Cerebral circulation - cognition and behavior最新文献

{"title":"Retinal Vasculometry and Cognitive Status: Insights from the UK Biobank","authors":"Misha Ramesh ,&nbsp;Royce Shakespeare ,&nbsp;Roshan Welikala ,&nbsp;Jiri Fajtl ,&nbsp;Sarah A. Barman ,&nbsp;Anthony P. Khawaja ,&nbsp;Paul J. Foster ,&nbsp;Alicja R. Rudnicka ,&nbsp;Christopher G. Owen","doi":"10.1016/j.cccb.2025.100413","DOIUrl":"10.1016/j.cccb.2025.100413","url":null,"abstract":"<div><h3>Introduction</h3><div>Retinal vasculometry (RV) offers a non-invasive window into microvascular health and has emerged as a potential biomarker for neurovascular and cognitive decline. While previous studies have explored RV in relation to cognitive function, the distinct contributions of smaller (&lt;50µm) and larger (≥50µm) width retinal vessels remain unclear. This study investigates the associations between cognitive status and artificial intelligence (AI)-derived RV metrics across the spectrum of retinal vessel calibres.</div></div><div><h3>Methods</h3><div>Composite cognitive scores (G4) were derived, using principal component analysis, for UK Biobank participants who had completed four cognitive tests (“pairs matching”, “reaction time,” “prospective memory,” and “fluid intelligence”). RV features (width, area, tortuosity, and width-variance) were extracted from retinal images using the Quantitative Analysis of Retinal vessel Topology and siZe (QUARTZ) Deep Learning AI algorithm. Multilevel linear regression models estimated associations between RV measures and G4, adjusting for demographic, socioeconomic, and cardiometabolic covariates, with additional exclusion of participants with self-reported cardiovascular events.</div></div><div><h3>Results</h3><div>Data from 69,040 (78%) participants (mean age 57 years, 54.5% female) with 124,477 retinal images were included. A one standard deviation increase in G4 was associated with wider arterioles (0.11 µm, 95%CI 0.06, 0.17μm), greater arteriolar tortuosity (0.41%, 95%CI 0.405,0.412%), and increased arteriolar area (0.03mm², 95%CI 0.029,0.039mm²). Similar positive associations were found for venular width (0.48μm, 95%CI 0.35,0.61μm) and area (0.06mm², 95%CI 0.05,0.07mm²), particularly in the 50–59 age group. Conversely, venular tortuosity (-0.577%, 95%CI -0.575, -0.579%) and vessel width-variance were inversely associated with G4. Notably, lower cognitive scores were associated with narrower venules and reduced arteriolar tortuosity, across smaller and larger sized vessels. Arteriolar width, however, showed varied results between different sized vessels. Reductions in vessel area with lower G4 were more pronounced in larger vessels, suggesting vessel size-specific patterns of association.</div></div><div><h3>Conclusions</h3><div>AI-derived RV features are significantly associated with cognitive performance, reinforcing their potential as non-invasive biomarkers of neurovascular health. The observed differential associations across vessel sizes highlight the importance of analysing both smaller and larger retinal vessels in cognitive and neurodegenerative research. These findings support further exploration of RV metrics as early indicators of cognitive decline and potential tools in dementia risk stratification.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100413"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture protects against cerebral ischemia-reperfusion injury via regulating P2×7R expression","authors":"Sijia Chen ,&nbsp;Ye Zhu ,&nbsp;Feihong Lin ,&nbsp;Hanming Jiang ,&nbsp;Haipeng Liu ,&nbsp;Shan Li ,&nbsp;Xuliang Huang ,&nbsp;Yunchang Mo ,&nbsp;Junlu Wang ,&nbsp;Qinxue Dai","doi":"10.1016/j.cccb.2025.100379","DOIUrl":"10.1016/j.cccb.2025.100379","url":null,"abstract":"<div><h3>Background</h3><div>Ischemic stroke is a serious clinical condition that is challenging to cure; therefore, slowing down the depletion of ATP is crucial to enhancing the tolerance of ischemic tissue through preconditioning. Electroacupuncture (EA) preconditioning induces tolerance to cerebral ischemia; however, the underlying mechanism remains unclear.</div></div><div><h3>Objective</h3><div>The P2×7 receptor (P2×7R) mediates the stimulation of microglial cells and is involved in the development of cerebral ischemia-reperfusion (I/R) damage. We hypothesized that the protective effect of EA preconditioning is associated with the downregulation of P2×7R expression.</div></div><div><h3>Methods</h3><div>We performed EA at the \"Baihui\" and \"Fengfu\" for 30 min before establishing a rat model of cerebral I/R induced based on the middle cerebral artery occlusion model (MCAO). MCAO rats were administered a ventricular injection of 2 '(3′)-O-(4-benzoyl) adenosine triphosphate (BzATP), a P2×7R agonist, 30 min before EA. Neurologic scoring, infarction volume, and expression of cytokines, Bcl-2 and Bax, Iba1, P2×7R, p38, and phosphorylated p38 (p-p38) in ischemia penumbra were detected 24 h after cerebral I/R.</div></div><div><h3>Results</h3><div>EA preconditioning ameliorated neurologic scoring, decreased infarction volume, and neuronal injury, and decreased cytokine release, while BzATP exacerbated cerebral I/R damage and inflammation events, unlike the favorable efficacy of EA. EA inhibited the expression of Iba-1, P2×7R, and p-p38/p38 in the ischemic penumbra, whereas BzATP reversed this effect.</div></div><div><h3>Conclusions</h3><div>EA could induce cerebral tolerance to I/R damage by suppressing P2×7R expression and release of inflammatory factors.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100379"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143478643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Where in the brain is human intelligence?✰","authors":"Lars Nyberg","doi":"10.1016/j.cccb.2024.100374","DOIUrl":"10.1016/j.cccb.2024.100374","url":null,"abstract":"<div><div>We still know relatively little about how the human brain supports intelligence. I this personal view I argue that adopting the framework of neurocognitive component processes (NCP) might advance the current state of knowledge. Integration of information processing across distributed brain regions is proposed as a potential NCP, and some possible clinical implications of adopting the NCP framework are outlined.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100374"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11699295/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Social cognitive function in stroke survivors: A scoping review","authors":"Ana Davlasheridze ,&nbsp;Lena Rafsten ,&nbsp;David Krabbe ,&nbsp;Farzaneh Badinlou ,&nbsp;Renate Reniers ,&nbsp;Terence J Quinn ,&nbsp;Tamar Abzhandadze","doi":"10.1016/j.cccb.2025.100398","DOIUrl":"10.1016/j.cccb.2025.100398","url":null,"abstract":"<div><h3>Objective</h3><div>We aimed to summarize current evidence on social cognitive function in stroke survivors by: identifying social cognition domains assessed; describing assessment tools; reporting impairment prevalence; and outlining interventions targeting impaired social cognition.</div></div><div><h3>Methods</h3><div>Updated methodological scoping review guidelines were followed. Database searches were conducted by a librarian on February 26, 2024 (starting from January 1, 2000), across multidisciplinary, international databases. Two authors who independently screened title, abstract, and full texts, resolved discrepancies through discussion or senior reviewer input. Standardized data extraction forms were used, and data were analyzed using descriptive statistics.</div></div><div><h3>Results</h3><div>Of 29,069 records, 62 studies, mostly hospital-based (52 %), using case-control designs (37 %), met the inclusion criteria. They included 3152 participants with stroke (62 % male), mainly with ischemic stroke (61 %), and right hemisphere lesions (39 %). The five domains (number, most common assessment instruments, and prevalence/or mean ± <em>s</em>.d.) of social cognitive function were: emotion perception and recognition (<em>n</em> = 38, “Ekman 60-Faces Test,” 7–100 %); theory of mind (<em>n</em> = 23, “Reading the Mind in the Eyes,” 15–64 %); empathy (<em>n</em> = 15, 24 %, “Balanced Emotional Empathy Scale,” 6–58 %); emotion regulation (<em>n</em> = 1, 2 %, “Difficulties in Emotion Regulation Scale,” range: 8.8 ± 3.87–72.07±21.54); and social problem-solving (<em>n</em> = 2, “Social Problem-Solving Fluency Task,” range: 18.02±4.62–98.1 ± 4.0). No study focused on interventions.</div></div><div><h3>Conclusion</h3><div>Social cognition after stroke research has mainly addressed emotion recognition, theory of mind, and empathy, with limited attention to other aspects. Although social cognition impairments were common, no studies have specifically targeted their rehabilitation, underscoring the need for focused interventions.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100398"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145219498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-stroke cognitive impairment and fatigue in patients with white matter hyperintensities. A prospective cohort study","authors":"Joakim Ölmestig ,&nbsp;Viktor Frederik Idin Sørensen ,&nbsp;Ingrid Grimsgaard ,&nbsp;Birgitte Fagerlund ,&nbsp;Christina Kruuse","doi":"10.1016/j.cccb.2025.100387","DOIUrl":"10.1016/j.cccb.2025.100387","url":null,"abstract":"<div><h3>Background</h3><div>Cognitive impairment, depression, and fatigue are often neglected symptoms post-stroke. This study aimed to identify how white matter hyperintensity (WMH), a marker for cerebral small vessel disease (CSVD), is associated with post-stroke cognitive impairment, fatigue, and depression.</div></div><div><h3>Methods</h3><div>This prospective cohort study included participants admitted with stroke or transient ischemic attack. Participants were classified into two groups based on WMH on magnetic resonance imaging (MRI) using the Fazekas scale (0–1: no CSVD, 2–3: CSVD). Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA), Symbol Digit Modalities Test (SDMT), and Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) in the acute stroke phase (≤14 days) and three months post-stroke. Fatigue and depression were evaluated with the Fatigue Severity Scale (FSS) and the Beck Depression Inventory-II (BDI-II).</div></div><div><h3>Results</h3><div>Two hundred and fifty-six participants were included with MRI. A high Fazekas score was associated with lower baseline SDMT (-4.17 ± 1.48, <em>p</em> = 0.005, <em>p</em>_adj = 0.019), three-months SDMT (-3.56 ± 1.66, <em>p</em> = 0.034, <em>p</em>_adj = 0.103), and higher baseline FSS (0.78 ± 0.26, <em>p</em> = 0.003, <em>p</em>_adj = 0.011) independently of age. There was no association between the Fazekas score and MoCA or BDI-II.</div></div><div><h3>Conclusion</h3><div>These findings highlight the association between WMH, lower processing speed on the SDMT test in the acute stroke phase, and higher fatigue post-stroke. We propose that the WMH burden should be considered in all patients admitted with stroke or transient ischemic attack to identify those at increased risk of post-stroke cognitive impairment and fatigue.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100387"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144306475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pre-stroke frailty and cognition as predictors to select patients for acute stroke treatment","authors":"I. Cova ,&nbsp;E. Salvadori ,&nbsp;L. Pantoni","doi":"10.1016/j.cccb.2025.100519","DOIUrl":"10.1016/j.cccb.2025.100519","url":null,"abstract":"","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100519"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145528142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effects of hypertension on the neurovasculature of the human prefrontal cortex at single cell resolution","authors":"Hope Han ,&nbsp;Gabriele Rocha ,&nbsp;Lara Robinson Hannah Sleven ,&nbsp;Anandhakumar Chandran ,&nbsp;Cesar Medina ,&nbsp;Robert Kitchen ,&nbsp;Zam Cader","doi":"10.1016/j.cccb.2025.100473","DOIUrl":"10.1016/j.cccb.2025.100473","url":null,"abstract":"<div><h3>Introduction</h3><div>Cardiovascular disorders including hypertension and diabetes are major risk factors that accelerate cognitive decline and increase the risk of neurodegenerative disease. However, the cellular and molecular mechanisms underlying their effects on the human brain remain poorly defined. Uncovering these mechanism may offer new approaches to protect the brain.</div></div><div><h3>Methods</h3><div>We employed single-nucleus RNA sequencing (snRNA-seq) of post-mortem prefrontal cortex tissue from 48 individuals hypertension and/or diabetes, alongside matched controls, to delineate cell-type-specific effects on the brain. We peformed single dissociation into vascular and parenchymal fractions followed by Split-Seq barcoding of extacted nuclei, library preparation and sequencing. Cell types were annotated to produce a prefrontal cortex single cell atlas. Downstream analysis included psuedobulk differential gene expresson, cell-type GWAS enrichement and cell-cell communication.</div></div><div><h3>Results</h3><div>We identify a striking enrichment of hypertension-associated genetic risk within brain vascular and glial cell populations, highlighting a potential causal role of brain cells in the development of hypertension. Furthermore, we find that despite having received antihypertensive treatment, hypertension continues to drive transcriptional alterations in brain vascular cells and astrocytes. Functional analyses reveal that these changes prominently involve genes implicated in synaptic structure and neuronal connectivity, suggesting an unanticipated role of these genes in vascular and glial cells. Co-expression network analysis further supports their functional importance, with a module of synaptic and axon guidance genes present in control tissue brain endothelial cells and specifically disrupted in hypertension.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that conventional antihypertensive therapies, even blood-brain-barrier penetrant angiotensin targeted treatments, may be insufficient to counteract hypertension-driven neurovascular dysfunction. This highlights the need for new interventions that preserve glia-vascular in hypertension to mitigate cognitive decline.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100473"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carotid Artery Disease in Cerebral Small Vessel Disease and Dementia","authors":"Gan Han ,&nbsp;Erika Kitajima ,&nbsp;Ashley Suwanda ,&nbsp;Dan Jobson ,&nbsp;Louise Allan ,&nbsp;Masafumi Ihara ,&nbsp;Newman S K Sze ,&nbsp;Yoshiki Hase ,&nbsp;Tuomo Polvikoski ,&nbsp;Raj Kalaria","doi":"10.1016/j.cccb.2025.100501","DOIUrl":"10.1016/j.cccb.2025.100501","url":null,"abstract":"<div><h3>Introduction</h3><div>Carotid artery disease (CAD) is a recognised important cause of stroke. However, its relationship with cerebral small vessel disease (SVD) and dementia remains unclear. We hypothesized that CAD in older individuals significantly affects cerebral perfusion, and leads to cerebral SVD.</div></div><div><h3>Methods</h3><div>We performed a clinicopathological study in patients from the Cognitive Function After Stroke (CogFAST) study and prospectively recruited dementia patients with evidence of cerebral SVD. In addition to brain tissues, we collected postmortem samples of the internal carotid arteries (ICA) from these cohorts in the Newcastle Brain Tissue Resource. Standard neuropathological examination was performed for diagnosis and assignment of the cases per current diagnostic criteria for vascular and neurodegenerative dementias and assessed for presence of types of vascular pathology including the degree of stenosis and sclerosis in vascular tissues.</div></div><div><h3>Results</h3><div>We evaluated a total of 159 ICA samples and brain tissues from all cases with evidence of SVD. Severity of ICA stenosis and sclerotic index correlated strongly with both clinical stroke and brain infarction (P&lt;0.0001). More than 90% of the subjects had one subtype of ICA lesion in the order: intimal thickening &gt;fibrocalcific &gt;fibrous cap (thick) &gt;fibrous cap (thin) &gt;thrombus group with a strong inflammatory reaction in fibrocalcific atheromas. Linear regression analysis showed that ICA stenosis was positively correlated to both SVD pathology scores and total number of vascular lesions (P&lt;0.034). We found that severity of stenosis was related to anterior circulation involvement and small infarcts in the subcortical structures including the white matter (WM) rather than the cortex. Total intracranial artery scores were correlated with ICA stenosis and sclerosis (P&lt;0.001). In the CogFAST group analysis, the smallest lesions in the WM but not in the cortex or basal ganglia, and thalamus were associated with severity of ICA stenosis (P&lt;0.05)</div></div><div><h3>Conclusions</h3><div>Carotid atherosclerosis promotes cerebral SVD types of changes and influences the cerebral arterial system. Our observations also suggest extracranial ICA athology impacts on the perfusion and integrity of the deep WM.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100501"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictors of microbleed emergence and increase may differ in CADASIL","authors":"Jessica Lebenberg ,&nbsp;Laura Tintore-Carbonell ,&nbsp;Louis Lambert ,&nbsp;Mohamed Saichi ,&nbsp;Hugues Chabriat","doi":"10.1016/j.cccb.2025.100458","DOIUrl":"10.1016/j.cccb.2025.100458","url":null,"abstract":"<div><h3>Introduction</h3><div>CADASIL is a severe monogenic cerebral small vessel disease leading to stroke, motor impairment, gait disturbances and cognitive decline. On cerebral MRI, several markers are observed during the disease course, including cerebral microbleeds (CMBs).</div><div>Although not directly correlated with clinical severity, CMBs reflect significant underlying vessel wall pathology, suggesting potential predictive value for disease progression.</div><div>However, as they are observed in only 1/3 of patients and test-retests showed a low reliable counting when their number increases, the factors associated with their appearance and increase remain poorly investigated. We searched its predictors in a large French cohort of patients.</div></div><div><h3>Methods</h3><div>In addition to the CMBs counted visually in 517 CADASIL patients recruited at the National Referral Centre in France, we collected for each individual age, sex, vascular risk factors, NOTCH3 mutation location and other biological and neuroimaging markers. To investigate the predictors of both the presence and burden of CMBs, a Hurdle modeling approach was used based on two parts: 1) the presence of CMBs was analyzed using a logistic regression model; 2) among individuals with CMBs, the total count was studied using a truncated negative binomial regression model to account for the overdispersion and absence of zero counts. All continuous predictors were standardized prior to analysis. A univariate screening step was first applied to exclude variables with weak associations with CMBs (p &gt; 0.3).</div></div><div><h3>Results</h3><div>The distribution of CMBs in our study was zero-inflated, with approximately 2/3 of participants without any lesion, positively skewed, with a small subset exhibiting more than 50 CMBs. Older age and higher number of lacunes were revealed as significant predictors of the presence of CMBs. In contrast, male sex and higher LDL cholesterol levels were found associated with a larger burden of CMBs among individuals with such lesions (Fig1).</div></div><div><h3>Conclusions</h3><div>Our results suggest that the predictors of the emergence and increase of CMBs differ in CADASIL. These findings support that the mechanisms underlying their appearance may change over time and that other factors, as the disease progresses, may contribute to an increase in their number. Further studies are needed to confirm these results in other cohorts and settings.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100458"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Demographic and Cardiovascular Risk Factors Influence Midlife Cognitive Function: Evidence from the i3C DECADE Study","authors":"Vanessa Fonseca Lomeli ,&nbsp;Ileana De Anda-Duran ,&nbsp;Shirine Moukaled ,&nbsp;Jessica G. Woo ,&nbsp;Elaine M. Urbina ,&nbsp;Ganesh Baliga ,&nbsp;David J. Libon ,&nbsp;Lydia A. Bazzano","doi":"10.1016/j.cccb.2025.100454","DOIUrl":"10.1016/j.cccb.2025.100454","url":null,"abstract":"<div><h3>Introduction</h3><div>Age, sex, race, and education are well-established determinants of cognitive performance in traditional testing, yet their impact on novel digital measures is less understood. Digital assessments offer scalable, precise evaluation of cognition and may reveal subtle demographic differences important for early risk detection. Leveraging three distinct cohorts from the Disparities and Equity in Childhood Cardiovascular Exposures and Alzheimer’s Dementia (DECADES) project, we examined demographic influences on two digital cognitive tools.</div></div><div><h3>Methods</h3><div>Participants included 236 community-dwelling adults (age 38-69 years; 79.5% female; 68.3% White) drawn from three midlife DECADES cohorts, each with distinct racial/ethnic and socioeconomic profiles. Demographic predictors of interest were age, sex, and race; obesity and hypertension were also considered, given their cognitive relevance. Cognitive performance was measured using two tablet-based instruments: (1) the Rowan Digital Cancellation Test (RDCT), which includes letter, symbol, and mixed conditions with outcomes of accuracy and processing speed, and (2) the Linus Digital Clock Drawing Task, which includes command and copy conditions with metrics of latency, stroke conformity, speed, and total completion time. Standardized protocols were used for administration across sites. One-way ANOVA models were used to test differences between demographic variables and digital outcomes. Significant differences were further examined with pairwise post hoc comparisons to delineate group differences.</div></div><div><h3>Results</h3><div>Older participants demonstrated slower processing across RDCT and clock tasks (letter speed F=36.5, p&lt;0.001; mixed speed F=29.8, p&lt;0.001). Women outperformed men on RDCT speed (letter F=22.9, p&lt;0.001; symbol F=9.6, p=0.002) and on clock copy time (F=4.9, p=0.027). Black participants exhibited longer clock command latencies (F=22.7, p&lt;0.001), more stroke errors (F=6.9, p&lt;0.001), and slower cancellation performance (letter speed F=10.5, p=0.001). Obesity was associated with slower digital processing, as indicated by reduced performance on clock average speed (F = 4.83, p = 0.02) and cancellation average speed (F = 4.82, p = 0.029), whereas hypertension did not show a significant association.</div></div><div><h3>Conclusions</h3><div>Demographic factors—including age, sex, and race—exert a strong influence on digital cognitive performance in midlife, paralleling traditional neuropsychological test findings. RDCT and digital clock drawing are sensitive to sociodemographic differences, underscoring their potential as scalable tools to identify at-risk groups before clinical symptoms emerge.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100454"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}