Rupal I. Mehta, Ana W. Capuano, Roshni Biswas, David A. Bennett, Zoe Arvanitakis
{"title":"Permutations of cerebrovascular pathologies in older adults with and without diabetes","authors":"Rupal I. Mehta, Ana W. Capuano, Roshni Biswas, David A. Bennett, Zoe Arvanitakis","doi":"10.1016/j.cccb.2025.100381","DOIUrl":"10.1016/j.cccb.2025.100381","url":null,"abstract":"<div><div>Permutations of cerebrovascular pathologies (CVP) in persons with diabetes mellitus (DM) have not been comprehensively investigated. Here, we examine diverse postmortem CVP outcomes, including permutations of single or mixed CVP, in 2163 older adults with or without DM who were followed in longitudinal studies of aging. Annual clinical evaluations included data to classify DM status by medical history (DM diagnosis), direct medication inspection (anti-diabetic therapy), and hemoglobin A1C level (≥6.5 %). Upon death, neuropathological examinations were performed and included evaluation for CVP (considering vessel pathologies and brain infarcts) and Alzheimer's disease neuropathologic change (AD-NC). Among all participants [mean age, 89.49 ± 6.89 years (SD)], single CVP were more common than mixed CVP. Logistic regression was used to analyze the association of DM with CVP permutations, controlling for age at death, sex, education, and AD-NC, and revealed increased odds of microinfarcts alone (odds ratio, 1.56 [95 %CI, 1.03–2.35]) and mixed microinfarcts and macroinfarcts (odds ratio, 1.90 [95 %CI, 1.16–3.13]). These associations remained after adjusting for demographic factors and cohort or vascular comorbidities including stroke, heart disease, hypertension, claudication, smoking, and systolic blood pressure. Furthermore, after controlling for demographic factors as well as AD-NC and APOE type, mixed microinfarcts and macroinfarcts were associated with approximate threefold increased risk of dementia (odds ratio, 2.95 [95 %CI, 1.13–7.70]) in participants with DM. Evidence suggests that older adults living with DM have higher odds of microinfarcts and mixed microinfarcts and macroinfarcts in the absence of intracranial vessel pathologies that cannot be explained by vascular comorbidities, and in this population mixed microinfarcts and macroinfarcts are associated with higher odds of dementia.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100381"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143682581","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}
Claire Seigworth , Isabelle Grassl , Dawn F. Wolfgram
{"title":"Measuring cerebrovascular reactivity in a hemodialysis cohort","authors":"Claire Seigworth , Isabelle Grassl , Dawn F. Wolfgram","doi":"10.1016/j.cccb.2025.100380","DOIUrl":"10.1016/j.cccb.2025.100380","url":null,"abstract":"<div><div>Introduction Cerebrovascular reactivity (CVR) can inform about cerebral vascular health and provide prognostic information on risk cerebral ischemic injury. Use of transcranial Doppler ultrasound (TCD) is a non-invasive and inexpensive method to measure CVR and often uses a stimulus of increase in arterial partial pressure of carbon dioxide (pCO<sub>2</sub>). We evaluate re-breathing and breath-hold to measure CVR in a medically complex hemodialysis cohort who are at risk for cerebral hypoperfusion due to circulatory stress of hemodialysis.</div><div>Methods CVR was measured using both a 30 s breath-hold and a re-breathing period. We used percent change in mean flow velocity of the middle cerebral artery, measured with TCD over the change in end-tidal CO<sub>2</sub> to calculate CVR. Paired T-test was used to compare the parameters of CVR and Pearson correlation to evaluate relevant risk factors for lower CVR.</div><div>Results 16 participants completed both CVR measurements, with mean (SD) age of 64.2 (11.2) years. CVR measured from each technique was similar 3.4 (2.9) %/mmHg (breath-hold) vs 2.7 (1.6) %/mmHg, (re-breathing) <em>p</em> = 0.37. Older age and history of stroke were associated with lower CVR when measured with re-breathing but not with breath-hold technique.</div><div>Conclusions <em>Re</em>-breathing to increase pCO<sub>2</sub> and measure CVR is well-tolerated by a frail older medically complex patient population and may be a way to measure cerebrovascular health.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100380"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143519720","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}
Naomi Vlegels , Hilde van den Brink , Anna Kopczak , Tine Arts , Stanley D.T. Pham , Jeroen C.W. Siero , Benno Gesierich , Alberto De Luca , Marco Duering , Jaco J.M. Zwanenburg , Martin Dichgans , Geert Jan Biessels
{"title":"The relation between cerebral small vessel function and white matter microstructure in monogenic and sporadic small vessel disease - the ZOOM@SVDs study","authors":"Naomi Vlegels , Hilde van den Brink , Anna Kopczak , Tine Arts , Stanley D.T. Pham , Jeroen C.W. Siero , Benno Gesierich , Alberto De Luca , Marco Duering , Jaco J.M. Zwanenburg , Martin Dichgans , Geert Jan Biessels","doi":"10.1016/j.cccb.2025.100383","DOIUrl":"10.1016/j.cccb.2025.100383","url":null,"abstract":"<div><div>In cerebral small vessel disease (cSVD), vascular dysfunction has been associated with cSVD-lesions across the brain. Here we further explore the relation between vascular dysfunction and cSVD-related brain injury. We tested two hypotheses: (1) that complementary measures of abnormal small vessel function relate to decreased white matter integrity, and (2) that local variance in vascular dysfunction relates to local variance in white matter integrity within individual patients.</div><div>We included 23 patients with monogenic cSVD (i.e. CADASIL) and 46 patients with sporadic cSVD. With whole-brain analyses, we tested if small vessel flow velocity and reactivity measures from 7T-MRI were associated with global peak-width-of-skeletonized-mean-diffusivity (PSMD). We also tested voxel-wise correlations between reactivity to hypercapnia and mean diffusivity (MD) in white matter.</div><div>Whole-brain analyses showed a negative association between blood flow velocity and PSMD for the perforating arteries in the centrum semiovale in CADASIL (<em>p</em> = 0.04) and in the basal ganglia in sporadic cSVD (<em>p</em> = 0.002). Global white matter reactivity to hypercapnia was not associated with PSMD. Within patients, both in CADASIL and sporadic cSVD, we observed significant voxel-wise negative correlations for endothelial-independent vascular reactivity and MD in the white matter.</div><div>These findings confirm our hypothesis that small vessel dysfunction in patients with cSVD is associated with microstructural white matter alterations, also at voxel level. The latter may reflect a direct relationship between local small vessel dysfunction and tissue injury.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100383"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143726097","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}
Brittany Monte , Judianne Davis , Xiaoyue Zhu , Feng Xu , Mark Majchrzak , Matthew J. Cabral , Waela M. Van Nostrand , Bethany Healey , Sunil Koundal , Hedok Lee , John K. Robinson , Helene Benveniste , William E. Van Nostrand
{"title":"A novel gene edited rat model of cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL)","authors":"Brittany Monte , Judianne Davis , Xiaoyue Zhu , Feng Xu , Mark Majchrzak , Matthew J. Cabral , Waela M. Van Nostrand , Bethany Healey , Sunil Koundal , Hedok Lee , John K. Robinson , Helene Benveniste , William E. Van Nostrand","doi":"10.1016/j.cccb.2025.100401","DOIUrl":"10.1016/j.cccb.2025.100401","url":null,"abstract":"<div><h3>Background</h3><div>Cerebral Autosomal Recessive Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CARASIL) is a rare hereditary cerebral small vessel disease associated with loss-of-function mutations in the High Temperature Requirement Serine Protease 1 (HTRA1). While previous mouse models have provided insight into the functions of HTRA1, they have incompletely replicated the pathogenesis of CARASIL.</div></div><div><h3>Methods</h3><div>A novel gene-edited rat model of CARASIL (designated CRHTRA1) was generated containing the loss-of-function <em>Htra1</em> mutation p.R302Q. Quantitative cognitive, physiological, pathological and transcriptomic analyses were conducted to assess the CARASIL phenotype.</div></div><div><h3>Results</h3><div>At 12 months, histopathological analyses revealed marked thickening of the cerebral arteriolar walls with concomitant lumen stenosis. Changes in elastic composition, vascular smooth muscle cells and extracellular matrix proteins were identified in cerebral arteries. Downstream pathological remodeling of vasculature is implicated in increased capillary tortuosity and changes in capillary coverage in specific brain regions. Focal hyperintensity regions associated with enlarged perivascular spaces were identified locally by <em>in vivo</em> proton density weighted MRI. Region-specific reductions of fractional anisotropy were identified using diffusion tensor imaging and correlated with a reduction in neuronal densities. Behavioral testing in CRHTRA1 rats revealed significant cognitive deficit and gait disturbances. Micro-computed tomography of spinal vertebrae revealed pronounced increases in osteophyte formation. Global cerebral RNA sequencing revealed changes in signaling pathways associated with the loss-of-function HTRA1 CARASIL mutation, including those associated with transforming growth factor-β signaling and extracellular matrix remodeling.</div></div><div><h3>Conclusion</h3><div>The CRHTRA1 rat recapitulates many pathological changes that are consistent with both clinical CARASIL pathology and studies of HTRA1 function <em>in vitro</em>.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"9 ","pages":"Article 100401"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145265202","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}
Sijia Chen , Ye Zhu , Feihong Lin , Hanming Jiang , Haipeng Liu , Shan Li , Xuliang Huang , Yunchang Mo , Junlu Wang , Qinxue Dai
{"title":"Electroacupuncture protects against cerebral ischemia-reperfusion injury via regulating P2×7R expression","authors":"Sijia Chen , Ye Zhu , Feihong Lin , Hanming Jiang , Haipeng Liu , Shan Li , Xuliang Huang , Yunchang Mo , Junlu Wang , 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}
Ana Davlasheridze , Lena Rafsten , David Krabbe , Farzaneh Badinlou , Renate Reniers , Terence J Quinn , Tamar Abzhandadze
{"title":"Social cognitive function in stroke survivors: A scoping review","authors":"Ana Davlasheridze , Lena Rafsten , David Krabbe , Farzaneh Badinlou , Renate Reniers , Terence J Quinn , 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}
Joakim Ölmestig , Viktor Frederik Idin Sørensen , Ingrid Grimsgaard , Birgitte Fagerlund , Christina Kruuse
{"title":"Post-stroke cognitive impairment and fatigue in patients with white matter hyperintensities. A prospective cohort study","authors":"Joakim Ölmestig , Viktor Frederik Idin Sørensen , Ingrid Grimsgaard , Birgitte Fagerlund , 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><sub>adj</sub> = 0.019), three-months SDMT (-3.56 ± 1.66, <em>p</em> = 0.034, <em>p</em><sub>adj</sub> = 0.103), and higher baseline FSS (0.78 ± 0.26, <em>p</em> = 0.003, <em>p</em><sub>adj</sub> = 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}
Arunima Kapoor , Shubir Dutt , Amy Nguyen , Trevor Lohman , Aimée Gaubert , John Paul M. Alitin , Isabel J Sible , Anisa Marshall , Fatemah Shenasa , Allison C Engstrom , David Robert Bradford , Kathleen Rodgers , Daniel A Nation
{"title":"Endothelial progenitor cells and cerebral small vessel disease in APOE4 carriers","authors":"Arunima Kapoor , Shubir Dutt , Amy Nguyen , Trevor Lohman , Aimée Gaubert , John Paul M. Alitin , Isabel J Sible , Anisa Marshall , Fatemah Shenasa , Allison C Engstrom , David Robert Bradford , Kathleen Rodgers , Daniel A Nation","doi":"10.1016/j.cccb.2025.100378","DOIUrl":"10.1016/j.cccb.2025.100378","url":null,"abstract":"<div><div><em>APOE4</em> carriers at genetic risk for Alzheimer's disease exhibit early cerebrovascular dysfunction, which may be triggered by endothelial dysfunction. Endothelial progenitor cells (EPCs) represent cell populations involved in promoting angiogenesis and facilitating vascular repair in response to injury. We examined whether elevated EPCs are associated with lower cerebral small vessel disease burden in <em>APOE4</em> carriers prior to cognitive decline. Independently living older adults (<em>N</em> = 109, mean age = 70.5 years; SD = 7.9; 34.9 % male) free of dementia or clinical stroke underwent brain MRI and venipuncture. Small vessel disease was determined using a validated scale. White matter hyperintensity (WMH) volume was determined using the lesion segmentation toolbox. PBMCs were cultured and EPCs were defined as number of colony forming units in vitro. Regression analysis revealed an association between average number of EPC colonies and lower small vessel disease load (<em>p</em> = .026) and WMH volume (<em>p</em> = .002), in <em>APOE4</em> carriers. Findings suggest that EPC colony count may indicate activation of mechanisms which protect cerebrovascular function in <em>APOE4</em> carriers prior to the development of cognitive decline.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100378"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143419271","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}
Ying Xu , G. Peggy McFall , Lina Rydén , Johan Skoog , Edward Chang , Lucette A. Cysique , Katie Harris , Sarah Kedwell , Mei Ling Lim , Kaarin J. Anstey , Craig S. Anderson , Roger A. Dixon , Ingmar Skoog , Phillip J. Tully , Ruth Peters
{"title":"Cumulative blood pressure load and cognitive decline in older adults: An observational analysis of two large cohorts","authors":"Ying Xu , G. Peggy McFall , Lina Rydén , Johan Skoog , Edward Chang , Lucette A. Cysique , Katie Harris , Sarah Kedwell , Mei Ling Lim , Kaarin J. Anstey , Craig S. Anderson , Roger A. Dixon , Ingmar Skoog , Phillip J. Tully , Ruth Peters","doi":"10.1016/j.cccb.2024.100375","DOIUrl":"10.1016/j.cccb.2024.100375","url":null,"abstract":"<div><h3>Introduction</h3><div>Cumulative blood pressure metrics may provide greater precision for measuring temporal risk exposure, especially in later life where data are mixed regarding associations of high blood pressure (BP) on cognitive function. We examined the relationship between greater cumulative exposure to high BP in later life and several domains of cognitive function.</div></div><div><h3>Methods</h3><div>Individual cognitive assessment scores and BP measurements in older adults (age ≥70 years) at baseline and over approximately 8 years of follow-up were available in the population-based Canadian Victoria Longitudinal Study (VLS) and Swedish Gothenburg H70 Birth Cohort Studies (H70). Linear mixed models were used to quantify associations between cumulative systolic and diastolic BP and change in cognitive scores.</div></div><div><h3>Results</h3><div>Each additional 100mmHg increase in cumulative BP was related to greater decline in the Rey Auditory Verbal Learning Test (RAVLT) List A, trials 1–5 total score over follow-up: -0.23 (95% confidence interval [CI] -0.32, -0.13) for systolic BP and -0.41 (95%CI -0.58, -0.23) for diastolic BP. Similarly increases cumulative systolic and diastolic BP were related to greater declines Digit Symbol Substitution Task (DSS) scores: -0.59 (95%CI -0.80, -0.38) and -1.04 (95% CI -1.40, -0.67), respectively. There were no associations of cumulative BP and temporal changes in general cognition, other measures of verbal episodic memory, or semantic fluency.</div></div><div><h3>Conclusions</h3><div>Higher cumulative BP is associated with greater declines in RAVLT measured immediate memory span and complex attention, information processing speed and visuospatial scanning in older adults, but the scale of change is small. Additional research is required to further define these relationships and identify opportunities for prevention.</div></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"8 ","pages":"Article 100375"},"PeriodicalIF":1.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142985722","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}