Risk Factor For Cognitive Decline Research Articles

Ventromedial frontoinsular connectivity is associated with long-term smoking behavior change in aging

Abstract A central question in the field of cognitive aging and behavioral neuroscience is what enables some individuals to successfully change their behavior more than others? Smoking is a significant risk factor for cognitive decline, particularly in vulnerable populations, including those who are at an elevated risk for Alzheimer’s disease (AD). Developing effective smoking reduction strategies is therefore a public health priority. The goal of the current study is to better understand the brain mechanisms underlying long-term smoking behavior change in cognitively normal, but at-risk, older adults. Neuroimaging and human lesion studies have implicated the insula and its functional network in subjective interoceptive awareness of cigarette craving and smoking-cue reactivity. We sought to characterize the extent to which anterior insular resting-state functional connectivity (RSFC) MRI predicted long-term smoking reduction (mean: 2.7 years, range 8 months–4 years) using a seed-to-voxel approach. Twenty-three (18 women; 26% APOE4 carriers; 61.5 years, SD = 3.7) cognitively unimpaired older individuals who smoked cigarettes at their baseline visit and have a first-degree family history of AD (at least one parent or multiple siblings affected) were included from a prospective longitudinal cohort, Pre-symptomatic Evaluation of Experimental or Novel Treatments for Alzheimer Disease (PREVENT-AD) in the current study. We found that reduced long-term smoking behavior was associated with enhanced antagonistic RSFC between bilateral anterior insula (aINS) and ventromedial prefrontal cortex (vmPFC). In a second pre-registered replication study within a larger, independent sample of 118 cognitively normal older adults who smoked cigarettes at baseline from the UK Biobank (73 women; 27.9% APOE4 carriers; 60.3 years, SD = 2.7), we found that baseline enhanced antagonistic RSFC between anterior insula and vmPFC predicted long-term smoking reduction (mean 5.2 years; ranging from 3 years to 7 years). To our knowledge, this is the largest study to examine the neural substrates of long-term smoking cessation in human aging. Our results suggest that antagonistic RSFC between aINS and vmPFC is a brain marker of future smoking reduction and disease prevention in older adults at risk for AD.

The Influence of Personality Type D and Coping Strategies on Cognitive Functioning in Students

The Influence of Personality Type D and Coping Strategies on Cognitive Functioning in Students

GLUT1-mediated microglial proinflammatory activation contributes to the development of stress-induced spatial learning and memory dysfunction in mice.

Stress is a recognized risk factor for cognitive decline, which triggers neuroinflammation involving microglial activation. However, the specific mechanism for microglial activation under stress and affects learning and memory remains unclear. The chronic stress mouse model was utilized to explore the relationship between microglial activation and spatial memory impairment. The effect of hippocampal hyperglycemia on microglial activation was evaluated through hippocampal glucose-infusion and the incubation of BV2 cells with high glucose. The gain-and loss-of-function experiments were conducted to investigate the role of GLUT1 in microglial proinflammatory activation. An adeno-associated virus (AAV) was employed to specifically knockdown of GLUT1 in hippocampal microglia to assess its impact on stressed-mice. Herein, we found that chronic stress induced remarkable hippocampal microglial proinflammatory activation and neuroinflammation, which were involved in the development of stress-related spatial learning and memory impairment. Mechanistically, elevated hippocampal glucose level post-stress was revealed to be a key regulator of proinflammatory microglial activation via specifically increasing the expression of microglial GLUT1. GLUT1 overexpression promoted microglial proinflammatory phenotype while inhibiting GLUT1 function mitigated this effect under high glucose. Furthermore, specific downregulation of hippocampal microglial GLUT1 in stressed-mice relieved microglial proinflammatory activation, neuroinflammation, and spatial learning and memory injury. Finally, the NF-κB signaling pathway was demonstrated to be involved in the regulatory effect of GLUT1 on microglia. We demonstrate that elevated glucose and GLUT1 expression induce microglia proinflammatory activation, contributing to stress-associated spatial memory dysfunction. These findings highlight significant interplay between metabolism and inflammation, presenting a possible therapeutic target for stress-related cognitive disorders.

Association of multiple metabolic and cardiovascular markers with the risk of cognitive decline and mortality in adults with Alzheimer's disease and AD-related dementia or cognitive decline: a prospective cohort study.

There is a scarcity of data stemming from large-scale epidemiological longitudinal studies focusing on potentially preventable and controllable risk factors for Alzheimer's disease (AD) and AD-related dementia (ADRD). This study aimed to examine the effect of multiple metabolic factors and cardiovascular disorders on the risk of cognitive decline and AD/ADRD. We analyzed a cohort of 6,440 participants aged 45-84 years at baseline. Multiple metabolic and cardiovascular disorder factors included the five components of the metabolic syndrome [waist circumference, high blood pressure (HBP), elevated glucose and triglyceride (TG) concentrations, and reduced high-density lipoprotein cholesterol (HDL-C) concentrations], C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), factor VIII, D-dimer, and homocysteine concentrations, carotid intimal-medial thickness (CIMT), and urine albumin-to-creatinine ratio (ACR). Cognitive decline was defined using the Cognitive Abilities Screening Instrument (CASI) score, and AD/ADRD cases were classified using clinical diagnoses. Over an average follow-up period of 13 years, HBP and elevated glucose, CRP, homocysteine, IL-6, and ACR concentrations were significantly associated with the risk of mortality in the individuals with incident AD/ADRD or cognitive decline. Elevated D-dimer and homocysteine concentrations, as well as elevated ACR were significantly associated with incident AD/ADRD. Elevated homocysteine and ACR were significantly associated with cognitive decline. A dose-response association was observed, indicating that an increased number of exposures to multiple risk factors corresponded to a higher risk of mortality in individuals with cognitive decline or with AD/ADRD. Findings from our study reaffirm the significance of preventable and controllable factors, including HBP, hyperglycemia, elevated CRP, D-dimer, and homocysteine concentrations, as well as, ACR, as potential risk factors for cognitive decline and AD/ADRD.

Effects of xylo-oligosaccharide on gut microbiota, brain protein expression, and lipid profile induced by high-fat diet

Midlife overweight and obesity are risk factors of cognitive decline and Alzheimer' s disease (AD) in late life. In addition to increase the risk of obesity and cognitive dysfunction, diets rich in fats also contributes to an imbalance of gut microbiota. Xylo-oligosaccharides (XOS) are a kind of prebiotics with several biological advantages, and can selectively promote the growth of beneficial microorganism in the gut. To explore whether XOS can alleviate cognitive decline induced by high-fat diet (HFD) through improving gut microbiota composition, mice were fed with normal control or 60% HFD for 9 weeks to induce obesity. After that, mice were supplemented with XOS (30 g or 60 g/kg-diet) or without, respectively, for 12 weeks. The results showed that XOS inhibited weight gain, decreased epidydimal fat weight, and improved fasting blood sugar and blood lipids in mice. Additionally, XOS elevated spatial learning and memory function, decreased amyloid plaques accumulation, increased brain-derived neurotrophic factor levels, and improved neuroinflammation status in hippocampus. Changes in glycerolipids metabolism-associated lipid compounds caused by HFD in hippocampus were reversed after XOS intervention. On the other hand, after XOS intervention, increase in immune-mediated bacteria, Faecalibacterium was observed. In conclusion, XOS improved gut dysbiosis and ameliorated spatial learning and memory dysfunction caused by HFD by decreasing cognitive decline-associated biomarkers and changing lipid composition in hippocampus.

Risk Factors for Cognitive Impairment in Multiple Sclerosis Patients

Cognitive impairment is one of the most significant burdens among the many neurological complaints in multiple sclerosis patients. Cognitive deficits negatively impact these patients’ quality of life, leading to partial or total loss of several mental functions, such as learning, memory, perception, or problem-solving. While the precise mechanisms involved in the onset and evolution of cognitive decline remain unknown, several risk factors have been associated with intellectual disability. With increasing data on this topic in recent years, the main aim of this review is to summarize the most relevant risk factors correlated with cognitive impairment in multiple sclerosis patients. Firstly, the authors demonstrate the importance of mental disability based on epidemiological data from multiple sclerosis patient cohorts. Subsequently, the intensely debated major risk factors for cognitive decline are discussed, with brief insights into the pathophysiology and possible underlying mechanisms. Finally, the authors describe the impact of medication on cognitive impairment in multiple sclerosis patients, highlighting the main research directions for future studies.

Tocotrienols Prevent the Decline of Learning Ability in High-Fat, High-Sucrose Diet-Fed C57BL/6 Mice.

Obesity has been increasing worldwide and is well-known as a risk factor for cognitive decline. It has been reported that oxidative stress in the brain is deeply involved in cognitive dysfunction in rodent models. While there are many studies on oxidation in the liver and adipose tissue of obese mice, the relationship between obesity-induced cognitive dysfunction and brain oxidation has not been elucidated. Here, we show that obesity induced by a high-fat, high-sucrose diet (HFSD) alters cognitive function in C57BL/6 male mice, and it may involve the acceleration of brain oxidation. Tocotrienols (T3s), which are members of the vitamin E family, can prevent HFSD-induced cognitive changes. To elucidate these mechanisms, respiratory metabolism, locomotor activity, temperature around brown adipose tissue, and protein profiles in the cerebrum cortex were measured. Contrary to our expectation, respiratory metabolism was decreased, and temperature around brown adipose tissue was increased in the feeding of HFSD. The proteins that regulate redox balance did not significantly change, but 12 proteins, which were changed by HFSD feeding and not changed by T3s-treated HFSD compared to control mice, were identified. Our results indicated that HFSD-induced obesity decreases mouse learning ability and that T3s prevent its change. Additionally, feeding of HFSD significantly increased brain oxidation. However, further study is needed to elucidate the mechanisms of change in oxidative stress in the brain by obesity.

Link among apolipoprotein E E4, gait, and cognition in neurodegenerative diseases: ONDRI study.

Apolipoprotein E E4 allele (APOE E4) and slow gait are independently associated with cognitive impairment and dementia. However, it is unknown whether their coexistence is associated with poorer cognitive performance and its underlying mechanism in neurodegenerative diseases. Gait speed, APOE E4, cognition, and neuroimaging were assessed in 480 older adults with neurodegeneration. Participants were grouped by APOE E4 presence and slow gait. Mediation analyses were conducted to determine if brain structures could explain the link between these factors and cognitive performance. APOE E4 carriers with slow gait had the lowest global cognitive performance and smaller gray matter volumes compared to non-APOE E4 carriers with normal gait. Coexistence of APOE E4 and slow gait best predicted global and domain-specific poorer cognitive performances, mediated by smaller gray matter volume. Gait slowness in APOE E4 carriers with neurodegenerative diseases may indicate extensive gray matter changes associated with poor cognition. APOE E4 and slow gait are risk factors for cognitive decline in neurodegenerative diseases. Slow gait and smaller gray matter volumes are associated, independently of APOE E4. Worse cognition in APOE E4 carriers with slow gait is explained by smaller GM volume. Gait slowness in APOE E4 carriers indicates poorer cognition-related brain changes.

Examining Demographic Factors, Psychosocial Wellbeing and Cardiovascular Health in Subjective Cognitive Decline in the Brain Health Registry Cohort

BackgroundSubjective cognitive decline (SCD) is defined as an individual’s perception of sustained cognitive decline compared to their normal state while still performing within boundaries for normal functioning. Demographic, psychosocial and medical factors have been linked to age-related cognitive decline, and Alzheimer’s dementia (AD). However, their relation to risk for SCD remains unclear. This study aims to identify demographic factors, psychosocial and cardiovascular health associated with SCD within the Brain Health Registry (BHR) online cohort.MethodsParticipants aged 55+ (N=27,596) in the BHR self-reported SCD measured using the Everyday Cognition Scale (ECog) and medical conditions, depressive symptoms, body mass index, quality of sleep, health, family history of AD, years of education, race, ethnicity and gender. Multivariable linear regression was used to examine whether SCD was associated with demographic, psychosocial, and medical conditions.ResultsWe found that advanced age, depressive symptoms, poorer sleep quality and poorer quality of health were positively associated with more self-reported SCD in all models. No race or ethnicity differences were found in association with SCD. Males who reported alcohol and tobacco use or underweight BMI had higher ECog scores compared with females.ConclusionIn addition to well-established risk factors for cognitive decline, such as age, our study consistently and robustly identified a strong association between psychosocial factors and self-reported cognitive decline in an online cohort. These findings provide further evidence that psychosocial health plays a pivotal role in comprehending the risk of SCD and early-stage cognitive ageing. Our findings emphasise the significance of psychosocial factors within the broader context of cardiovascular and demographic risk factors.

The Social and Cognitive Online Training (SCOT) project: A digital randomized controlled trial to promote socio-cognitive well-being in older adults

ObjectivesEffective prevention programs targeting risk factors for cognitive decline in the elderly are recommended given the progressive increase in the aging of the general population. The Social and Cognitive Online Training (SCOT) project is a randomized, controlled, parallel clinical trial designed to prevent the age-related decline in executive and social functions. MethodsThe study included 60 cognitively healthy older adults (age = 71.8±5.3, education = 12.3±3.7, MoCA = 25.1±2.4). Participants underwent a baseline clinical and neuropsychological assessment and were then assigned to either an experimental group (SCOT) or a non-specific cognitive training group (CON). Both 8-week digital interventions included two individual cognitive training sessions and one group meeting per week. Post-intervention assessment evaluated the efficacy of the training on specific outcome measures: the Tower of London for executive functioning, the Ekman-60 Faces test, and the Mini-Social cognition & Emotional Assessment battery for social cognition. A measure of loneliness was included as an exploratory outcome. ResultsBaseline demographic and neuropsychological characteristics were balanced between SCOT (n = 29) and CON (n = 28) groups. Pre-post-intervention analyses showed improvements in executive functioning and social cognition in both groups, without significant interaction effects. Exploratory post-hoc analyses stratifying the SCOT group by training performance showed significant post-training improvements in executive functioning, emotion recognition, and cognitive theory of mind for high-performing participants. DiscussionResults provide preliminary evidence for the beneficial effects of SCOT training, particularly for those who performed best during the training. The SCOT training could represent a new intervention to promote socio-cognitive well-being in the context of active ageing and dementia prevention.

Nutrition is associated with differences in multisensory integration in healthy older adults

ABSTRACT Diet can influence cognitive functioning in older adults and is a modifiable risk factor for cognitive decline. However, it is unknown if an association exists between diet and lower-level processes in the brain underpinning cognition, such as multisensory integration. We investigated whether temporal multisensory integration is associated with daily intake of fruit and vegetables (FV) or products high in fat/sugar/salt (FSS) in a large sample (N = 2,693) of older adults (mean age = 64.06 years, SD = 7.60; 56% female) from The Irish Longitudinal Study on Ageing (TILDA). Older adults completed a Food Frequency Questionnaire from which the total number of daily servings of FV and FSS items respectively was calculated. Older adults’ susceptibility to the Sound Induced Flash Illusion (SIFI) measured the temporal precision of audio-visual integration, which included three audio-visual Stimulus Onset Asynchronies (SOAs): 70, 150 and 230 ms. Older adults who self-reported a higher daily consumption of FV were less susceptible to the SIFI at the longest versus shortest SOAs (i.e. increased temporal precision) compared to those reporting the lowest daily consumption (p = .013). In contrast, older adults reporting a higher daily consumption of FSS items were more susceptible to the SIFI at the longer versus shortest SOAs (i.e. reduced temporal precision) compared to those reporting the lowest daily consumption (p < .001). The temporal precision of multisensory integration is differentially associated with levels of daily consumption of FV versus products high in FSS, consistent with broader evidence that habitual diet is associated with brain health.

Polygenic burden and its association with baseline cognitive function and postoperative cognitive outcome in temporal lobe epilepsy

ObjectiveDemographic and disease factors are associated with cognitive deficits and postoperative cognitive declines in adults with pharmacoresistant temporal lobe epilepsy (TLE), but the role of genetic factors in cognition in TLE is not well understood. Polygenic scores (PGS) for neurological and neuropsychiatric disorders and IQ have been associated with cognition in patient and healthy populations. In this exploratory study, we examined the relationship between PGS for Alzheimer’s disease (AD), depression, and IQ and cognitive outcomes in adults with TLE. Methods202 adults with pharmacoresistant TLE had genotyping and completed neuropsychological evaluations as part of a presurgical work-up. A subset (n = 116) underwent temporal lobe resection and returned for postoperative cognitive testing. Logistic regression was used to determine if PGS for AD, depression, and IQ predicted baseline domain-specific cognitive function and cognitive phenotypes as well as postoperative language and memory decline. ResultsNo significant findings survived correction for multiple comparisons. Prior to correction, higher PGS for AD and depression (i.e., increased genetic risk for the disorder), but lower PGS for IQ (i.e., decreased genetic likelihood of high IQ) appeared possibly associated with baseline cognitive impairment in TLE. In comparison, higher PGS for AD and IQ appeared as possible risk factors for cognitive decline following temporal lobectomy, while the possible relationship between PGS for depression and post-operative cognitive outcome was mixed. SignificanceWe did not observe any relationships of large effect between PGS and cognitive function or postsurgical outcome; however, results highlight several promising trends in the data that warrant future investigation in larger samples better powered to detect small genetic effects.

A high fat diet potentiates neonatal iron overload-induced memory impairments in rats.

The present study aimed at evaluating possible synergistic effects between two risk factors for cognitive decline and neurodegenerative disorders, i.e. iron overload and exposure to a hypercaloric/hyperlipidic diet, on cognition, insulin resistance, and hippocampal GLUT1, GLUT3, Insr mRNA expression, and AKT phosporylation. Male Wistar rats were treated with iron (30mg/kg carbonyl iron) or vehicle (5% sorbitol in water) from 12 to 14th post-natal days. Iron-treated rats received a standard laboratory diet or a high fat diet from weaning to adulthood (9months of age). Recognition and emotional memory, peripheral blood glucose and insulin levels were evaluated. Glucose transporters (GLUT 1 and GLUT3) and insulin signaling were analyzed in the hippocampus of rats. Both iron overload and exposure to a high fat diet induced memory deficits. Remarkably, the association of iron with the high fat diet induced more severe cognitive deficits. Iron overload in the neonatal period induced higher insulin levels associated with significantly higher HOMA-IR, an index of insulin resistance. Long-term exposure to a high fat diet resulted in higher fasting glucose levels. Iron treatment induced changes in Insr and GLUT1 expression in the hippocampus. At the level of intracellular signaling, both iron treatment and the high fat diet decreased AKT phosphorylation. The combination of iron overload with exposure to a high fat diet only led to synergistic deleterious effect on emotional memory, while the effects induced by iron and by the high fat diet on AKT phosphorylation were comparable. These findings indicate that there is, at least to some extent, an additive effect of iron combined with the diet. Further studies investigating the mechanisms associated to deleterious effects on cognition and susceptibility for the development of age-associated neurodegenerative disorders are warranted.

Which Are the Most Reliable Sleep Parameters that Predict Cognitive Decline and Alzheimer's Disease?

Sleep disorders can represent an independent risk factor for cognitive decline and Alzheimer's disease (AD). It remains to be clarified if specific sleep parameters could be considered biomarkers of AD-related neurodegeneration. Several studies solely investigated the results of cross-sectional research, without providing conclusive evidence. Few longitudinal studies showed some inconsistencies in macrostructural and microstructural sleep findings. Methodological heterogeneity among studies can explain the discrepancies in the results. Moreover, the polysomnographic findings are usually related to only one-night recording. The combination of actigraphic recordings with sleep EEG monitoring for some consecutive days should be considered in future research.

Association between abdominal adiposity and cognitive decline in older adults: a 10-year community-based study

ObjectivesThis study aimed to investigate the association between abdominal adiposity and change in cognitive function in community-dwelling older adults. Design, Setting, and ParticipantsThis longitudinal study included older adults aged ≥60 years without cognitive impairment who participated in the National Institute for Longevity Sciences – Longitudinal Study of Aging. MeasurementsCognitive function was evaluated biennially using the Mini-Mental State Examination (MMSE) over 10 years. Waist circumference (WC) was measured at the naval level, and subcutaneous fat area (SFA) and visceral fat area (VFA) were assessed using baseline computed tomography scans. WC, SFA, and VFA areas were stratified into sex-adjusted tertiles. A linear mixed model was applied separately for men and women. ResultsThis study included 873 older adults. In men, the groups with the highest levels of WC, SFA, and VFA exhibited a greater decline in MMSE score than the groups with the lowest levels (β [95% confidence interval]: WC, –0.12 [–0.23 to –0.01]; SFA, –0.13 [–0.24 to –0.02]; VFA, –0.11 [–0.22 to –0.01]). In women, the group with the highest level of WC and SFA showed a greater decline in MMSE score than the group with the lowest level (WC, –0.12 [–0.25 to –0.01]; SFA, –0.18 [–0.30 to –0.06]), but VFA was not associated with cognitive decline. ConclusionHigher WC, SFA, and VFA in men and higher WC and SFA in women were identified as risk factors for cognitive decline in later life, suggesting that abdominal adiposity involved in cognitive decline may differ according to sex.

Social Disconnectedness, Perceived Loneliness, and Cognitive Functioning: The Role of Neighborhood Environment.

Social disconnectedness and loneliness pose significant challenges for older Chinese immigrants. Yet, it remains unclear whether they are associated with an increased risk of cognitive decline in this population. This study aimed to investigate the association of social disconnectedness and loneliness with cognitive functioning and examine the moderation role of neighborhood contexts. This longitudinal analysis examined a sample of individuals aged 60 years and older from the Population Study of Chinese Elderly in Chicago (N = 2,044). Global cognition was assessed using the averaged z-scores of cognitive performance tests. Social disconnectedness was constructed using 5 indicators about structural aspects of social relationships. Loneliness was assessed with the R-UCLA loneliness scale. Neighborhood socioeconomic status (NSES) and neighborhood segregation index were constructed using 2010-2014 American Community Survey data at the census tract level. Individual perceptions about neighborhood environments were used to construct neighborhood cohesion index and neighborhood disorder index (NDI). Latent growth curve models with adjusted cluster robust standard errors were estimated. More loneliness was associated with a higher level of initial cognitive functioning (B = 0.030, p < .01), but also with a faster decline rate over time (B = -0.007, p < .01) after adjusting for covariates. High NSES and less neighborhood segregation buffered the negative effects of loneliness on cognitive decline, respectively. High NDI amplified the positive relationship between loneliness and initial functioning, but accelerated the rate of cognitive decline associated with loneliness. The study revealed that perceived loneliness, but not social disconnectedness, is a risk factor for cognitive decline among older Chinese immigrants. Living in a neighborhood with low socioeconomic status, more segregation, and high disorder elevated the detrimental effect of loneliness on long-term cognitive decline. Further research needs to investigate the complex interplay between social relationships, neighborhood environment, and cognition.

Neuropsychiatric symptoms and ApoE genotype in older adults without dementia: a cross-sectional study.

The ApoE genotype and neuropsychiatric symptoms (NPS) are known risk factors for cognitive decline in older adults. However, the interaction between these variables is still unclear. The aim of this study was to determine the association between the presence of the ApoE ε4 allele and the occurrence of NPS in older adults without dementia. In this cross-sectional investigation we determined the apolipoprotein E (ApoE) genotype of 74 older adults who were either cognitively normal (20.3% / Clinician Dementia Rating Scale (CDR): 0) or had mild cognitive impairment (MCI: 79.7% / CDR: 0.5). We used a comprehensive cognitive assessment protocol, and NPS were estimated by the Neuropsychiatric Inventory-Clinician Rating Scale (NPI-C), Mild Behavioural Impairment-Checklist (MBI-C), Hamilton Rating Scale for Depression (HAM-D), and Apathy Inventory. ApoE ε4 carriers had higher MBI-C total scores than ApoE ε4 noncarriers. Correlations between NPS and ApoE genotype were observed for two NPI-C domains, although in opposite directions: the ApoE ε4 allele was associated with a 1.8 unit decrease in the estimated aberrant motor disturbance score and with a 1.3 unit increase in the estimated appetite/eating disorders score. All fitted models were significant, except for the one fitted for the domain delusions from the NPI-C. Among individuals with amnestic MCI, ε4 carriers presented higher depression score (HAM-D) than noncarriers; in turn, ε4 noncarriers exhibited higher aggression score (NPI-C) than ε4 carriers. Our analyses showed associations between NPS and the presence of the ApoE ε4 allele in two NPI-C domains, despite the sample size. Furthermore, compared to noncarriers, the presence of the ApoE ε4 correlated positively with appetite/eating disorders and negatively with aberrant motor disturbance domain. Examination of the amnestic MCI group displayed significant, although weak, associations. Therefore, ε4 carriers exhibited higher depression scores according to the HAM-D scale compared to ε4 noncarriers. Conversely, ε4 noncarriers had higher scores in the aggression domain of the NPI-C than ε4 carriers.

Montelukast Ameliorates 2K1C-Hypertension Induced Endothelial Dysfunction and Associated Vascular Dementia.

Declined kidney function associated with hypertension is a danger for cognitive deficits, dementia, and brain injury. Cognitive decline and vascular dementia (VaD) are serious public health concerns, which highlights the urgent need for study on the risk factors for cognitive decline. Cysteinyl leukotriene (CysLT1) receptors are concerned with regulating cognition, motivation, inflammatory processes, and neurogenesis. This research aims to examine the consequence of montelukast (specific CysLT1 antagonist) in renovascular hypertension 2-kidney-1-clip-2K1C model-triggered VaD in experimental animals. 2K1C tactics were made to prompt renovascular hypertension in mature male rats. Morris water maze was employed to measure cognition. Mean arterial pressure (MAP), serum nitrite levels, aortic superoxide content, vascular endothelial activity, brain's oxidative stress (diminished glutathione, raised lipid peroxides), inflammatory markers (IL-10, IL-6, TNF-α), cholinergic activity (raised acetylcholinesterase), and cerebral injury (staining of 2, 3, 5- triphenylterazolium chloride) were also examined. Montelukast in doses of 5.0 and 10.0 mg kg-1 was used intraperitoneally as the treatment drug. Along with cognitive deficits, 2K1C-operated rats showed elevated MAP, endothelial dysfunction, brain oxidative stress, inflammation, and cerebral damage with diminished serum nitrite/nitrate. Montelukast therapy significantly and dose-dependently mitigated the 2K1Chypertension-provoked impaired behaviors, biochemistry, endothelial functions, and cerebral infarction. The 2K1C tactic caused renovascular hypertension and associated VaD, which was mitigated via targeted regulation of CysLT1 receptors by montelukast administration. Therefore, montelukast may be taken into consideration for the evaluation of its complete potential in renovascular-hypertension-induced VaD.

Enhancing cognitive function in older adults: dietary approaches and implications.

Natural aging encompasses physiological and psychological changes that impact overall health and quality of life. Mitigating these effects requires physical and mental exercise, coupled with proper nutrition. Notably, protein malnutrition emerges as a potential risk factor for senile dementia, with insufficient intake correlating with premature cognitive decline. Adequate protein intake in the elderly positively associates with memory function and lowers cognitive impairment risk. Considering diet as a modifiable risk factor for cognitive decline, extensive research has explored diverse dietary strategies to prevent dementia onset in older adults. However, conclusive results remain limited. This review aims to synthesize recent evidence on effective dietary approaches to enhance cognitive function and prognosis in older individuals. Specifically, the study evaluates complex multicomponent programs, protein-rich diets, and branched-chain amino acid supplementation. By addressing the nexus of nutrition and cognitive health, this review contributes to understanding viable interventions for promoting cognitive well-being in aging populations.

Cognitive Impairment in Renal Replacement Therapy: Comparison between Methods

Cognitive impairment (CI) can be defined as a clinical syndrome characterized by a decline in at least two of several domains of cognitive function. Chronic kidney disease (CKD) is an independent risk factor for cognitive decline, and the prevalence in patients with end-stage renal disease is estimated at 50% - 80%. However, it appears that CI in patients on renal replacement therapy (RRT) may be underdiagnosed. In this cross-sectional study, 33 patients on Peritoneal Dialysis from the AOU Federico II were recruited, and matched by sex, age, and dialysis age to 33 patients on Hemodialysis and 33 controls belonging to healthy volunteers. The total 66 patients and their 33 controls were assessed for cognitive function using the Cognitive Reserve Index Questionnaire (CRIq) test. Between PD and HD patients, a statistically significant difference emerged in all subscores and in the total CRI. Between PD patients and controls, a statistically significant difference emerged in education, CRI- CRI-leisure time, and the total CRI. Therefore, CI may occur in patients undergoing PD earlier and with a greater frequency than in the general population, but with a lower incidence than in patients on HD. These considerations should be communicated to patients when they are educated about different replacement methods.