Exploring the risk of microplastics to pollinators: focusing on honey bees.

The rapid increase in global plastic production and usage has led to global environmental contamination, with microplastics (MPs) emerging as a significant concern. Pollinators provide a crucial ecological service, while bee populations have been declining in recent years, and MPs have been recognized as a new risk factor contributing to their losses. Despite the pervasive distribution and persistence of MPs, understanding their risks to honey bees remains a critical knowledge gap. This review summarizes recent studies that investigate the toxicity of MPs on honey bee health from different perspectives. The findings revealed diverse and material-/size-/dosage-dependent outcomes, emphasizing the need for comprehensive assessments in the follow-up studies. MPs have been detected in honey and in bees' organs (e.g., gut and brain), posing potential threats to bee fitness, including altered behavior, cognitive abilities, compromised immunity, and dysfunction of the gut microbiota. It should be noticed that despite several laboratory studies suggesting the aforementioned adverse effects of MPs, field/semi-field experiments are still warranted. The synergistic toxicity of MPs with other environmental contaminants (pesticides, antibiotics, fungicides, heavy metals, etc.) still requires further investigation. Our review highlights the critical need to understand the relationships between MPs, pollinators, and the ecosystem to mitigate potential risks and ensure the sustainability of vital services provided by honey bees.

Correlations between plasma markers and brain Aß deposition across the AD continuum: Evidence from SILCODE.

BACKGROUND: Previous studies have found that Alzheimer's disease (AD)-related plasma markers are associated with amyloid beta (Aß) deposition, but the change of this association in different Aß pathological stages remains unclear. METHODS: Data were obtained from the SILCODE. According to the standardized uptake value ratio (SUVR) and Aß stage classification, correlation analysis was performed among plasma biomarkers, and voxel/SUVR values in the regions of interest (ROI) and clinical scale information, respectively. Mediation analysis was used to study the possible pathways. RESULTS: The proportion of cognitively normal (CN) and subjective cognitive decline (SCD) was the highest in stages A0 to 1, while in stages A2 to 4, the proportion of mild cognitive impairment (MCI) and AD increased. Plasma phosphorylated tau (p-tau)181 and glial fibrillary acidic protein (GFAP) levels were significantly lower in stage A0 compared to the later phases. Two pathways demonstrated fully mediated effects: positron emission tomography (PET) SUVR-plasma p-tau181-Mini-Mental State Examination (MMSE) and PET SUVR-plasma GFAP-MMSE. DISCUSSION: This study demonstrated the role of plasma biomarkers in the early stage of AD, especially in SCD, from both the clinical diagnosis and Aß stage dimensions. HIGHLIGHTS: Plasma ptau181 and GFAP level serve as indicators of early Alzheimer's disease and the pathologic Aß staging classification. A possible ceiling effect of GFAP was observed in the mid-to-late stages of the AD course. This study confirms the role of AD plasma markers in promoting Aß deposition at an early stage, particularly in females with subjective cognitive decline(SCD). The overlapping brain regions of plasma p-tau181, GFAP, and neurofilament light for Aß deposition in the brain in early AD were distributed across various regions, including the posterior cingulate gyrus, rectus gyrus, and inferior temporal gyrus.

State-Level Education Quality and Trajectories of Cognitive Function by Race and Educational Attainment.

Policy Points Education-cognition research overlooks the role of education quality in shaping cognitive function at midlife and older ages, even though quality may be more responsive to federal and state investment in public schooling than attainment. For older US adults who attended school during the early to mid-20th century, the quality of US education improved considerably as federal and state investment increased. Ensuring access to high-quality primary and secondary education may protect against poor cognitive function at midlife and older ages, particularly among Black Americans and persons who complete less education. It may also play an important role in reducing health inequities. CONTEXT: Although educational attainment is consistently associated with better cognitive function among older adults, we know little about how education quality is related to cognitive function. This is a key gap in the literature given that the quality of US education improved considerably during the early to mid-20th century as state and federal investment increased. We posit that growing up in states with higher-quality education systems may protect against poor cognitive function, particularly among Black adults and adults who completed fewer years of school. METHODS: We used prospective data on cognitive function from the Health and Retirement Study linked to historical data on state investment in public schools, restricting our sample to non-Hispanic White and Black adults born between 1914 and 1959 (19,096 White adults and 4,625 Black adults). Using race-stratified linear mixed models, we considered if state-level education quality was associated with level and decline in cognitive function and if these patterns differed by years of schooling and race. FINDINGS: Residing in states with higher-resourced education systems during childhood was associated with better cognitive function, particularly among those who completed less than 12 years of schooling, regardless of race. For White adults, higher-resourced state education systems were associated with higher scores of total cognitive function and episodic memory, but there were diminishing returns as resources increased to very high levels. For Black adults, the relationship between state education resources and cognitive function varied by age with positive associations in midlife and generally null or negative associations at the oldest ages. CONCLUSIONS: Federal and state investment in public schools may provide students with opportunities to develop important cognitive resources during schooling that translate into better cognitive function in later life, especially among marginalized populations.

Predicting progression from subjective cognitive decline to mild cognitive impairment or dementia based on brain atrophy patterns.

BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder where pathophysiological changes begin decades before the onset of clinical symptoms. Analysis of brain atrophy patterns using structural MRI and multivariate data analysis are an effective tool in identifying patients with subjective cognitive decline (SCD) at higher risk of progression to AD dementia. Atrophy patterns obtained from models trained to classify advanced AD versus normal subjects, may not be optimal for subjects at an early stage, like SCD. In this study, we compared the accuracy of the SCD progression prediction using the 'severity index' generated using a standard classification model trained on patients with AD dementia versus a new model trained on ß-amyloid (Aß) positive patients with amnestic mild cognitive impairment (aMCI). METHODS: We used structural MRI data of 504 patients from the Swedish BioFINDER-1 study cohort (cognitively normal (CN), Aß-negative = 220; SCD, Aß positive and negative = 139; aMCI, Aß-positive = 106; AD dementia = 39). We applied multivariate data analysis to create two predictive models trained to discriminate CN individuals from either individuals with Aß positive aMCI or AD dementia. Models were applied to individuals with SCD to classify their atrophy patterns as either high-risk "disease-like" or low-risk "CN-like". Clinical trajectory and model accuracy were evaluated using 8 years of longitudinal data. RESULTS: In predicting progression from SCD to MCI or dementia, the standard, dementia-based model, reached 100% specificity but only 10.6% sensitivity, while the new, aMCI-based model, reached 72.3% sensitivity and 60.9% specificity. The aMCI-based model was superior in predicting progression from SCD to MCI or dementia, reaching a higher receiver operating characteristic area under curve (AUC = 0.72; P = 0.037) in comparison with the dementia-based model (AUC = 0.57). CONCLUSION: When predicting conversion from SCD to MCI or dementia using structural MRI data, prediction models based on individuals with milder levels of atrophy (i.e. aMCI) may offer superior clinical value compared to standard dementia-based models.

Modern neurophysiological techniques indexing normal or abnormal brain aging.

Brain aging is associated with a decline in cognitive performance, motor function and sensory perception, even in the absence of neurodegeneration. The underlying pathophysiological mechanisms remain incompletely understood, though alterations in neurogenesis, neuronal senescence and synaptic plasticity are implicated. Recent years have seen advancements in neurophysiological techniques such as electroencephalography (EEG), magnetoencephalography (MEG), event-related potentials (ERP) and transcranial magnetic stimulation (TMS), offering insights into physiological and pathological brain aging. These methods provide real-time information on brain activity, connectivity and network dynamics. Integration of Artificial Intelligence (AI) techniques promise as a tool enhancing the diagnosis and prognosis of age-related cognitive decline. Our review highlights recent advances in these electrophysiological techniques (focusing on EEG, ERP, TMS and TMS-EEG methodologies) and their application in physiological and pathological brain aging. Physiological aging is characterized by changes in EEG spectral power and connectivity, ERP and TMS parameters, indicating alterations in neural activity and network function. Pathological aging, such as in Alzheimer's disease, is associated with further disruptions in EEG rhythms, ERP components and TMS measures, reflecting underlying neurodegenerative processes. Machine learning approaches show promise in classifying cognitive impairment and predicting disease progression. Standardization of neurophysiological methods and integration with other modalities are crucial for a comprehensive understanding of brain aging and neurodegenerative disorders. Advanced network analysis techniques and AI methods hold potential for enhancing diagnostic accuracy and deepening insights into age-related brain changes.

Ovomemolins: Egg-derived peptides that improved cognitive decline after oral administration in mice.

Eggs not only contain all the molecules necessary to nurture new life but are also rich in nutrients such as high-quality protein. For example, epidemiologic studies have shown that egg intake is positively correlated with cognitive function. Thus, we specifically examined the effect of ovalbumin, a major protein present in egg whites, on cognitive function. First, we found that an orally administered enzymatic digest of ovalbumin improves cognitive function in mice fed a high-fat diet. Then, we narrowed down candidate peptides based on the prediction of peptide production according to enzyme-substrate specificity and comprehensive peptide analysis of the digest. We found that three peptides, namely ILPEY, LYRGGLEP, and ILELP, improve cognitive function after oral administration. We also showed that ILPEY, LYRGGLEP, and ILELP were present in the digest and named them ovomemolins A (OMA), B, and C, respectively. Notably, ovomemolins are the first peptides derived from egg whites that have been shown to improve cognitive function. The cognitive improvement induced by OMA, the most abundant of the peptides in the digest, was inhibited by methyllycaconitine, an antagonist of α7nAChR, which is known to be related to memory. These results suggest that OMA improves cognitive function through the acetylcholine system. After OMA administration, brain-derived neurotrophic factor (BDNF) mRNA expression and the number of 5-bromo-2'-deoxyuridine-positive cells suggested that OMA increases hippocampal BDNF expression and neurogenesis.

Predictive value of synaptic plasticity for functional decline in patients with multiple sclerosis.

Background: Previous research suggested that quadripulse (QPS)-induced synaptic plasticity is associated with both cognitive and motor function in patients with multiple sclerosis (MS) and does not appear to be reduced compared to healthy controls (HCs). Objective: This study aimed to explore the relationship between the degree of QPS-induced plasticity and clinically significant decline in motor and cognitive functions over time. We hypothesized that MS patients experiencing functional decline would exhibit lower levels of baseline plasticity compared to those without decline. Methods: QPS-induced plasticity was evaluated in 80 MS patients (56 with relapsing-remitting MS and 24 with progressive MS), and 69 age-, sex-, and education-matched HCs. Cognitive and motor functions, as well as overall disability status were evaluated annually over a median follow-up period of 2 years. Clinically meaningful change thresholds were predefined for each outcome measure. Linear mixed-effects models, Cox proportional hazard models, logistic regression, and receiver-operating characteristic analysis were applied to analyse the relationship between baseline plasticity and clinical progression in the symbol digit modalities test, brief visuospatial memory test revised (BVMT-R), nine-hole peg test (NHPT), timed 25-foot walk test, and expanded disability status scale. Results: Overall, the patient cohort showed no clinically relevant change in any functional outcome over time. Variability in performance was observed across time points in both patients and HCs. MS patients who experienced clinically relevant decline in manual dexterity and/or visuospatial learning and memory had significantly lower levels of synaptic plasticity at baseline compared to those without such decline (NHPT: ß = -0.25, p = 0.02; BVMT-R: ß = -0.50, p = 0.005). Receiver-operating characteristic analysis underscored the predictive utility of baseline synaptic plasticity in discerning between patients experiencing functional decline and those maintaining stability only for visuospatial learning and memory (area under the curve = 0.85). Conclusion: Our study suggests that QPS-induced plasticity could be linked to clinically relevant functional decline in patients with MS. However, to solidify these findings, longer follow-up periods are warranted, especially in cohorts with higher prevalences of functional decline. Additionally, the variability in cognitive performance in both patients with MS and HCs underscores the importance of conducting further research on reliable change based on neuropsychological tests.

New method for taxonomic descriptions with coded notation, producing dynamic and interchangeable output.

A proposal for taxonomic species description notation is presented to replace the traditional descriptive texts for a coded matrix, avoiding redundant adjectives and subjective descriptions. This is an attempt to enhance the species description rate and to make the descriptions output available to other scientific disciplines, machine learning, interactive and computer-assisted identification keys, metadata analysis and its applications. The method consists of presenting the description of the overall morphology in a coded matrix, following a character list with detailed observed conditions for each character. The method is dynamic and open to amendments and new data addition as they become available. We test the new method describing five new species of Collembola Symphypleona of the genus Pararrhopalites as a generalized model and made the coded output available. We conclude that a coded taxonomic description is an advance to the traditional taxonomic text, with potential to enhance the global descriptions rate. The generated descriptions are dynamic, expandable and can be easily used in other fields of science, allowing non-experts to access the data for phylogenetic, biogeographic, ecological studies and metadata analysis. Even though an experienced taxonomist will always be necessary to make a detailed taxonomic description, it is a step forward to a general template to semi-automated taxon recognition and to future development of auxiliary tools for species description using machine learning and templates to speed up the time-consuming phase of schematic figures preparation, after the expert interpretations are done.

The McCusker Subjective Cognitive Impairment Inventory (McSCI): a novel measure of perceived cognitive decline.

BACKGROUND: Subjective cognitive decline (SCD), i.e. self/other-reported concerns on one's cognitive functioning without objective evidence of significant decline, is an indicator of dementia risk. There is little consensus on reliability and validity of the available SCD measures. Therefore, introducing a novel and psychometrically sound measure of SCD is timely. OBJECTIVE: The psychometric properties of a new SCD measure, the McCusker Subjective Cognitive Impairment Inventory-Self-Report (McSCI-S), are reported. METHODS: Through review of previously published measures as well as our clinical and research data on people with SCD, we developed a 46-item self-report questionnaire to assess concerns on six cognitive domains, namely, memory, language, orientation, attention and concentration, visuoconstruction abilities and executive function. The McSCI-S was examined in a cohort of 526 participants using factor analysis, item response theory analysis and receiver operating characteristic (ROC) curve. RESULTS: A unidimensional model provided acceptable fit (CFI = 0.94, TLI = 0.94, RMSEA [90% CI] = 0.052 [.049, 0.055], WRMR = 1.45). The McSCI-S internal consistency was excellent (.96). A cut-off score of ≥24 is proposed to identify participants with SCDs. Higher McSCI-S scores were associated with poorer general cognition, episodic verbal memory, executive function and greater memory complaints and depressive scores (P < .001), controlling for age, sex and education. CONCLUSIONS: Excellent reliability and construct validity suggest the McSCI-S estimates SCDs with acceptable accuracy while capturing self-reported concerns for various cognitive domains. The psychometric analysis indicated that this measure can be used in cohort studies as well as on individual, clinical settings to assess SCDs.

Effect of semaglutide on kidney function across different levels of baseline HbA1c, blood pressure, body weight and albuminuria in SUSTAIN 6 and PIONEER 6.

BACKGROUND AND HYPOTHESIS: This post-hoc analysis explored the semaglutide effects on eGFR slope by baseline glycemic control, blood pressure (BP), body mass index (BMI), and albuminuria status in people with type 2 diabetes and high cardiovascular risk. METHODS: Pooled SUSTAIN 6 and PIONEER 6 data were analyzed for change in estimated glomerular filtration (eGFR) slope by baseline HbA1c (<8%/≥8%; <64 mmol/mol/≥64 mmol/mol), systolic BP (<140/90 mmHg/≥140/90 mmHg), and BMI (<30 kg/m2/≥30 kg/m2). SUSTAIN 6 data were analyzed by baseline urinary albumin: creatinine ratio (UACR; <30/30 - 300/>300 mg/g). RESULTS: The estimated absolute treatment differences (ETD) overall in eGFR slope [95% confidence intervals] favored semaglutide versus placebo in the pooled analysis (0.59 [0.29;0.89] mL/min/1.73m2/year) and in SUSTAIN 6 (0.60 [0.24;0.96] mL/min/1.73m2/year); the absolute benefit was consistent across all HbA1c, BP, BMI, and UACR subgroups (all p-interaction > 0.5). CONCLUSION: A clinically meaningful reduction in risk of chronic kidney disease progression was observed with semaglutide versus placebo regardless of HbA1c, BP, BMI, and UACR levels.

Physical decline, falls, and hospitalization among vulnerable older patients in the trajectory of colorectal cancer treatment.

INTRODUCTION: Resilience to anticancer treatment for colorectal cancer (CRC) among older patients varies. Many experience weight loss, physical decline, falls, and hospitalization during treatment, often leading to early discontinuation of otherwise effective chemotherapy. Screening for vulnerability might help to identify patients at risk of these adverse outcomes in older adults. MATERIALS AND METHODS: This is a secondary analysis from the GERICO trial. Patients aged ≥70 years assessed for chemotherapy for CRC were screened for eligibility for the GERICO trial with the geriatric-8 (G8) frailty screening tool. The present study population comprised patients who were (1) screened with G8 but for reasons not included in the GERICO study and (2) patients who were randomized to the GERICO control group. We evaluated whether patients identified as vulnerable with G8 (≤14/17) or retrospectively constructed mG8 (≥6/35) had higher risk of experiencing decline in performance status (PS), falls, and unplanned hospitalization during treatment. The association between frailty status and the adverse outcomes was analyzed with univariate and multivariate logistic regression. The discriminative ability of G8/mG8 to predict outcomes was analyzed using the area under the curve for receiver operating characteristics curves. RESULTS: In total, 238 patients (median age 74 years [range 70-91]) were included in this analysis. More vulnerable than fit patients experienced decline in PS (G8: 41% vs. 14%, p = 0.006 and mG8: 28% vs. 17%, p = 0.04) during treatment. Furthermore, more vulnerable than fit patients experienced falls (G8 14% vs. 6% p = 0.04) and unplanned hospitalization (G8: 31% vs. 14%, p = 0.009 and mG8: 34% vs. 13%, p < 0.001). Multivariate analyses showed an association between G8 vulnerability and decline in PS, falls, and hospitalization. DISCUSSION: Patients with G8 or mG8 vulnerability were more likely to experience decline in PS and unplanned hospitalization during chemotherapy for CRC than fit patients. More G8 vulnerable patients experienced falls compared with fit patients. Appropriate interventions should be offered to older patients with CRC assessed as vulnerable with G8 or mG8 to maintain PS during chemotherapy.

Analysis of changes in social isolation, loneliness, or both, and subsequent cognitive function among older adults: Findings from a nationwide cohort study.

INTRODUCTION: The study aimed to investigate the associations of changes in social isolation, loneliness, or both, with cognitive function. METHODS: Data were from 7299 older adults in the Chinese Longitudinal Healthy Longevity Survey. We defined four change patterns (no, incident, transient, and persistent) for social isolation and loneliness, and created nine-category variable to represent the joint changes. Tobit regression models and Cox models were performed. RESULTS: Incident, transient, and persistent social isolation or loneliness may accelerate cognitive decline (p < 0.05). Incident, transient, and persistent social isolation were associated with higher cognitive impairment risk, while only persistent loneliness was associated with higher cognitive impairment risk (p < 0.001). Notably, short-term or persistent social isolation was associated with accelerated cognitive decline and incident cognitive impairment, regardless of different loneliness change status (p < 0.05). DISCUSSION: Short-term or persistent social isolation and persistent loneliness may be a salient risk factor for cognitive decline and cognitive impairment. HIGHLIGHTS: Incident, transient, and persistent social isolation were associated with accelerated cognitive decline and higher cognitive impairment risk. Persistent loneliness was associated with accelerated cognitive decline and higher cognitive impairment risk. Short-term or persistent social isolation with concurrent different loneliness change status accelerated cognitive decline and higher cognitive impairment risk.

Autophagy Regulation Attenuates Neuroinflammation and Cognitive Decline in an Alzheimer's Disease Mouse Model with Chronic Cerebral Hypoperfusion.

This study investigates the role of autophagy regulation in modulating neuroinflammation and cognitive function in an Alzheimer's disease (AD) mouse model with chronic cerebral hypoperfusion (CCH). Using the APP23/PS1 mice plus CCH model, we examined the impact of autophagy regulation on cognitive function, neuroinflammation, and autophagic activity. Our results demonstrate significant cognitive impairments in AD mice, exacerbated by CCH, but mitigated by treatment with the autophagy inhibitor 3-methyladenine (3-MA). Dysregulation of autophagy-related proteins, accentuated by CCH, underscores the intricate relationship between cerebral blood flow and autophagy dysfunction in AD pathology. While 3-MA restored autophagic balance, rapamycin (RAPA) treatment did not induce significant changes, suggesting alternative therapeutic approaches are necessary. Dysregulated microglial polarization and neuroinflammation in AD+CCH were linked to cognitive decline, with 3-MA attenuating neuroinflammation. Furthermore, alterations in M2 microglial polarization and the levels of inflammatory markers NLRP3 and MCP1 were observed, with 3-MA treatment exhibiting potential anti-inflammatory effects. Our findings shed light on the crosstalk between autophagy and neuroinflammation in AD+CCH and suggest targeting autophagy as a promising strategy for mitigating neuroinflammation and cognitive decline in AD+CCH.

The relationship between male and female endogenous reproductive hormones levels and subjective cognitive decline score: A cross-sectional analysis of the Pingyin cohort study.

OBJECTIVE: Reproductive hormones might impact disease course in cognitive decline. We examined the association between male and female endogenous reproductive hormones and subjective cognitive decline (SCD) score. DESIGN, PATIENTS AND MEASUREMENTS: A cross-sectional study design was used with baseline data from the Pingyin cohort study, involving 1943 participants aged 45-70 years. Oestrogen (E2), testosterone, follicle stimulating hormone (FSH) and luteinizing hormone (LH) were measured in females and E2 and testosterone were measured in males. We categorised hormones into three levels of low, intermediate and high level. The 9-item subjective cognitive decline questionnaire (SCD-Q9) scores were collected to assess the symptoms of SCD. Multivariable logistic regression models were used to estimate odds ratios (ORs) and 95% confidence interval (CI) between categorised hormone levels and SCD status. Multivariable linear regression models were also used. RESULTS: Overall, 1943 participants were involved and 1285 (66.1%) were female. The mean age at baseline was 59.1 (standard deviation 7.1) years. Women with high testosterone levels had a higher probability of having SCD compared with those with low testosterone levels (OR 1.43, 95% CI 1.01-2.05). Men with a high level of testosterone (0.59, 0.35-0.98) and high testosterone/E2 ratio (0.55, 0.33-0.90) were related to decreased chances of having SCD. Each one-unit increase of testosterone was linked to reduced SCD score in males [(ß: -.029, 95% CI (-0.052, -0.007)]. CONCLUSION: There was sex-specific relationship between hormone levels and SCD abnormal. Those with higher testosterone levels in females may increase likelihood of experiencing SCD. Males with higher testosterone levels and higher testosterone/E2 ratio may be associated with reduced likelihood of SCD. The roles of endogenous reproductive hormone levels and their dynamic changes in cognitive function need further investigation.

Critical Assessment of the Neurological Complications during High-Risk Anesthesia Procedures.

Damage to the peripheral and central nervous systems is frequently irreversible. Surgically induced neurological damage and anesthesia may result in catastrophic situations for patients and their families. The incidence of significant neurological complications during the perioperative period is examined in this article. In contrast to other organs like the kidney, heart, liver, lungs, and skeletal system, native neurological function cannot be replaced with artificial parts or devices soon. Ignoring brain function during the perioperative period has been a systemic problem in anesthesiology, even though the central and peripheral nervous systems are crucial. This bold claim is intended to draw attention to the fact that, unlike the circulatory and respiratory systems, which have been routinely monitored for decades, the brain and other neural structures do not have a standard monitoring during surgery and anesthesia. Given that the brain and spinal cord are the principal therapeutic targets of analgesics and anesthetics, this deficiency in clinical care is even more alarming. Organs that are notoriously hard to repair or replace after damage have, up until now, received comparatively little attention. In this article, a succinct overview of five neurological complications associated with surgery and anesthesia is presented. After critically reviewing the literature on the subject, the article is focused to common (delirium), controversial (postoperative cognitive decline), and potentially catastrophic (stroke, spinal cord ischemia, or postoperative visual loss) adverse events in the neurological surgery setting. The findings will increase awareness of major neurological complications to the involved surgical and anesthesia team and enhance preventive and treatment strategies during the perioperative period.

Predictors for the development of motoric cognitive risk syndrome in older adults.

BACKGROUND: Motoric cognitive risk (MCR) syndrome refers to a condition where both slow gait and memory complaints coexist, which heightens their vulnerability to developing dementia. Considering that the risk factors of MCR are elucidated from cross-sectional studies and also likely vary based on socioeconomic status, we conducted a community-based longitudinal study to determine the predictors of MCR among older adults in Malaysia. METHODS: Out of 1,249 older participants (aged 60 years and above) without MCR at baseline (Wave II of LRGS-TUA cohort study), 719 were successfully followed up after 3.5 years to identify predictors of subsequent MCR development. A comprehensive interview-based questionnaire was administered for sociodemographic information, cognitive function, psychosocial, functional status, and dietary intake. Anthropometric measurements, body composition, and physical performance were assessed. Univariate analyses were performed for each variable, followed by a hierarchical logistic regression analysis to identify the predictors of MCR that accounted for confounding effects between the studied factors. RESULTS: The incidence rate of MCR was 4.0 per 100 person-years. Smoking (Adjusted Odd Ratio (Adj OR) = 1.782; 95% Confidence Interval (CI):1.050-3.024), hypertension (Adj OR = 1.725; 95% CI:1.094-2.721), decreased verbal memory as assessed by the lower Rey Auditory Verbal Learning Test (RAVLT) (Adj OR = 1.891; 95% CI:1.103-3.243), and decreased functional status measured using instrumental activity of daily living (IADL) (Adj OR = 4.710; 95% CI:1.319-16.823), were predictors for MCR incidence. CONCLUSIONS: Our study results provide an initial reference for future studies to formulate effective preventive management and intervention strategies to reduce the growing burden of adverse health outcomes, particularly among Asian older adults.

Confronting Alzheimer's Disease Risk in Women: A Feasibility Study of Memory Screening as Part of the Annual Gynecological Well-Woman Visit.

Objective: Routine health care visits offer the opportunity to screen older adults for symptoms of Alzheimer's disease (AD). Many women see their gynecologist as their primary health care provider. Given this unique relationship, the Women's Preventive Services Initiative and the American College of Obstetrics and Gynecology advocate for integrated care of women at all ages. It is well-established that women are at increased risk for AD, and memory screening of older women should be paramount in this effort. Research is needed to determine the feasibility and value of memory screening among older women at the well-woman visit. Materials and Methods: Women aged 60 and above completed a 5-item subjective memory screener at their well-woman visit at the Columbia University Integrated Women's Health Program. Women who endorsed any item were considered to have a positive screen and were given the option to pursue clinical evaluation. Rates of positive screens, item endorsement, and referral preferences were examined. Results: Of the 530 women approached, 521 agreed to complete the screener. Of those, 17.5% (n = 91) were classified as positive. The most frequently endorsed item was difficulty with memory or thinking compared with others the same age. Among women with positive screens, 57.5% were interested in pursuing clinical referrals to a memory specialist. Conclusion: Results support the feasibility and potential value of including subjective memory screening as part of a comprehensive well-woman program. Early identification of memory loss will enable investigation into the cause of memory symptoms and longitudinal monitoring of cognitive change.

Brain structure, amyloid, and behavioral features for predicting clinical progression in subjective cognitive decline.

As a potential preclinical stage of Alzheimer's dementia, subjective cognitive decline (SCD) reveals a higher risk of future cognitive decline and conversion to dementia. However, it has not been clear whether SCD status increases the clinical progression of older adults in the context of amyloid deposition, cerebrovascular disease (CeVD), and psychiatric symptoms. We identified 99 normal controls (NC), 15 SCD individuals who developed mild cognitive impairment in the next 2 years (P-SCD), and 54 SCD individuals who did not (S-SCD) from ADNI database with both baseline and 2-year follow-up data. Total white matter hyperintensity (WMH), WMH in deep (DWMH) and periventricular (PWMH) regions, and voxel-wise grey matter volumes were compared among groups. Furthermore, using structural equation modelling method, we constructed path models to explore SCD-related brain changes longitudinally and to determine whether baseline SCD status, age, and depressive symptoms affect participants' clinical outcomes. Both SCD groups showed higher baseline amyloid PET SUVR, baseline PWMH volumes, and larger increase of PWMH volumes over time than NC. In contrast, only P-SCD had higher baseline DWMH volumes and larger increase of DWMH volumes over time than NC. No longitudinal differences in grey matter volume and amyloid was observed among NC, S-SCD, and P-SCD. Our path models demonstrated that SCD status contributed to future WMH progression. Further, baseline SCD status increases the risk of future cognitive decline, mediated by PWMH; baseline depressive symptoms directly contribute to clinical outcomes. In conclusion, both S-SCD and P-SCD exhibited more severe CeVD than NC. The CeVD burden increase was more pronounced in P-SCD. In contrast with the direct association of depressive symptoms with dementia severity progression, the effects of SCD status on future cognitive decline may manifest via CeVD pathologies. Our work highlights the importance of multi-modal longitudinal designs in understanding the SCD trajectory heterogeneity, paving the way for stratification and early intervention in the preclinical stage. PRACTITIONER POINTS: Both S-SCD and P-SCD exhibited more severe CeVD at baseline and a larger increase of CeVD burden compared to NC, while the burden was more pronounced in P-SCD. Baseline SCD status increases the risk of future PWMH and DWMH volume accumulation, mediated by baseline PWMH and DWMH volumes, respectively. Baseline SCD status increases the risk of future cognitive decline, mediated by baseline PWMH, while baseline depression status directly contributes to clinical outcome.

Traumatic brain injury and cognitive change over 30 years among community-dwelling older adults.

INTRODUCTION: There is limited evidence regarding the rate of long-term cognitive decline after traumatic brain injury (TBI) among older adults. METHODS: In this prospective cohort study, time-varying TBI was defined by self-report and International Classification of Disease diagnostic codes. Cognitive testing was performed at five visits over 30 years and scores were combined into a global cognition factor score. Adjusted linear mixed-effects models estimated the association of TBI with cognitive change. RESULTS: A total of 11,701 Atherosclerosis Risk in Communities (ARIC) Study participants (mean baseline age 58 years, 58% female, 25% Black) without TBI at baseline were included. Over follow-up, 18% experienced TBI. The adjusted average decline in cognition per decade (standard deviation units) was more than twice as fast among individuals with ≥ 2 incident TBIs (𝛽 = -0.158, 95% confidence interval [CI] = -0.253,-0.063), but not among individuals with 1 TBI (𝛽 = -0.052, 95% CI = -0.107, 0.002), compared to without TBI (𝛽 = -0.057, 95% CI = -0.095, -0.020). DISCUSSION: This study provides robust evidence that TBIs fundamentally alter the trajectories of cognitive decline. HIGHLIGHTS: The adjusted average decline in cognition per decade (standard deviation units) was more than twice as fast among individuals with ≥ 2 incident traumatic brain injuries (TBIs; 𝛽 = -0.158, 95% confidence interval [CI] = -0.253, -0.063), but not with 1 TBI (𝛽 = -0.052, 95% CI = -0.107, 0.002), compared to without TBI (𝛽 = -0.057, 95% CI = -0.095, -0.020). Over a period of 30 years, this difference in cognitive decline is equivalent to individuals with ≥ 2 TBIs being 9.7 years older at baseline. Associations of TBI were stronger among individuals with one or two apolipoprotein E (APOE) ε4 alleles than among individuals with zero APOE ε4 alleles (P interaction = 0.007).