bluuebunny/crossref_metadata_2025_split huggingface dataset:
Whose voices are still silent: Applying an intersectionality lens to existing evidence on cognitive impairment in older adults with combined hearing and vision impairment
Authors: Jaiswal Atul , Santhakumaran Sangeetha , Gupta Shikha , Dumassais Shirley , Aubin Gabrielle , Wittich Walter 
Published: December 2021

AbstractBackgroundAge‐related sensory loss is a significant yet understudied public health problem. Evidence suggests that sensory loss in older adults is associated with an increased risk of cognitive impairment, functional decline, and social isolation. However, older adults with combined vision and hearing impairment (dual sensory impairment/DSI) are often overlooked in ageing as well as Alzheimer’s research. We synthesized existing evidence on cognitive impairment in older adults with DSI. Given the importance of diversity and inclusion in ageing and healthcare research, we applied the lens of intersectionality to the review data with the aim of exploring whose voices among older adults with DSI are not represented and whose voices are captured in the existing evidence.MethodWe conducted a scoping review using the methodological framework by Arskey and O’Malley (2005). The review considered empirical studies that explored cognitive impairment in older adults with DSI. The search was conducted across eleven scientific databases (CINAHL, Embase, Global Health, Mednar, OAIster, OpenGrey, PsycEXTRA, PsycINFO, PubMed, Web of Science, and WorldWideScience) in June 2020. Following the content analysis approach, the extracted data were later analyzed applying the intersectionality lens to capture attributes such as age, sex, gender identity, class, culture, disability, education, ethnicity, geography, indigeneity, and immigration status.ResultOf 11,595 studies retrieved, fifty‐six (n = 56) were included in the review, demonstrating how limited the evidence is that exists on cognitive impairment among older adults with DSI. The majority of studies focused on older men with DSI from high‐income countries (Australia, Canada, Japan, Netherlands, UK, and the USA), with the exception of one study from India. Only a few studies reported binary gender differences, with no studies reporting cognitive impairment in gender diverse older population. Attributes such as immigration status and indigeneity were not reported, though the race and ethnicity of older adults were presented in some studies.ConclusionThe review highlights important knowledge gaps related to cognitive impairment in older adults with DSI, which is a heterogeneous group. Researchers need to go beyond traditional approaches to promote the intersectionality paradigm in their research to provide evidence that is more representative and inclusive in nature.
Associations between social networks and cognitive declines in later life in longitudinal aging studies: A systematic review and meta‐analysis
Authors: Zhang Yun , Clouston Sean AP 
Published: December 2021

AbstractBackgroundIt remains unclear whether and how various aspects of social networks and cognitive declines are associated bidirectionally.MethodWe systematically searched the databases of PubMed, Web of Science and PsycINFO for longitudinal cohort studies that examined associations between social networks and cognitive declines in the general population up through February 2019. Characteristics of study designs, conclusions, and research trends were summarized. For meta‐analyses, estimates extracted from included studies were recalculated into odds ratios with 95% confidence intervals (95%CI). They were stratified by different classification criteria and pooled into random‐effect inverse‐variance weighted aggregations. Heterogeneity was tested by Q‐tests and I2 indexes. Publication bias was assessed by funnel plots and Egger’s tests.ResultWe identified 37 studies for systematic review and 24 for meta‐analysis. When researching effects of social network on subsequent cognitive decline, poor social networks were significant risk factors for cognitive declines (OR: 0.824, 95% CI: 0.769, 0.883; p<0.001; k=23) in longitudinal research. Stratified by social network characteristics, social network size (OR: 0.814, 95% CI: 0.663, 0.999; p=0.049; k=7), structure and function (OR: 0.879, 95%CI: 0.826, 0.936; p<0.001; k=17), and emotional feedback from network members (OR: 0.860, 95% CI: 0.652, 1.134; p=0.285; k=3) were all significant risk factors. When researching effects of cognitive declines on subsequent changes of social network, only a few studies (n=5) were included, which consistently supported that worse cognitive declines were associated with smaller size and less complex structure of social networks, however, their heterogeneous methods and study designs were not fit for meta‐analysis.ConclusionThere are both significant effects of social networks on subsequent cognitive declines and significant effects of cognitive declines on changes of size and complexity of social networks in subsequent years. Most studies focused on effects of social networks on changes of social networks, only a few explored the opposite direction. The association between dynamic changes of social networks and cognitive declines is an under‐studied topic.
Late‐life social activity moderates the association between temporal lobe atrophy and episodic memory decline
Authors: Jo Jihyeon , Kim Hairin , Youm Yoosik , Chey Jeanyung 
Published: December 2021

AbstractBackgroundRetirement and loss of important social relationships, including spouse and friends, make older adults more vulnerable to social isolation. Therefore, social activity could be important for older adults in maintaining life satisfaction and everyday functioning. Although several studies found protective roles of social activity against cognitive decline in late life, only a few studies examined the protective effects of social activity using longitudinal data. In this study, the effects of social activity on the relationship between brain aging and cognitive decline in older adults were examined during a four‐year period.MethodThirty‐two older adults with normal cognition (mean age = 70.69, SD: 6.27, mean education = 7.75, SD: 3.94 at baseline) were recruited from the Korean Social Life, Health, and Aging Project (KSHAP). Neuropsychological and brain imaging data, and social survey, were acquired in 2015 and 2019. Elderly Verbal Learning Test (EVLT) performance and cortical volumes from Magnetic Resonance Imaging (MRI) were the main measures of interest. The participants were asked to respond either “yes” or “no” to social survey items, including participation in community senior center events, volunteering for charities, religious activities, socializing events, leisure activities, and community activities. Social activity was explored in terms of level, consistency, and types of social activities. The Computational Anatomy Toolbox (CAT) was used to calculate temporal lobe gray matter volume selected as regions of interest (ROI) for its role in episodic memory. Hierarchical regressions were conducted to examine the effects of social activity on the relationship between temporal lobe atrophy and episodic memory decline.ResultWe found that the temporal lobe atrophy was associated with the delayed recall decline (r = 0.49, p = 0.003). More involvement in social activity at baseline decreased the effects of temporal lobe atrophy on delayed recall decline, controlling for age, sex, education, and self‐rated health as covariates. Further, consistent involvement in social activity, especially volunteering, attenuated the association between temporal lobe atrophy and delayed recall decline.ConclusionThese findings suggest that social activities in late life function as cognitive reserve to buffer against the effects of temporal lobe atrophy on episodic memory decline in older adults.
Professional stress: A major risk factor in Alzheimer’s disease
Authors: Doscan Ana Maria M 
Published: December 2021

AbstractBackgroundEarly brain ageing (objectified by decreasing the age of onset of neurocognitive impairment) in the 35‐50 age segment has become a major concern for longevity medicine. Hence the need to extensively investigate chronic occupational stress and its effects on human brain, especially when acting as a risk factor for early Alzheimer’s disease. Preventive diagnosis of stress vulnerability, identification of demands that may exceed the individual's ability to respond effectively, quantification and objectification of stress, will help deceleration of early brain aging process.MethodThe study as designed to evaluate professional chronic stress that includes: history of stress in patients’ life, neurocognitive stress scales evaluation, biological evaluation of stress hormones ‐ urinary determination of serotonin, melatonin, adrenalin /noradrenalin, dopamine and salivary cortisol and measurement of heart rate variability.ResultOur study results, based on the evaluation of 100 patients aged between 35‐65 years old, who work in stressful environment, show the link between elevated cortisol levels and the occurrence of clinical manifestations of neurocognitive impairment in the context of persistent occupational stress, and also the presence of depressive disorder in patients’ life history, in the context of changes in stress biomarkers.ConclusionPersistent professional stress can cause changes in the body's normal defense response to stress factors. Early identification of occupational stressors, clinical and biological knowledge of stress as well as the development of preventive and personalized measures, may define a future approach in the context of preventing stress induced pathologies like depression and anxiety, but also neurocognitive disorders (from mild cognitive impairment to early Alzheimer’s disease).
Racial differences in biomarkers of Alzheimer’s disease and inflammation
Authors: Hu William T. , Wharton Whitney , Parker Monica W. 
Published: December 2021

AbstractBackgroundIn clinically diagnosed Alzheimer’s disease (AD) dementia, older Black/African American (B/AA) adults were previously identified to have genetic risks, cognitive profiles, and longitudinal progression which differed from older White adults. Socioeconomic status and biological factors may each contribute to these findings. To determine if race modified biochemical as well as clinical AD phenotypes, we sought to analyze biomarker differences between B/AA and White adults across the aging spectrum.MethodThree cohorts (n=237) were included in this Atlanta‐based study. We prospectively recruited people with normal cognition (NC, n=158) from community events across the greater Atlanta area, and people with mild cognitive impairment or AD dementia (MCI/AD, n=79) from the Emory Cognitive Neurology Clinic and the AD Research Center. Participants underwent detailed clinical, neuropsychological, CSF, and MRI analysis. CSF levels of AD biomarkers, neurofilament light (NfL), and seven cytokines were measured using Luminex in Atlanta with the exception that AD biomarkers for the middle‐aged cohort were measured using ELISA in Sweden.ResultCompared to White adults with NC, B/AA adults showed reduced t‐Tau and p‐Tau181 levels across the aging spectrum by 25‐40%. This difference persisted in subjects with MCI/AD and after accounting for geographic socioeconomic conditions. CSF Aβ42 and NfL levels differed only according to diagnosis (NC vs. MCI/AD) but not race. Older B/AA adults also had lower CSF IL‐9 levels than older White adults, and AD‐associated alterations were only observed in B/AA. In keeping with this, neuropathologic and transcriptomic analysis showed race‐associated differences in the IL‐9 pathway.ConclusionB/AA adults had lower CSF levels of tau‐related protein than White adults across multiple cohorts, and different profiles of CSF and brain cytokine alterations in the presence of AD pathology. Distinct tau‐ and IL‐9‐related processes need to be further investigated according to genetic ancestry and cross‐generational social determinants of health.
Changes in subjective and objective cognitive decline in non‐depressed, non‐demented patients with Parkinson's disease: A 1 to 2 years’ follow‐up
Authors: Rattanabannakit Chatchawan , Wongkanjana Nutchaphol , Munjit Rabwas , Warunyuwong Wikrom , Srivanitchapoom Prachaya , Senanarong Vorapun 
Published: December 2021

AbstractBackgroundSubjective and objective cognitive impairments were prevalent in patients with Parkinson’s disease (PD), but there is no data on longitudinal cognitive change in these patients in Thailand. We aimed to evaluate the cognition, perception of cognitive decline, and the diagnosis of cognitive impairment in Thai patients with PD after 1‐2 follow‐up.MethodNon‐demented, non‐depressed PD patients were included from the Movement Disorder Clinic at Siriraj Hospital. Patients with severe motor symptoms that interfered with cognitive tests were excluded. We used the Montreal Cognitive Assessment‐Thai version (MoCA) to assess cognition. Perception of cognitive decline was assessed by using the Cognitive Change Index (CCI) rated by patients (CCI‐S) and their informants (CCI‐I). All parameters were assessed at baseline and re‐evaluated at 1‐2 years. Association of MoCA, CCI‐S, CCI‐I, the discrepancy of CCI (CCI‐D; CCI‐S minus CCI‐I), apathy score, and patients’ clinical characteristics were analyzed.ResultSixty‐two participants were followed for 18.59±4.55 months. The mean age at baseline was 63.38±9.63 years, and the mean duration of PD diagnosis was 5.63±3.49 years. The MoCA score slightly declined from 20.6±5.1 at baseline to 20.1±4.9 (mean changes ‐0.53±3.2, p=0.195). 47.1% of patients with normal cognition at baseline converted to PD‐MCI. Most (77.8%) PD‐MCI patients remained in the MCI stage, 11.1% turned to dementia, and 11.1% reverted to normal. The CCI‐I and apathy scores increased significantly after 1‐2 years (p=0.003 and <0.001, respectively), but not the CCI‐S. After controlling with age, gender, and education, the 14‐item Starkstein Apathy Scale score at follow‐up was significantly associated with the CCI‐I and the MoCA scores (r = 0.37 and ‐0.34, respectively, both p<0.01). Moreover, change in MoCA scores was significantly associated with the score of CCI‐D at follow‐up (r=‐0.29, p=0.03). Participants with orthostatic hypotension had a lower MoCA score at follow‐up (p=0.04).ConclusionApathy, informant perception of cognitive decline, but not the cognition, were changed significantly in non‐demented PD patients after 1‐2 years follow‐up. Apathy, the discrepancy of perception of cognitive decline between participant and informant, and orthostatic hypotension may be related to the lower cognition at follow‐up. Further studies with a larger sample size and more extensive neuropsychological evaluation are required.
Association between cerebral small‐vessel disease and Alzheimer’s disease pathologies
Authors: Cai Yuan , Mok Vincent C.T. , Liu Wanting , Fan Xiang , Shi Lin , Au Lisa W.C. 
Published: December 2021

AbstractBackgroundControversy exists regarding the etiological role of cerebral small vessel disease (CSVD) in Alzheimer's disease (AD). We thus evaluated the association between brain Aβ/tau burden and white matter hyperintensity (WMH) volume among subjects with varying severity levels of cognitive impairment.MethodA total of 84 stroke‐free subjects (healthy controls [HC]=10; subjective cognitive decline [SCD]=32; mild cognitive impairment [MCI]=26; dementia =16) were included. All patients underwent structural MRI, 11C‐ PIB, and 18F‐T807 PET to measure CSVD makers, Aβ deposition (A+) and pathologic tau (T+), respectively. WMH volume was quantified by automatic segmentation using AccuBrain® IV 1.1 (BrainNow Medical Technology Company Ltd.).ResultNo significant association was found between A+T+ and WMH volume in the overall population (β =‐0.03 ;95% CI, ‐0.04‐0.11; p=0.10). There was also no significant association found within different cognitive diagnostic group except in those with dementia, where we found that increasing global 11C‐ PIB SUVR correlated with lower WMH volume (B=‐1.76 ;95% CI, ‐2.92‐ ‐0.59; p=0.007). No significant association between 18F‐T807 SUVR and WMH volume was observedConclusionWe found no association between brain Aβ/tau burden and WMH volume except an inverse association was noted between Aβ and WMH in dementia patients. PiB retention might be restrained by WMH in those patients with higher CSVD burden.
Physical activity attenuates or even eliminates the risk of all‐cause dementia associated with aging in older adults: A population‐based cohort study
Authors: Feter Natan , Leite Jayne S , Rombaldi Airton 
Published: December 2021

AbstractBackgroundFrom 2016 to 2040 the number of people with all‐cause dementia in the United Kingdom is expected to increase by 57%, while 70% percent of it is due to a higher life expectancy. It is meaningful to examine whether physical activity could mitigate the risk of all‐cause dementia associated with aging in older adults. We aimed to examine the overall and age‐stratified effect of physical activity on the risk of all‐cause dementia in older adults.MethodOlder adults aged 50 or more participants of the English Longitudinal Study of Aging (ELSA) were followed during a 17‐years follow‐up, between 2002 and 2019. Physical activity was accessed using a self‐reported, validated questionnaire in each wave (2002‐2019). Participants were classified as inactive, low, or moderate‐to‐high levels of physical activity. Medical diagnosis of dementia was asked in each wave for either the cohort member or by a proxy interview with family or caregivers. Additionally, the Informant Questionnaire on Cognitive Decline in the Elderly was used to determine the presence of all‐cause dementia (cut‐off = 3.5).ResultData from 8,270 older adults were analyzed (55.6% women; mean [SD] age, 63.9 [9.7]). Over a 17‐year follow‐up, 7.8% (95%: 7.3 to 8.4) were diagnosed with all‐cause dementia. For each year increased in age, the odds of all‐cause dementia increased 6.1% (95%CI: 5.1% to 7.1%). On the other hand, participants engaging in low (OR: 0.27; 95%CI: 0.22 to 0.33) or moderate‐to‐high level (OR: 0.12; 95%CI: 0.09 to 0.16) of physical activity had lower odds of incidence of all‐cause dementia through the follow‐up period. Participants aged 80 or over who engaged in a moderate‐to‐high level of physical activity had a lower risk of all‐cause dementia than inactive adults aged between 50‐69 years. Results were sustained after sensitive analysis to reduce the impact of reverse causality.ConclusionAlthough aging is the strongest risk factor for all‐cause dementia, physical activity could eliminate the risk associated with aging in older adults. Public health policies should consider that for older adults, engaging in physical activity below recommended levels may be an accessible and achievable strategy to prevent all‐cause dementia.
Exercise training improves cognition in chronic stroke: A 6‐month randomized controlled trial
Authors: Liu‐Ambrose Teresa , Falck Ryan S , Best John R , Hsiung Ging‐Yuek Robin , Middleton Laura E , Hall Peter A , Davis Jennifer C , Eng Janice J 
Published: December 2021

AbstractBackgroundA stroke doubles one’s risk for dementia. Impairment in multiple domains of cognition are common following stroke. Thus, stroke survivors represent a target population in need of intervention strategies to promote cognitive function and prevent dementia. We assessed whether targeted exercise training or cognitive and social enrichment activities would promote cognitive function in community‐dwelling adults with chronic stroke (i.e., > 12 months since stroke event).MethodsA three‐arm parallel, single‐blinded, 6‐month randomized controlled trial with 120 adults with chronic stroke who were randomized (2:2:3) to: 1) targeted exercise training (EX; n=34)) modeled after the Fitness And Mobility Exercise (FAME) program (Eng, Top Geriatr Rehabil, 2010); 2) cognitive and social enrichment activities (Cog‐Plus; n=34); and 3) an active control group (CON; n=52). Each experimental arm was group‐based and 2x/week. The primary outcome was the ADAS‐Cog‐Plus, a global measure of cognitive performance using multidimensional item response theory to summarize scores from the 13‐item ADAS‐Cog and other standard cognitive assessments (i.e., Trail Making Test Parts A and B, Digit Span Forward and Backward, and Animal and Vegetable Fluency). Lower ADAS‐Cog‐Plus scores represent better cognitive performance; ADAS‐Cog‐Plus scores of approximately −1.0 indicate healthy cognitive performance, 0.0 indicate mild cognitive impairment, and 1.0 indicate dementia. The primary analysis using linear mixed model compared changes in ADAS‐Cog‐Plus performance from baseline to month 6, with baseline ADAS‐Cog‐Plus and Mini‐Mental State Examination scores as covariates. Two planned simple contrasts (i.e., EX vs. CON; Cog‐Plus vs. CON) were performed using the Dunnett test.ResultMean baseline Fugl‐Meyer score was 81.21 (SD=23.85; range: 6‐100) and mean baseline Montreal Cognitive Assessment score was 21.89 points out of 30. An overall attrition rate of 14% was observed (EX=6; Cog‐Plus=5; CON=6). Participants in the EX group had significantly better ADAS‐Cog Plus performance than CON at trial completion (estimated mean difference: ‐0.23; 95%CI:[‐0.43, ‐0.03]; p=.024). There was no significant difference in ADAS‐Cog Plus performance between the Cog‐Plus and CON group at trial completion (estimated mean difference: ‐0.10; 95% CI:[‐0.30, 0.10]; p=.314).ConclusionTargeted exercise training may be efficacious in improving cognition in adults with chronic stroke and should be promoted among individuals with chronic stroke.
Using amyloid PET as a biomarker to detect progression of early Alzheimer’s disease
Authors: Ali Muhammad , Farias Fabiana H.G. , Sung Yun Ju , Wang Fengxian , Cruchaga Carlos 
Published: December 2021

AbstractBackgroundAlzheimer’s disease (AD), the most common form of dementia, is a complex polygenic disease with genetic, cellular, pathologic, and clinical heterogeneity. Recently, significant attempts have been made for identifying AD biomarkers for reliably tracking disease progression in its early asymptomatic stages. To this end, amyloid imaging technique has provided a breakthrough in deciphering the pathophysiology and accumulation of amyloid beta (Aβ) and hyperphosphorylated tau deposits in the brain. As such, our lab and multiple other research groups have used biomarker levels such as CSF Aβ tau, TREM2, and amyloid positivity for genetic association studies and identified novel genes and loci associated to AD. In a recent study, Raghavan et al., analyzed 4,314 participants and identified a novel locus for amyloidosis within RBFOX1 gene, however, this finding has not been replicated yet.MethodIn order to investigate the underlying genetic basis for brain amyloidosis in AD, we aim at systematically analyzing the largest collection of amyloid imaging (N=6,243), data across multiple ethnicities from multicenter cohorts (ADRC, A4, DIAN, ADNI, and ADNIDOD) as a quantitative trait to identify the functional variants and genes driving the association of AD.ResultResults and key findings will be presented at the AAIC meeting.ConclusionWe will leverage these datasets to generate prediction models for amyloid positivity and Mandelian Randomization (MR) analyses. Furthermore, the identification of AD‐specific molecular signatures and pathways will enable the characterization of appropriate therapeutic targets for the prevention and/or treatment of AD.