Risk Factor For Cognitive Decline Research Articles

Design and Methods of the Early Age-Related Hearing Loss Investigation Randomized Controlled Trial.

Hearing loss has been identified as a major modifiable risk factor for cognitive decline. The Early Age-Related Hearing Loss Investigation (EARHLI) study will assess the mechanisms linking early age-related hearing loss (ARHL) and cognitive impairment. Randomized, controlled, single-site, early phase II, superiority trial. Tertiary academic medical center. One hundred fifty participants aged 55 to 75 years with early ARHL (severity defined as borderline to moderate) and amnestic mild cognitive impairment will be included. Participants will be randomized 1:1 to a best practice hearing intervention or a health education control. The primary study outcome is cognition measured by the Alzheimer Disease Cooperative Study-Preclinical Alzheimer Cognitive Composite. Secondary outcomes include additional measures of cognition, social engagement, and brain organization/connectivity. Trial enrollment will begin in early 2024. After its completion in 2028, the EARHLI trial should offer evidence on the effect of hearing treatment versus a health education control on cognitive performance, social engagement, and brain organization/connectivity in 55- to 75-year-old community-dwelling adults with early ARHL and amnestic mild cognitive impairment.

Relationship between Social Participation and Cognitive Impairment in Low-Educated Older Adults Based on Indonesian Family Life Survey-5.

The increasing older adult population requires attention in terms of education and health, as higher education levels contribute to cognitive reserve and may protect against age-related cognitive impairment. Cognitive reserve is an individual's cognitive flexibility in using cognitive functions affected by brain aging, neurological diseases, and injury. Indonesia has a high prevalence of low-educated older adults, which strongly correlates with progressive cognitive impairment. Identifying risk factors for cognitive decline in this population is crucial. This study determines the factors affecting cognitive impairment in low-educated older adults using cross-sectional data from the Indonesian Family Life Survey-5. This descriptive study analyzed 2,313 low-educated older adults ≥60 years old. Univariate and bivariate analyses were used to describe the sample and identify the relationships between categorical variables. Logistic regression identified the most significant factor affecting cognitive impairment. The prevalence of cognitive impairment in low-educated older adults is 22.6%. The chi-square test revealed significant relationships between those who are aged 75 years, a status other than married, female, living in rural areas, and not participating in social activities. Age is the most prominent factor affecting cognitive impairment in such adults (P<0.001; adjusted odds ratio, 3.232; 95% confidence interval, 2.500-4.180). Cognitive impairment in the aforementioned adults is associated with being ≥75 years old, being a status other than married, being female, living in rural areas, and not participating in social activities. After controlling other variables, low-educated older adults who participated in at least ≥1 social activity in the last 12 months experienced cognitive impairment 0.64 times compared to those who did not participate in social activities.

The taxonomy of subjective cognitive decline: proposal and first clinical evidence from the Geneva memory clinic cohort.

Subjective Cognitive Decline (SCD) is characterized by subjective cognitive concerns without objective cognitive impairment and is considered a risk factor for cognitive decline and dementia. However, most SCD patients will not develop neurodegenerative disorders, yet they may suffer from minor psychiatric, neurological, or somatic comorbidities. The aim of the present study is to provide a taxonomy of the heterogeneous SCD entity by isolating homogenous SCD subgroups with specific clinical features and cognitive trajectoriesand to conduct a preliminary validation using data from a memory clinic sample. Participants were fifty-five SCD individuals consecutively recruited at the Geneva Memory Center. Based on clinical reports, they were classified into three clinically pre-defined subgroups: (i) those with psychological or psychiatric comorbidities (Psy), (ii) those with somatic comorbidities (SomCom), (iii) and those with no apparent cause (NAC). Baseline demographics, clinical, cognitive, and biomarker differences among the SCD subgroups were assessed. Longitudinal cognitive changes (average 3 years follow-up) were modeled using a linear mixed model. Out of the 55 SCD cases, 16 were SomCom, 18 Psy, and 21 NAC. 47% were female, mean age was 71 years. We observed higher frequency of APOE ε4 carriers in NAC (53%) compared to SomCom (14%) and Psy (0%, P=0.023) and lower level of plasma Aβ42 in NAC (6.8±1.0) compared to SomCom (8.4±1.1; P=0.031). SomCom subjects were older (74 years) than Psy (67 years, P=0.011), and had greater medial temporal lobe atrophy (1.0±1.0) than Psy (0.2±0.6) and NAC (0.4±0.5, P=0.005). SomCom have worse episodic memory performances (14.5±3.5) than Psy (15.8±0.4) and NAC (15.8±0.7, P=0.032). We observed a slightly steeper, yet not statistically significant, cognitive decline in NAC (β=-0.48) compared to Psy (β=-0.28) and SomCom (β=-0.24). NAC feature higher proportion of APOE ε4 carriers, lower plasma Aβ42 and a trend towards steeper cognitive decline than SomCom and Psy. Taken together, these findings suggest that NAC are at higher risk of cognitive decline due to AD. The proposed clinical taxonomy might be implemented in clinical practice to identify SCD at higher risk. However, such taxonomy should be tested on an independent cohort with larger sample size.

Modifiable Risk Factors Associated With Cognitive Decline in Late Life Depression: Findings From the Canadian Longitudinal Study on Aging: Facteurs de risque modifiables associés au déclin cognitif dans la dépression en fin de vie : constatations de l'Étude longitudinale canadienne sur le vieillissement.

Depression in later life is associated with a two-fold increased risk of dementia. It is not clear to what extent potentially modifiable risk factors account for this association. Older adults (age 50 + ) with objective health measures (n = 14,014) from the Canadian Longitudinal Study on Aging were followed for a mean duration of 35 months. Linear regression analyses were used to determine if clinically significant depression (Centre for Epidemiologic Studies Depression scale score (CESD) ≥ 10) was associated with global cognitive decline, assessed with a neuropsychological battery during follow-up, and if modifiable risk factors mediated this association. Depression was associated with an excess of risk factors for cognitive decline including: vascular disease, hypertension, diabetes, apnoea during sleep, higher body mass index, smoking, physical inactivity and lack of social participation. In regression analyses depression remained independently associated with cognitive decline over time (beta -0.060, P = 0.038) as did cerebrovascular disease (beta -0.197, P < 0.001), HbA1C (beta -0.059, P < 0.001), visual impairment (beta -0.070, P = 0.007), hearing impairment (beta -0.098, P < 0.001) and physical inactivity (beta -0.075, P = 0.014). In mediation analyses, we found that cerebrovascular disease (z = -3.525, P < 0.001), HbA1C (z = -4.976, P < 0.001) and physical inactivity (z = -3.998, P < 0.001) partially mediated the association between depression and cognitive decline. In this large sample of Canadian older adults incorporating several objective health measures, older adults with depression were at increased risk of cognitive decline and had an excess of potentially modifiable risk factors. Clinicians should pay particular attention to control of diabetes, physical inactivity and risk factors for cerebrovascular disease in older adults presenting with depression as they can contribute to accelerated cognitive decline and may be addressed during routine clinical care.

Multi-night acoustic stimulation is associated with better sleep, amyloid dynamics, and memory in older adults with cognitive impairment.

Sleep is a potential early, modifiable risk factor for cognitive decline and dementia. Impaired slow wave sleep (SWS) is pronounced in individuals with cognitive impairment (CI). Cognitive decline and impairments of SWS are bi-directionally linked in a vicious cycle. SWS can be enhanced non-invasively using phase-locked acoustic stimulation (PLAS), potentially breaking this vicious cycle. Eighteen healthy older adults (HC, agemean±sd, 68.3 ± 5.1) and 16 older adults (agemean±sd, 71.9 ± 3.9) with CI (Montreal Cognitive Assessment ≤ 25) underwent one baseline (sham-PLAS) night and three consecutive stimulation nights (real-PLAS). EEG responses and blood-plasma amyloid beta Aβ42/Aβ40 ratio were measured pre- and post-intervention, as was episodic memory. The latter was again evaluated 1week and 3months after the intervention. In both groups, PLAS induced a significant electrophysiological response in both voltage- and time-frequency analyses, and memory performance improved in association with the magnitude of this response. In the CI group, both electrophysiological and associated memory effects were delayed compared to the healthy group. After 3 intervention nights, electrophysiological response to PLAS was no longer different between CI and HC groups. Only in the CI sample, stronger electrophysiological responses were significantly associated with improving post-intervention Aβ42/Aβ40 ratios. PLAS seems to improve SWS electrophysiology, memory, and amyloid dynamics in older adults with CI. However, effects on memory require more time to unfold compared to healthy older adults. This indicates that PLAS may become a potential tool to ameliorate cognitive decline, but longer interventions are necessary to compensate for declining brain integrity. This study was pre-registered (clinicaltrials.gov: NCT04277104).

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.

Propofol enhancement of slow wave sleep to target the nexus of geriatric depression and cognitive dysfunction: protocol for a phase I open label trial

IntroductionLate-life treatment-resistant depression (LL-TRD) is common and increases risk for accelerated ageing and cognitive decline. Impaired sleep is common in LL-TRD and is a risk factor for cognitive decline. Slow...

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

Academic and emotional challenges faced by medical students can affect their psychological well-being and health. Personal characteristics may also predispose one to the manifestation of distress reactions. Individuals with type D personality have an increased tendency to develop depressive reactions and somatic diseases, including the presence of cognitive dysfunction. In students, the presence of cognitive dysfunction may additionally adversely affect academic and psycho-emotional problems. The purpose of this study was to examine the influence of type D personality and coping strategies on cognitive functioning in medical students. A cross-sectional study included 258 medical students (age 19 ± 1.2 years, 79 men). All participants completed psychological questionnaires (DS-14 to identify type D personality, and The Coping Strategy Indication, CSI-to determine coping strategies), as well as extensive neuropsychological testing of cognitive functions. Among the medical students examined, the frequency of identification of type D personality was 44%. In persons with personality type D, according to psychometric testing, a decrease in the level of functional mobility of nervous processes (FMNP) was noted, which was manifested in an increase in the test completion time (p < 0.001) and an increase in the number of errors (p < 0.001) during the FMNP test, and an increase in the test completion time in the attention concentration test. In addition, in type D participants, an increase in the test execution time during the attention test was noted (p = 0.007). Personality type D was an independent risk factor for cognitive decline in students in multiple linear regression analysis, when type D was analyzed as a dichotomous construct. Assessing personal characteristics and identifying personality type D is advisable for medical students, to develop subsequent programs to increase their resistance to academic challenges, improve cognitive function, and also to prepare for future stress loads during professional activities in the field of healthcare.

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.

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 increasing 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 prebiotic with several biological advantages, and can selectively promote the growth of beneficial microorganisms 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.

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.

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.

Abstract 44: Soluble CD14 and Risk of Incident Cognitive Impairment: The Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study

Introduction: Black adults in the U.S. experience a greater burden of systemic inflammation and cognitive impairment and dementia compared with White adults. Increasing evidence suggests peripheral inflammation is a risk factor for cognitive decline, however few longitudinal studies have investigated these relationships. CD14 is a pattern recognition receptor expressed by monocytes and macrophages that promotes inflammation. Concentrations of the soluble form of CD14 (sCD14) vary by race, and higher sCD14 was associated with incident coronary heart disease (CHD) and stroke in Black but not White participants in the REGARDS cohort study. We hypothesized higher sCD14 would also be more strongly associated with incident cognitive impairment (ICI) in Black compared to White adults. Methods: We performed a nested case-control study of ICI in the REGARDS study, a biracial cohort of 30,239 American adults ≥45 years old. Cases were 495 participants without cognitive impairment or stroke at baseline who developed ICI during a median 3.5 years of follow-up based on abnormal scores on ≥2 of 3 cognitive tests. 587 controls were selected from a cohort random sample and free of cognitive impairment or stroke at baseline. Logistic regression models estimated odds ratios (OR) of ICI by concentration of sCD14 measured from stored baseline serum samples. We tested for a sCD14-by-race interaction a priori. Results: The sCD14-by-race interaction term was statistically significant in each model (p-interaction &lt;0.05). In analyses stratified by race, adjusting for demographic factors (age, sex, and region), a 1-SD increment sCD14 was associated with a 40% higher odds of ICI among Black adults (OR: 1.40; 95% CI: 1.07, 1.95) with no association among White adults (OR: 1.08; 95% CI: 0.90, 1.28). In models adjusted for cognitive and vascular risk factors (income, education, systolic blood pressure, hypertension medication use, dyslipidemia, BMI, history of heart disease, atrial fibrillation, diabetes, smoking, and alcohol use), the relationship was attenuated in Black participants (OR: 1.33; 95% CI: 0.96, 1.84) and remained null among White participants (OR: 0.99; 95% CI: 0.81, 1.22). Comparing those with sCD14 concentration &gt;90th percentile to below, adjusted for risk factors, Black participants had a 2.47 (95% CI: 1.08, 5.67) higher odds of ICI with no association in White participants (OR: 0.91; 95% CI: 0.46, 1.80). Discussion: Higher sCD14 was associated with ICI risk in Black but not White adults, similar to prior observations for stroke. Results suggest that sCD14-associated inflammatory responses may be a risk factor for ICI among Black adults.

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.

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.

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.

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.