9 (PCSK9), a pivotal protein regulating lipid metabolism, has been implicated in promoting microthrombotic formation and inflammatory cascades, thereby contributing to cardiovascular ischemia/reperfusion (I/R) injury. However, its involvement in cerebral I/R injury and its potential role in microcirculation protection remain unexplored. In this investigation, we utilized a middle cerebral artery occlusion/reperfusion (MCAO/R) mouse model to simulate ischemic stroke. Different concentrations of evolocumab (1, 5, 10mg/kg, i.v.), a PCSK9 inhibitor, were administered to assess its impact. Immunofluorescence staining was employed to analyze changes in the expression of occludin, claudin-5, thrombocyte, ICAM-1, VCAM-1, and CD45, providing insights into blood-brain barrier integrity, platelet adhesion, and immune cell infiltration. Moreover, the Morris water maze and elevated plus maze were utilized to evaluate neurological and behavioral functions in MCAO/R mice, shedding light on the effects of PCSK9 inhibition. Our findings revealed a surge in plasma PCSK9 levels post-MCAO/R, peaking at 24h post-reperfusion. Evolocumab (10mg/kg) treatment significantly mitigated brain infarction and neurological deficits, evidenced by enhanced locomotor function and reduced post-stroke anxiety. However, it did not ameliorate cognitive impairment following MCAO/R. Additionally, evolocumab administration led to diminished leakage of evans blue solution and upregulated expression of occludin and claudin-5. Thrombocyte, ICAM-1, VCAM-1, and CD45 levels were notably reduced in the penumbral area post-evolocumab treatment. These protective effects are speculated to be mediated through the inhibition of the ERK/NF-κB pathway. The PCSK9 inhibitor evolocumab holds promise as a therapeutic agent during the acute phase of stroke, exerting its beneficial effects by modulating the ERK/NF-κB signaling pathway.

Development and validation of a risk prediction model for cognitive impairment in breast cancer patients.

Breast cancer patients often experience cognitive impairment as a complication during treatment, which seriously affects their quality of life. This study aimed to assess the risk factors associated with cognitive impairment in breast cancer patients and to construct and validate a nomogram model to predict cognitive impairment in this population. In this study, we used a convenience sampling method to select 423 breast cancer patients who attended the Department of Breast Surgery at the First Hospital of Jinzhou Medical University from September 2023 to March 2024. We analyzed these patients' cognitive impairment risk factors through LASSO regression and logistic regression analysis to develop a predictive model. The model was evaluated using the area under the curve (AUC) from the receiver operating characteristic (ROC) curve and the calibration curve and decision curve analysis. This study found a prevalence of cognitive impairment of 19.62% among breast cancer patients. A nomogram model was developed based on six influencing factors: age, educational level, pathological type, treatment program, emotional state, and fatigue. The area under the curve (AUC) for the model's training and validation groups was 0.944 and 0.931, respectively. The model calibration curves showed a high degree of consistency, and the decision curve analysis (DCA) indicated good clinical applicability of the model. This nomogram demonstrates good discrimination, calibration, and clinical applicability, making it a more intuitive predictor of the risk of cognitive impairment in breast cancer patients.

The prevalence and clinical correlation factors of cognitive impairment in patients with major depressive disorder hospitalized during the acute phase

ObjectiveThis study aimed to investigate the prevalence of cognitive impairment among patients with major depressive disorder (MDD) hospitalized during the acute phase and to analyze the in-depth association between this cognitive impairment and clinical correlation factors.MethodsIn this cross-sectional study, we recruited 126 patients aged between 18 and 65 years who were diagnosed with MDD. All these patients were inpatients from the Department of Psychiatry at the Second People’s Hospital of Hunan Province. We employed a series of assessment tools, including the Pittsburgh Sleep Quality Index (PSQI), the 16-item Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS-16), the Pre-sleep Arousal Scale (PSAS), the Morningness-Eveningness Questionnaire (MEQ), the Hamilton Anxiety Rating Scale (HAMA), and the 17-item Hamilton Depression Rating Scale (HAMD-17). The patients were divided into a cognitive impairment group and a non-cognitive impairment group based on their scores on the Montreal Cognitive Assessment Scale (MoCA). Through Spearman’s correlation analysis, we explored the correlation between the total MoCA score and the score of each factor. Additionally, we utilized binary logistic regression analysis to investigate the relationship between cognitive impairment and clinically relevant factors in MDD patients hospitalized during the acute phase and plotted ROC curves to evaluate their clinical efficacy.ResultsIn this study, we found that the prevalence of cognitive impairment among MDD patients hospitalized during the acute phase was as high as 63.49%. Through statistical analysis, we observed significant differences between the cognitive impairment group and the non-cognitive impairment group in terms of age, place of residence, education level, and HAMD-17 scores. In the Spearman correlation analysis, we noted the following trends: visuospatial and executive abilities were negatively correlated with the HAMD-17 score (P < 0.05); naming ability was positively correlated with the PSAS score but negatively correlated with the MEQ score (P < 0.05); memory was also negatively correlated with the MEQ score (P < 0.05); attention was negatively correlated with the HAMA score; and abstract cognitive ability was negatively correlated with the MEQ score (P < 0.05). Through binary logistic regression analysis, we further revealed the relationship between cognitive impairment and factors such as living in a rural area (OR = 2.7, 95% CI = 1.083-6.731, P < 0.05), increased age (OR = 1.049, 95% CI = 1.013-1.087, P < 0.01), and the HAMD-17 score (OR = 1.10295, 95% CI = 1.031-11.79, P < 0.01). Additionally, ROC curve analysis demonstrated a significant correlation between the HAMD-17 score and the prediction of cognitive function in MDD patients hospitalized during the acute phase (P < 0.001). Specifically, the AUC for the HAMD-17 score was 0.73, with an optimal cut-off value of 19.5, sensitivity of 70.0%, and specificity of 63.0%. Furthermore, the AUC for age was 0.71, with an optimal cut-off value of 33.5, sensitivity of 59.0%, and specificity of 80.0%.ConclusionsThis study indicates that MDD patients hospitalized during the acute phase have a higher prevalence of cognitive impairment. This phenomenon reflects a significant correlation between clinical factors such as age, sleep-related characteristics, and the severity of depression with cognitive impairment. Therefore, regular assessment of cognitive function in MDD patients and early intervention may be crucial for the treatment and prognosis of the disease.

WMH Contributions to Cognitive Impairment: Rationale and Design of the Diverse VCID Study.

As awareness of dementia increases, more individuals with minor cognitive complaints are requesting clinical assessment. Neuroimaging studies frequently identify incidental white matter hyperintensities, raising patient concerns about their brain health and future risk for dementia. Moreover, current US demographics indicate that ≈50% of these individuals will be from diverse backgrounds by 2060. Racial and ethnic minority populations bear a disproportionate burden of vascular risk factors magnifying dementia risk. Despite established associations between white matter hyperintensities and cognitive impairment, including dementia, no study has comprehensively and prospectively examined the impact of individual and combined magnetic resonance imaging measures of white matter injury, their risk factors, and comorbidities on cognitive performance among a diverse, nondemented, stroke-free population with cognitive complaints over an extended period of observation. The Diverse VCID (Diverse Vascular Cognitive Impairment and Dementia) study is designed to fill this knowledge gap through 3 assessments of clinical, behavioral, and risk factors; neurocognitive and magnetic resonance imaging measures; fluid biomarkers of Alzheimer disease, vascular inflammation, angiogenesis, and endothelial dysfunction; and measures of genetic risk collected prospectively over a minimum of 3 years in a cohort of 2250 individuals evenly distributed among Americans of Black/African, Latino/Hispanic, and non-Hispanic White backgrounds. The goal of this study is to investigate the basic mechanisms of small vessel cerebrovascular injury, emphasizing clinically relevant assessment tools and developing a risk score that will accurately identify at-risk individuals for possible treatment or clinical therapeutic trials, particularly individuals of diverse backgrounds where vascular risk factors and disease are more prevalent.

Factors associated with eating performance in nursing home residents living with dementia and other comorbidities.

Eating performance is the functional ability to get food into the mouth and chew/swallow it. Nursing home residents with dementia commonly experience compromised eating performance and subsequent consequences. Prior work examined the association between resident eating performance and their cognitive and functional ability. Yet, the associations between resident eating performance and behavioral and psychological symptoms, psychotropic medication use, and comorbidities are less studied. This study aimed to examine the association between eating performance and cognition, functional ability, behavioral and psychological symptoms, psychotropic medication use, and comorbidities in nursing home residents with dementia. This was a secondary analysis using baseline data from two randomized controlled trials, testing the impact of Function Focused Care on function and behavioral symptoms in 882 residents with moderate-to-severe dementia (mean age 86.55 years, 71% female, 30% non-white, 68.5% severe dementia) from 67 nursing homes in two states between 2014 and 2020. Eating performance (dependent variable) was measured using the single self-feeding item of Barthel Index. Independent variables included cognitive impairment, functional ability (Barthel Index total score excluding the self-feeding item score), behavioral and psychological symptoms (agitation, depression, resistiveness-to-care), psychotropic medication use (anti-depression, sedative, anti-psychotics, anti-seizure, anti-anxiety), and comorbidities. Nearly 39% of residents were dependent in eating. On average, residents had five documented comorbidities (SD = 3.06, range = 0-12) and were on approximately one psychotropic medication (SD = 1.25, range = 0-5). Eating performance was associated with cognitive impairment (OR = 0.53, 95% CI = 0.35, 0.79, p = .002), functional ability (OR = 1.05, 95% CI = 1.04, 1.06, p < .001), depressive symptoms (OR = 0.94, 95% CI = 0.89, 0.98, p = .007), and anxiolytic use (OR = 0.64, 95% CI = 0.42, 0.99, p = .046). Findings supported that better eating performance was associated with less cognitive impairment, higher functional ability, fewer depressive symptoms, and less anxiolytic use. Targeted interventions to accommodate to cognitive function, optimize functional ability, minimize anxiolytic use, and manage depressive symptoms are encouraged to support eating performance in residents with dementia.

Cognitive Function in Individuals with Chronic Hypoparathyroidism - A Prospective Observational Study.

"Brain fog" is a frequently reported, distressing experience among individuals with chronic hypoparathyroidism, characterized by reduced concentration and reduced ability to perform day-to-day tasks. However, evidence linking chronic hypoparathyroidism to cognitive impairment is limited and inconsistent. This study aimed to explore cognitive function in these patients using a validated neurocognitive test battery, compare results with a matched healthy control group, and analyze the frequency of cognitive impairment based on normative data. The participants' cognitive performance was tested using a cognitive test battery, including the Trail Making Test A/B, the Color-Word Interference Test, and the California Verbal Learning Test. These tests were used to evaluate the cognitive domains of "attention and processing speed," "verbal learning and memory, " and "executive function." In total, 30 individuals with hypoparathyroidism and 30 healthy controls were included. 24 patients were women (80.0%), with a median age of 44.5±13.1 and a median disease duration of 8.7 years (±5.3). Individuals with chronic hypoparathyroidism showed poorer cognitive performance in "attention and processing speed" (F(1,57) = 8.65, p = 0.005*, η² = 0.13) compared to healthy controls. A significantly higher percentage of patients had cognitive deficits in both "attention and processing speed" (56.7% vs. 3.3%) and "executive function" (60.0% vs. 16.7%). This study provides evidence that cognitive dysfunction, particularly in "attention and processing speed" is common in chronic hypoparathyroidism. Recognizing cognitive impairment in these patients is crucial, especially when discussing workability. Neuropsychological training as an adjunct therapy strategy may be beneficial in managing these cognitive deficits.

The protective role of basal metabolic rate in cognitive decline: evidence from epidemiological and genetic studies.

This study aims to explore the relationship between basal metabolic rate (BMR) and cognitive impairment and assess the potential of BMR as a protective factor against cognitive decline. This investigation initially conducted a cross-sectional study of American adults from 2011 to 2014 using data from the National Health and Nutrition Examination Survey. It examined the correlation between participants' BMR and cognitive functions, exploring the association with cognitive impairment. Subsequently, publicly available genome-wide association study data was used to examine potential causal links between genetically determined BMR and specific cognitive disorders using Mendelian randomization. Cross-sectional findings revealed a significant positive correlation between higher BMR and cognitive scores. In Mendelian randomization analysis, BMR demonstrated an inverse causal relationship with Alzheimer's disease and Parkinson's dementia, suggesting BMR as a potential protective factor against these diseases. No causal links were found with vascular dementia, Lewy body dementia, and frontotemporal dementia. This study supports the role of BMR as a potential protective factor against Alzheimer's disease and Parkinson's dementia, suggesting that BMR may play an important role in preventing cognitive decline. However, due to the limitations of cross-sectional studies, further prospective studies and broader demographic samples are necessary to verify these results and explore underlying biological mechanisms. Key messages What is already known on this topic: Existing knowledge suggests a close relationship between BMR and health and cognitive functions, but detailed studies on its connection with specific cognitive impairments are still needed. What this study adds: This study found a significant positive correlation between higher BMR and cognitive improvement, potentially aiding in the prevention of Alzheimer's and Parkinson's dementia. How this study might affect research, practice, or policy: This finding guides public health strategies and personalized medicine, emphasizing the necessity for further research to validate BMR's protective effects.

The effect of neuroticism on mobile phone addiction among undergraduate nursing students: a moderated mediation model.

Mobile phone addiction (MPA) has numerous deleterious effects on college students, including depression, anxiety, cognitive impairments, and sleep disorders. Undergraduate nursing students play a crucial role as a significant reserve workforce in clinical nursing practice, and their compromised mental health status significantly influences the quality of nursing work and nurse-patient relationships in the future. This study aims to investigate the associations between neuroticism and MPA among undergraduate nursing students, the mediating effect of self-control and the moderating effect of psychological capital. A total of 900 undergraduate nursing students participated in the survey, wherein the Eysenck Personality Questionnaire Short Form Scale China Version-Neuroticism Subscale (EPQ-RSC-N), Self-Control Scale (SCS), Positive Psychological Capital Questionnaire (PPQ), and Mobile Phone Addiction Tendency Scale (MPATS) were employed for assessment. To analyze the available data, various statistical methods were utilized, including common method bias test examination, descriptive statistics, chi-square tests, independent samples t-tests, Pearson's correlation analyses, as well as the Hayes' PROCESS Macro models 4 and 14. (1) The prevalence of MPA in this study was found to be 34.89%. (2) The MPA was positively correlated with neuroticism (r = 0.287, p < 0.001), and was negatively correlated with self-control (r = -0.467, p < 0.001) and psychological capital (r = -0.260, p < 0.001). (3) Self-control played a partially mediating role in the association between neuroticism and MPA, with an effect size of 0.151, accounting for 52.98% of the total effect. (4) Psychological capital played a moderating role in the association between self-control and MPA. More specifically, with an increase in the level of psychological capital increases, the predictive effect of self-control on MPA gradually strengthens (β = -0.072, SE = 0.019, t = -3.708, p < 0.001). The prevalence of MPA was relatively high among undergraduate nursing students, with neuroticism exerting a direct influence on it. Self-control served as a mediating factor that could partially alleviate MPA associated with neuroticism. Psychological capital has the ability to regulate the relationship between self-control and MPA. Therefore, enhancing self-control capabilities and cultivating psychological capital levels can effectively manage MPA among undergraduate nursing students.