Risk Factor For Cognitive Decline Research Articles

Tinnitus and Cognitive Decline

Tinnitus, defined as the perception of sound in the absence of any external stimuli, is a condition which affects a significant number of people worldwide. Although the pathophysiology of tinnitus is not fully understood, hearing loss is known to be a major contributor. To date, many studies have investigated the relationship between hearing loss and cognitive function, and hearing loss is now considered a modifiable risk factor for cognitive decline. In this context, recent studies have investigated whether tinnitus, which is closely associated with hearing loss, is also a risk factor for cognitive decline. However, conflicting results have been reported regarding the relationship between these two conditions. Several studies have reported cognitive decline in tinnitus patients, particularly in areas related to working memory and attention. The consideration of patient age is crucial, as older people seem to be more affected by tinnitus-related cognitive issues. In contrast, some studies have indicated no direct association between tinnitus and cognitive decline, with some even indicating potential cognitive improvement in tinnitus patients. In this article, we review the current research on the relationship between tinnitus and cognitive function and discuss the potential association between these two conditions.

The joint effects of sarcopenia and cardiometabolic risk factors on declined cognitive function: Evidence from a 7-year cohort study

BackgroundSarcopenia and cardiometabolic risk factors are very common in the middle-aged and older population. This study aimed to explore the joint effect of sarcopenia and cardiometabolic risk factors on cognitive performance and cognitive decline. MethodsThe definition of sarcopenia status was referenced in the AWGS 2019 algorithm. Linear regression models were used to explore the association of sarcopenia status with cognitive performance at baseline. Mixed effect models and multinomial logistic regression models were used to evaluate the long-term effect of sarcopenia status. The additive interaction between the effects of sarcopenia and cardiometabolic risk factors on cognitive performance was also evaluated. ResultsIn the cross-sectional analysis, sarcopenia and possible sarcopenia were associated with worse cognitive performance. In the longitudinal analysis, the participant with sarcopenia had a 0.34 [95 % CI (−0.43, −0.24)] lower global cognition score, and those with possible sarcopenia had a 0.20 [95 % CI (−0.27, −0.14)] lower global cognition score, compared with participants with no-sarcopenia. Sarcopenia and possible sarcopenia were identified as significant risk factors for cognitive decline. Sarcopenia combined with hypertension, type 2 diabetes, dyslipidemia, or abdominal obesity was associated with worse cognitive function. LimitationsThe assessment of cognitive function was not diagnosed accurately. ConclusionsSarcopenia and possible sarcopenia had adverse effects on cognitive performance and cognitive decline, sarcopenia combined with cardiometabolic risk factors can significantly enhance these effects. Therefore, the prevention of sarcopenia in the older population is crucial.

Association of Chronic Pain with Biomarkers of Neurodegeneration, Microglial Activation, and Inflammation in Cerebrospinal Fluid and Impaired Cognitive Function.

Debate surrounds the role of chronic pain as a risk factor for cognitive decline and dementia. This study aimed at examining the association of chronic pain with biomarkers of neurodegeneration using data from the Alzheimer's Disease Neuroimaging Initiative. Participants were classified using the ATN (amyloid, tau, neurodegeneration) classification. Chronic pain was defined as persistent or recurrent pain reported at baseline. For each ATN group, analysis of covariance models identified differences in cerebrospinal fluid (CSF) levels of amyloid β1-42 , phosphorylated tau 181 (ptau181 ), total tau (t-tau), soluble triggering receptor expressed on myeloid cells 2 (sTREM2), and cognitive function between chronic pain states. Differences in CSF levels of inflammatory markers between chronic pain states were further analyzed. Linear mixed effect models examined longitudinal changes. The study included 995 individuals, with 605 (60.81%) reporting chronic pain at baseline. At baseline, individuals with suspected non-Alzheimer pathophysiology and chronic pain showed increased CSF levels of t-tau and sTREM2. Chronic pain was associated with increased tumor necrosis factor α levels, irrespective of the ATN group. Longitudinally, an increase in ptau181 CSF levels was observed in chronic pain patients with negative amyloid and neurodegeneration markers. Amyloid-positive and neurodegeneration-negative chronic pain patients showed higher memory function cross-sectionally. No significant longitudinal decline in cognitive function was observed for any ATN group. Our study suggests that chronic pain induces neuronal damage and microglial activation in particular subgroups of patients along the AD spectrum. Further studies are needed to confirm these findings. ANN NEUROL 2023.

Specific quinone reductase 2 inhibitors reduce metabolic burden and reverse Alzheimer's disease phenotype in mice.

Biological aging can be described as accumulative, prolonged metabolic stress and is the major risk factor for cognitive decline and Alzheimer's disease (AD). Recently, we identified and described a quinone reductase 2 (QR2) pathway in the brain, in which QR2 acts as a removable memory constraint and metabolic buffer within neurons. QR2 becomes overexpressed with age, and it is possibly a novel contributing factor to age-related metabolic stress and cognitive deficit. We found that, in human cells, genetic removal of QR2 produced a shift in the proteome opposing that found in AD brains while simultaneously reducing oxidative stress. We therefore created highly specific QR2 inhibitors (QR2is) to enable evaluation of chronic QR2 inhibition as a means to reduce biological age-related metabolic stress and cognitive decline. QR2is replicated results obtained by genetic removal of QR2, while local QR2i microinjection improved hippocampal and cortical-dependent learning in rats and mice. Continuous consumption of QR2is in drinking water improved cognition and reduced pathology in the brains of AD-model mice (5xFAD), with a noticeable between-sex effect on treatment duration. These results demonstrate the importance of QR2 activity and pathway function in the healthy and neurodegenerative brain and what we believe to be the great therapeutic potential of QR2is as first-in-class drugs.

Basic Mechanisms of Brain Injury and Cognitive Decline in Hypertension.

Dementia affects almost 50 million adults worldwide, and remains a major cause of death and disability. Hypertension is a leading risk factor for dementia, including Alzheimer disease and Alzheimer disease-related dementias. Although this association is well-established, the mechanisms underlying hypertension-induced cognitive decline remain poorly understood. By exploring the mechanisms mediating the detrimental effects of hypertension on the brain, studies have aimed to provide therapeutic insights and strategies on how to protect the brain from the effects of blood pressure elevation. In this review, we focus on the basic mechanisms contributing to the cerebrovascular adaptions to elevated blood pressure and hypertension-induced microvascular injury. We also assess the cellular mechanisms of neurovascular unit dysfunction, focusing on the premise that cognitive impairment ensues when the dynamic metabolic demands of neurons are not met due to neurovascular uncoupling, and summarize cognitive deficits across various rodent models of hypertension as a resource for investigators. Despite significant advances in antihypertensive therapy, hypertension remains a critical risk factor for cognitive decline, and several questions remain about the development and progression of hypertension-induced cognitive impairment.

Interaction between air pollution and risk factors for cognitive decline: a comparison study in China and the UK cohorts

Interaction between air pollution and risk factors for cognitive decline: a comparison study in China and the UK cohorts

Cognitive transitions based on functional status in older adults with heart failure: a population-based study.

Cognitive impairment and functional status are both important determinants of poor outcomes in heart failure (HF). However, little is known about how functional status impacts the changes in cognitive status during the disease course. This study aimed to describe the cognitive transitions in patients with HF and assess the relationship of these transitions to functional status, which was assessed by the dependency of activities of daily living (ADL). This retrospective cohort study included 1764 patients with an International Classification of Diseases-10 code of HF (≥65years, mean age 82.3±7.9years, 39% male) from a long-term care and medical insurance database from Nobeoka city, a rural city of south-western Japan. Cognitive status at baseline and 6, 12, 18, and 24month time points was collected, and participants were stratified based on ADL status at baseline. Generalized estimating equations and multi-state modelling were used to examine associations between ADL dependency and cognitive changes/mortality. Transition probabilities were estimated using multi-state modelling. At baseline, there were 1279 (73%) and 485 (27%) patients with independent and dependent ADL, respectively. In overall patients, 1656 (93.9%) patients had normal/mild cognitive status and 108 (6%) patients had a moderate/severe cognitive status at baseline. The majority [104 (96%) patients] of patients with moderate/severe cognitive status at baseline had dependent ADL. In patients with moderate/severe cognitive status, the number of patients with dependent ADL always outnumbered that of the independent ADL throughout the follow-up. Multi-state modelling estimated that patients with dependent ADL and normal/mild cognitive status at baseline had 47% probability of maintaining the same cognitive status at 24months, while the probability of maintaining the same cognitive status was 86% for those with independent ADL. Patients with normal/mild cognitive status in the dependent ADL group at baseline had a higher risk of experiencing a transition to moderate/severe cognitive status at any time point during 24months compared with those with independent ADL [hazard ratio 5.24 (95% confidence interval 3.47-7.90)]. In older patients with HF, the prevalence of cognitive impairment was always higher for those with reduced functional status. Despite having a normal/mild cognitive status at baseline, patients with dependent ADL are at high risk of experiencing cognitive decline over 24months with substantially less chance of maintaining their cognitive status. ADL dependency was an important risk factor of cognitive decline in patients with HF.

Identifying predictors of cognitive decline in long-term care: a scoping review

BackgroundCognitive impairment can cause social, emotional, and financial burdens on individuals, caregivers, and healthcare providers. This is especially important in settings such as long-term care (LTC) homes which largely consist of vulnerable older adults. Thus, the objective of this study is to review and summarize current research examining risk factors of cognitive decline in older adults within LTC.MethodsThis scoping review includes primary observational research studies assessing within-person change in cognition over time in LTC or equivalent settings in high resource countries. A mean participant age of ≥ 65 years was required. Searches were conducted in Medline, Embase, Cumulative Index to Nursing and Allied Health Literature (CINAHL), and PyscInfo on June 27th, 2022 and included articles published during or after the year 2000. Title, abstract, and full-text screening was performed by two independent reviewers using Covidence. Specific predictors along with their associated relation with cognitive decline were extracted by a team of reviewers into a spreadsheet.ResultsThirty-eight studies were included in this review. The mean sample size was 14 620. Eighty-seven unique predictors were examined in relation to cognitive decline. Dementia was the most studied predictor (examined by 9 of 38 studies), and the most conclusive, with eight of those studies identifying it as a risk factor for cognitive decline. Other predictors that were identified as risk factors included arterial stiffness (identified by 2 of 2 studies), physical frailty (2 of 2 studies), sub-syndromal delirium (2 of 2 studies), and undergoing the first wave of COVID-19 lockdowns (2 of 2 studies). ADL independence was the most conclusive protective factor (3 of 4 studies), followed by social engagement (2 of 3 studies). Many remaining predictors showed no association and/or conflicting results.ConclusionsDementia was the most common risk factor, while ADL independence was the most common protective factor associated with cognitive decline in LTC residents. This information can be used to stratify residents by risk severity and provide better personalized care for older adults through the targeted management of cognitive decline.

Depression, Inflammation, and Intestinal Permeability: Associations with Subjective and Objective Cognitive Functioning throughout Breast Cancer Survivorship.

About one-in-three breast cancer survivors have lingering cognitive complaints and objective cognitive impairment. Chronic inflammation and intestinal permeability (i.e., leaky gut), two risk factors for cognitive decline, can also fuel depression-another vulnerability for cognitive decline. The current study tested whether depression accompanied by high levels of inflammation or intestinal permeability predicted lower subjective and objective cognitive function in breast cancer survivors. We combined data from four breast cancer survivor studies (n = 613); some had repeated measurements for a total of 1015 study visits. All participants had a blood draw to obtain baseline measures of lipopolysaccharide binding protein-a measure of intestinal permeability, as well as three inflammatory markers that were incorporated into an inflammatory index: C-reactive protein, interleukin-6, and tumor necrosis factor-α. They reported depressive symptoms on the Center for Epidemiological Studies depression scale (CES-D), and a binary variable indicated clinically significant depressive symptoms (CES-D ≥ 16). The Kohli (749 observations) and the Breast Cancer Prevention Trial (591 observations) scales assessed subjective cognitive function. Objective cognitive function tests included the trail-making test, Hopkins verbal learning test, Conners continuous performance test, n-back test, FAS test, and animal-naming test (239-246 observations). Adjusting for education, age, BMI, cancer treatment type, time since treatment, study visit, and fatigue, women who had clinically elevated depressive symptoms accompanied by heightened inflammation or intestinal permeability reported poorer focus and marginally poorer memory. However, poorer performance across objective cognitive measures was not specific to inflammation-associated depression. Rather, there was some evidence of lower verbal fluency; poorer attention, verbal learning and memory, and working memory; and difficulties with visuospatial search among depressed survivors, regardless of inflammation. By themselves, inflammation and intestinal permeability less consistently predicted subjective or objective cognitive function. Breast cancer survivors with clinically significant depressive symptoms accompanied by either elevated inflammation or intestinal permeability may perceive greater cognitive difficulty, even though depression-related objective cognitive deficits may not be specific to inflammation- or leaky-gut-associated depression.

Abstract 083: Neurovascular And Cognitive Dysfunction In Middle-Aged Mice With High Blood Pressure Variability

Blood pressure variability (BPV) is a novel risk factor for cognitive decline. This study tested the hypothesis that BPV disrupts cellular function and communication at the neurovascular complex (vascular, glia, and neuron) contributing to BPV-induced neurovascular dysfunction. A main goal of the study was to establish a murine BPV model and examine how this risk factor impacts key functional outputs of the neurovascular complex. Middle-aged C57BL6 mice were implanted a cranial window and injected GCaMP viral vectors to monitor Ca 2+ activity in cortical neurons or astrocytes. DSI telemetry was used to monitor cardiovascular variables simultaneously ( in vivo ) with arteriole diameter and astrocyte/neuronal Ca 2+ responses via two-photon imaging. In addition, mice were implanted a programmable pump and infused 6-8 pulses/day of saline (Control) or angiotensin II (Ang II, 18 μg/day) for 20-25 days. Ang II infusions evoked transient BP increases (Δ 23±2 mmHg, mean arterial pressure (MAP, P=0.0001, n=14)), and increased BPV (P=0.04, n=12) measured by the average real variability. The 24-hour MAP was not different compared to Controls, allowing for the investigation of BPV-evoked changes in neurovascular function in the absence of hypertension. BPV mice displayed cognitive decline (NOR, P=0.006, n=10). Myogenic responses were lost in parenchymal arterioles of BPV mice but preserved in Controls (P<0.01 n=6). In addition to impaired vascular function, during Ang II-induced BP increases, astrocytes of BPV mice exhibited greater Ca 2+ event frequency (P<0.0001, n=4-6), but of lesser amplitude and reduced area (P=0.02, n=4-6). Furthermore, the neurovascular coupling response, evoked via whisker stimulation, was blunted in mice with high BPV (P<0.0001, n=6-10). Relevant to inflammation, microglial cells from BPV mice had elevated Iba1 (P=0.03, n=4-5) and CD68+ (P=0.003), an inflammatory marker. These findings show that BPV, in the absence of hypertension, result in a loss of cerebral autoregulation, a shift in spontaneous astrocyte Ca 2+ dynamics during blood pressure fluctuations, and increased microglia reactivity. Future mechanistic studies are needed to determine how BPV contributes to cognitive decline.

Lower 25-hydroxyvitamin D is associated with severer white matter hyperintensity and cognitive function in patients with non-disabling ischemic cerebrovascular events

ObjectivesThis study aimed to investigate the potential correlations among serum 25-hydroxyvitamin D [25(OH)D] levels, white matter hyperintensity (WMH) and cognitive function in patients with non-disabling ischemic cerebrovascular events (NICE). MethodsThis was a prospective investigation of 160 NICE patients with age of 40 years or older. Cognitive function was evaluated by the Montreal Cognitive Assessment (MoCA). White matter lesions were evaluated by WMH using Fazekas scores. Spearman correlation analysis and linear regression models were used to identify the associations between serum 25(OH)D levels and cognitive function. Binary logistic regression analysis models were used to evaluate the predictable value of serum 25(OH)D levels and WMH for cognitive impairment. ResultsPatients with inadequate 25(OH)D levels had lower MoCA score (P=0.008), and a higher proportion of severe WMH (P=0.043). Spearman correlation analysis demonstrated that serum 25(OH)D concentrations were positively associated with MoCA score (rs=0.185, P=0.019) while negatively related to the proportion of severe WMH (sWMH) (rs=-0.166, P=0.036).The association between 25(OH)D concentrations and MoCA score remained significant in linear regression (adjusted β=0.012, 95%CI:0.001-0.203).Adjusted binary logistic regression analysis showed that the odds ratio of cognitive impairment with insufficient 25(OH)D concentration was 5.038 (95%CI:1.154-21.988) compared with the sufficient group and the sWMH (OR=2.728, 95%CI:1.230-6.051) was identified as an independent risk factor for cognitive decline in NICE patients. ConclusionSerum 25(OH)D levels and white matter lesions were independently and significantly associated with cognitive impairment in NICE patients.

Association of metabolic dysfunction with cognitive decline and Alzheimer's disease: A review of metabolomic evidence

The discovery of new biomarkers that can distinguish Alzheimer's disease (AD) from mild cognitive impairment (MCI) in the early stages will help to provide new diagnostic and therapeutic strategies and slow the transition from MCI to AD. Patients with AD may present with a concomitant metabolic disorder, such as diabetes, obesity, and dyslipidemia, as a risk factor for AD that may be involved in the onset of both AD pathology and cognitive impairment. Therefore, metabolite profiling, or metabolomics, can be very useful in diagnosing AD, developing new therapeutic targets, and evaluating both the course of treatment and the clinical course of the disease. In addition, studying the relationship between nutritional behavior and AD requires investigation of the role of conditions such as obesity, hypertension, dyslipidemia, and elevated glucose level. Based on this literature review, nutritional recommendations, including weight loss by reducing calorie and cholesterol intake and omega-3 fatty acid supplementation can prevent cognitive decline and dementia in the elderly. The underlying metabolic causes of the pathology and cognitive decline caused by AD and MCI are not well understood. In this review article, metabolomics biomarkers for diagnosis of AD and MCI and metabolic risk factors for cognitive decline in AD were evaluated.

A Cluster Analysis of Oral and Cognitive Health Indicators in the CLSA: An Exploratory Study on Cholinergic Activity as the Link.

Poor oral health has been suggested as a risk factor for cognitive decline. Yet, biologically plausible mechanisms explaining this relationship remain unknown. We aimed (1) to identify oral and cognitive health clustering patterns among middle-aged to elderly Canadians and (2) to investigate the extent to which these patterns could be explained by bone mineral density (BMD), a proxy measure of the cholinergic neurons' activity. This cross-sectional study used baseline data from the Comprehensive cohort of the Canadian Longitudinal Study of Aging (CLSA). Oral health was assessed by a self-report questionnaire, and 7 task-based instruments measured cognitive health. We identified oral and cognitive health clusters, our outcome variables, using latent class analysis. Two sets of multivariate logistic regression and 95% confidence intervals were used to investigate whether BMD explains the odds of membership in a certain oral and cognitive health group. The final models were adjusted for socioeconomic, health, and lifestyle factors. Our study sample (N = 25,444: 13,035 males, 12,409 females) was grouped into 5 and 4 clusters based on the oral health status and performance on the cognitive tasks, respectively. After adjusting for all potential covariates, increase in BMD was not associated with higher odds of membership in classes with better oral health (odds ratio [OR] = 1.58 [95% confidence interval {CI}: 0.85-2.92]) and cognitive health (OR = 1.61 [95% CI: 1-2.6]) compared with the groups with the least favorable oral and cognitive health status, respectively. Middle-aged and elderly Canadians show different oral and cognitive health profiles, based on their denture-wearing status and performance on cognitive tests. No evidence could be found to support BMD in place of cholinergic neurons' activity as the common explanatory factor behind the association between oral health and cognitive health. This study is probably the first of its kind to shed light on the cholinergic system as a potential pathway influencing oral and cognitive health. Our findings may support the notion that any potential association between poor oral health and cognitive health might be explained by common contributors, helping clinicians to find the common risk factors for both conditions.

Atlas of the aging mouse brain reveals white matter as vulnerable foci

Aging is the key risk factor for cognitive decline, yet the molecular changes underlying brain aging remain poorly understood. Here, we conducted spatiotemporal RNA sequencing of the mouse brain, profiling 1,076 samples from 15 regions across 7 ages and 2 rejuvenation interventions. Our analysis identified a brain-wide gene signature of aging in glial cells, which exhibited spatially defined changes in magnitude. By integrating spatial and single-nucleus transcriptomics, we found that glial aging was particularly accelerated in white matter compared with cortical regions, whereas specialized neuronal populations showed region-specific expression changes. Rejuvenation interventions, including young plasma injection and dietary restriction, exhibited distinct effects on gene expression in specific brain regions. Furthermore, we discovered differential gene expression patterns associated with three human neurodegenerative diseases, highlighting the importance of regional aging as a potential modulator of disease. Our findings identify molecular foci of brain aging, providing a foundation to target age-related cognitive decline.

Methyl donor supplementation reduces phospho-Tau, Fyn and demethylated protein phosphatase 2A levels and mitigates learning and motor deficits in a mouse model of tauopathy.

Reduced folate status and elevated levels of circulating homocysteine are modifiable risk factors for cognitive decline and dementia. Disturbances in one-carbon metabolism are associated with the pathological accumulation of phosphorylated tau, a hallmark feature of prevalent dementia, including Alzheimer's disease and subgroups of frontotemporal dementia. Here, using transgenic TAU58/2 mouse models of human tauopathy, we tested whether dietary supplementation with L-methylfolate (the active folate form), choline and betaine can reduce tau phosphorylation and associated behavioural phenotypes. TAU58/2 mice fed with the methyl donor-enriched diet showed reduced phosphorylation of tau at the pathological S202 (CP13) and S396/S404 (PHF-1) epitopes and alleviation of associated motor and learning deficits. Compared with mice on the control diet, the decrease in cortical phosphorylated tau levels in mice fed with the methyl donor-enriched diet was associated with enhanced methylation of protein phosphatase 2A, the major brain tau Ser/Thr phosphatase. It also correlated with a reduction in protein levels of Fyn, a tau tyrosine kinase that plays a central role in mediating pathological tau-induced neurodegeneration. Conversely, Fyn expression levels were increased in mice with deficiencies in folate metabolism. Our findings provide the first experimental evidence that boosting one-carbon metabolism with L-methylfolate, choline and betaine can mitigate key pathological, learning and motor deficits in a tauopathy mouse model. They give support to using a combination of methyl donors as a preventive or disease-modifying strategy for tauopathies.

Visit-to-Visit Glucose Variability, Cognition, and Global Cognitive Decline: The Multi-Ethnic Study of Atherosclerosis.

Higher visit-to-visit glucose variability (GV) is associated with dysglycemia and type 2 diabetes (T2D), key risk factors for cognitive decline. Evaluate the association of GV with cognitive performance and decline in racially/ethnically diverse older populations with and without T2D. We calculated the standard deviation of glucose (SDG), average real variability (ARV), and variability independent of the mean (VIM) among 4367 Multi-Ethnic Study of Atherosclerosis participants over 6 clinical examinations. Participants completed a cognitive assessment at the fifth examination, and a subset completed a second assessment 6 years later. We used multivariable linear regression to estimate the association of intraindividual GV with cognitive test scores after adjustments for cardiovascular risk factors and mean glucose level over the study period. Two-fold increments in the VIM and SDG were associated with worse Cognitive Abilities Screening Instrument (CASI) performance, while two-fold increments in VIM and ARV were associated with worse Digit Symbol Coding test score. GV measures were not associated with change in CASI performance among 1834 participants with repeat CASI data 6 years later. However, among 229 participants with incident T2D, the SDG and VIM were associated with decline in CASI (-1.7 [95% CI: -3.1, -0.3] and -2.1 [-3.7, -0.5] points, respectively). In contrast, single-timepoint glucose and HbA1c were not associated with CASI decline among participants with or without incident T2D. Higher visit-to-visit GV over 16 to 18 years is associated with worse cognitive performance in the general population, and with modest global cognitive decline in participants with T2D.

Obesity and Postoperative Cognitive Dysfunction: A Curious Association.

Postoperative cognitive dysfunction (POCD) is a medical condition that impacts cognitive function after surgery, particularly major procedures. Patients with POCD may experience physical symptoms, such as depression, anxiety, and fatigue, severely undermining their quality of life. Research establishes the connection between obesity and cognitive dysfunction since patients diagnosed with obesity are more susceptible to cognitive decline. Although obesity poses a significant risk factor for cognitive impairment, the link between obesity and POCD is still inadequately understood. Therefore, this systematic review explores the correlation between obesity and POCD by detailing potential mechanisms underlying this relationship and identifying areas for further research. Following the guidelines for systematic reviews, we conducted a literature search between August 2022 and April 2023, which identified studies with a substantial number of patients with POCD after major surgeries, including coronary artery bypass grafting, gastrointestinal procedures, cholecystectomy, and carotid endarterectomy. Our findings also demonstrated that a significant percentage of these had obesity, which was statistically significant as a risk factor for cognitive decline. Pathological processes, such as changes in vascular endothelium integrity, systemic inflammation induced by obesity, and apolipoprotein E-epsilon-4 expression, have been identified to contribute to POCD after surgery. Despite the promising results, there remains a gap in the literature. Thus, it is crucial to investigate the relationship between obesity and POCD further, uncover more potential underlying pathophysiological processes, and identify therapeutic targets. These measures would enable healthcare practitioners to prevent or reduce cognitive dysfunction associated with obesity in surgical patients.

Analysis of factors related to cognitive impairment in a community-based, complete enumeration survey in Japan: the Nakayama study.

The number of patients with cognitive disorders is rapidly increasing in the world, becoming not only a medical problem, but also a social problem. There have been many reports that various factors are associated with cognitive dysfunction, but the factors have not yet been fully identified. This was a community-based complete enumeration study which aimed to identify risk and protective factors for dementia. The first phase included all residents aged 65 years or older in a town in Japan. They completed many examinations, such as living conditions questionnaires, physical examination, Mini-Mental State Examination, and brain magnetic resonance imaging. The participants with suspected cognitive impairment underwent additional examinations for detailed evaluation in the second phase. Statistical analysis was performed to identify risk and protective factors for dementia after all participants were diagnosed. There were 927 participants in the baseline evaluation; 611 (65.9%) were healthy, 165 (17.8%) had mild cognitive impairment (MCI), and 151 (16.3%) had dementia. The age-standardised prevalence of dementia was 9.5%. Statistical analyses for amnestic MCI and Alzheimer's disease showed that risk factors for cognitive decline were diabetes mellitus, low activities of daily living, and living alone, and that protective factors were history of exercise and drinking habit. The present findings suggest that several lifestyle-related diseases and factors are associated with cognitive decline. These results support similar findings from previous studies and will be helpful for preventing dementia in the future.

In Case You Haven't Heard…

Scientists have known for some time that addressing hearing loss can reduce a person's chances of developing Alzheimer's disease, but a study released on July 18 shows just how much, a news release from UsAgainstAlzheimer's stated. According to the ACHIEVE study, “A landmark study of the effect of hearing intervention on brain health in older adults,” published in The Lancet, treating hearing loss in older adults who had more risk factors for cognitive decline slowed down the loss of thinking and memory abilities by 48% over three years. The study's findings were also presented by its author, Frank Lin, M.D., Ph.D., of the Johns Hopkins University School of Medicine and Bloomberg School of Public Health, at the annual Alzheimer's Association's International Conference. One in three Americans between the ages of 65 and 74 has hearing loss, according to the National Institutes of Health. Worldwide, mid‐ and late‐life hearing loss is identified as the single largest potentially modifiable risk factor for dementia. The ACHIEVE study is the first randomized clinical trial to investigate whether treating hearing loss in older adults reduces the cognitive decline that can occur with aging.

Hearing intervention versus health education control to reduce cognitive decline in older adults with hearing loss in the USA (ACHIEVE): a multicentre, randomised controlled trial

Hearing loss is associated with increased cognitive decline and incident dementia in older adults. We aimed to investigate whether a hearing intervention could reduce cognitive decline in cognitively healthy older adults with hearing loss. The ACHIEVE study is a multicentre, parallel-group, unmasked, randomised controlled trial of adults aged 70-84 years with untreated hearing loss and without substantial cognitive impairment that took place at four community study sites across the USA. Participants were recruited from two study populations at each site: (1) older adults participating in a long-standing observational study of cardiovascular health (Atherosclerosis Risk in Communities [ARIC] study), and (2) healthy de novo community volunteers. Participants were randomly assigned (1:1) to a hearing intervention (audiological counselling and provision of hearing aids) or a control intervention of health education (individual sessions with a health educator covering topics on chronic disease prevention) and followed up every 6 months. The primary endpoint was 3-year change in a global cognition standardised factor score from a comprehensive neurocognitive battery. Analysis was by intention to treat. This trial was registered at ClinicalTrials.gov, NCT03243422. From Nov 9, 2017, to Oct 25, 2019, we screened 3004 participants for eligibility and randomly assigned 977 (32·5%; 238 [24%] from ARIC and 739 [76%] de novo). We randomly assigned 490 (50%) to the hearing intervention and 487 (50%) to the health education control. The cohort had a mean age of 76·8 years (SD 4·0), 523 (54%) were female, 454 (46%) were male, and most were White (n=858 [88%]). Participants from ARIC were older, had more risk factors for cognitive decline, and had lower baseline cognitive scores than those in the de novo cohort. In the primary analysis combining the ARIC and de novo cohorts, 3-year cognitive change (in SD units) was not significantly different between the hearing intervention and health education control groups (-0·200 [95% CI -0·256 to -0·144] in the hearing intervention group and -0·202 [-0·258 to -0·145] in the control group; difference 0·002 [-0·077 to 0·081]; p=0·96). However, a prespecified sensitivity analysis showed a significant difference in the effect of the hearing intervention on 3-year cognitive change between the ARIC and de novo cohorts (pinteraction=0·010). Other prespecified sensitivity analyses that varied analytical parameters used in the total cohort did not change the observed results. No significant adverse events attributed to the study were reported with either the hearing intervention or health education control. The hearing intervention did not reduce 3-year cognitive decline in the primary analysis of the total cohort. However, a prespecified sensitivity analysis showed that the effect differed between the two study populations that comprised the cohort. These findings suggest that a hearing intervention might reduce cognitive change over 3 years in populations of older adults at increased risk for cognitive decline but not in populations at decreased risk for cognitive decline. US National Institutes of Health.