Cerebral circulation - cognition and behavior最新文献

{"title":"Association between angiogenic factors and vascular risk, white matter hyperintensities and CSF amyloid beta","authors":"Lene Pålhaugen ,&nbsp;Berglind Gísladóttir ,&nbsp;Jonas Alexander Jarholm ,&nbsp;Bjørn-Eivind Kirsebom ,&nbsp;Per Selnes ,&nbsp;Tormod Fladby","doi":"10.1016/j.cccb.2024.100304","DOIUrl":"10.1016/j.cccb.2024.100304","url":null,"abstract":"<div><h3>Introduction</h3><p>Angiogenic mediators like placental growth factor (PlGF) and vascular endothelial growth factors (VEFG-C and VEFG-A) in cerebrospinal fluid (CSF) are suggested markers of cerebral small vessel disease (SVD). SVD is a cause of vascular cognitive impairment and dementia (VCID), but studies have shown that both non-amyloid SVD related to vascular risk factors and cerebral amyloid angiopathy (CAA) often exist in patients with Alzheimer's Disease (AD). CSF amyloid beta (Abeta) 42 is reduced in AD due to trapping in parenchymal plaques. Abeta40 is mainly deposited in the vasculature, and low CSF concentrations are seen in CAA. In this cross-sectional study, we examine the associations between these angiogenic factors, vascular risk and white matter hyperintensities (WMH) on MRI, as well as Abeta peptides in CSF.</p></div><div><h3>Methods</h3><p>We recruited non-demented participants from the Norwegian Dementia Disease Initiation cohort. We measured PlGF, VEGF-C and VEGF-A in CSF. Vascular risk was assessed with the Framingham Risk Score (FRS) for cardiovascular disease. WMH volumes were calculated by an automated algorithm. We used linear regression to examine associations between angiogenic markers and FRS, CSF levels of Abeta42 and Abeta40. Associations with WMH load were assessed in models without (Model 1) and with (Model 2) correction for amyloid status. Continuous variables were standardized. Age and sex were covariates.</p></div><div><h3>Results</h3><p>In total, 240 individuals (mean age 63.4 years, 128 female/112 male, 124 cognitively normal/116 cognitively impaired) were included. Reduced VEGF-C was associated with higher FRS (B=-0.292, p&lt;0.001) and reduced Abeta42 (B=0.261, p&lt;0.001) and Abeta40 (B=0.574, p&lt;0.001). We also found a negative association between WMH load and VEGF-C (B=-0.233, p&lt;0.001), that remained significant after correction for amyloid status. Increased PlGF was associated with higher FRS (B=0.186, p&lt;0.001), lower Abeta40 (B=-0.111, p=0.029) and increased WMH load (B=0.188, p=0.026), the latter remaining significant after correction for amyloid status.</p></div><div><h3>Discussion</h3><p>Both angiogenic factors VEGF-C and PlGF are associated with vascular risk, Abeta40 and WMH load, suggesting a role in both SVD and AD pathogenesis. These factors should be included in longitudinal studies to further confirm their impact on disease processes and elucidate mechanisms involved in the interaction between SVD and AD.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100304"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024001053/pdfft?md5=4ceab7c6227e5c2d0cc95fda8a291c28&pid=1-s2.0-S2666245024001053-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142121696","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":"Angiotensin-converting enzyme 2 (ACE-2) is dysregulated in Alzheimer's disease but not Vascular dementia","authors":"Ozge Guzel,&nbsp;Hannah Mary Tayler,&nbsp;James Scott Miners,&nbsp;Patrick Gavin Kehoe","doi":"10.1016/j.cccb.2024.100298","DOIUrl":"10.1016/j.cccb.2024.100298","url":null,"abstract":"<div><h3>Introduction</h3><p>The brain renin-angiotensin system (RAS) is dysregulated in dementia. We have previously shown that ACE-2, a central regulator of the protective counter-regulatory arm of RAS, is inversely associated with disease pathology in Alzheimer's disease (AD). We have investigated whether ACE-2 is similarly deficient in Vascular dementia (VaD) and mixed dementia (AD-VaD), in addition to AD. We also investigated whether ACE-2 is related to vascular pathology including CAA and SVD and explored whether ACE-2 varies according to gender, hypertension status, and ACE-2 genotype.</p></div><div><h3>Methods</h3><p>We studied brain tissue (frontal cortex) from 147 dementia cases (AD (n=94), VaD (n=20) and AD-VaD (n=33)) and 104 age-matched non-demented controls from the South West Dementia Brain Bank, University of Bristol. Amyloid β (Aβ) and tau pathology and levels, had previously been measured by IHC and ELISA, respectively. ACE-2 protein levels were measured by ELISA, and ACE-2 enzyme activity was measured using a fluorometric sensolyte kit (Anaspec). ACE-1 activity was measured using a fluorogenic assay; Ang-II and Ang-(1-7) were measured by in-house direct ELISA. ACE-2 genotypes (rs2285666 and rs4240157) were obtained by PCR.</p></div><div><h3>Results</h3><p>ACE-2 enzyme activity was significantly reduced in AD and AD-VaD cases (p&lt;0.0001 and p=0.0039, respectively) but not VaD. ACE-2 protein levels were unchanged between dementia groups. ACE-2 activity correlated inversely with parenchymal Aβ (r=-0.223, p=0.0005) and tau load (r=-0.294, p&lt;0.0001) and with insoluble Aβ40 and Aβ42 levels (r=-0.267 and r=-0.289, both p&lt;0.0001). ACE-2 activity correlated inversely with ACE-1 activity (r=−0.227, p=0.0004), and the ratio of ACE-1 to ACE-2 was significantly increased in AD and AD-VaD cases (p&lt;0.0001 and p=0.0029, respectively) but not in VaD. ACE-2 activity was lower in females with AD (p=0.0015). There is no relationship with CAA/SVD. ACE-2 activity was higher in people with late-stage hypertension (p=0.044), and females with hypertension have lower enzyme activity than males (p=0.041). ACE-2 levels and activity werenot associated with ACE-2 genotypes.</p></div><div><h3>Discussion</h3><p>These findings indicate that, despite strong vascular properties, changes in ACE-2 function are AD-related and not altered in VaD. The reduction in ACE-2 in females in AD warrants further investigation. We did not find any association with ACE-2 genotypes.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100298"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000990/pdfft?md5=8b7a017a0f50fecbe251364f6a3fce3a&pid=1-s2.0-S2666245024000990-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122043","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":"Baseline levels of soluble amyloid precursor proteins predict conversion to subcortical small-vessel disease","authors":"Petronella Kettunen ,&nbsp;Francesco Locatelli ,&nbsp;Emir Basic ,&nbsp;Maria Bjerke ,&nbsp;Michael Jonsson ,&nbsp;Johan Svensson ,&nbsp;Anders Wallin","doi":"10.1016/j.cccb.2024.100301","DOIUrl":"10.1016/j.cccb.2024.100301","url":null,"abstract":"<div><h3>Introduction</h3><p>The Gothenburg Mild Cognitive Impairment (MCI) study is a longitudinal mono-center study of patients seeking help for cognitive complaints at the memory clinic in Gothenburg, Sweden. The study includes both pre-clinical diagnoses, e.g. subjective cognitive impairment (SCI) and mild cognitive impairment (MCI), as well as patients with manifest dementia, including Alzheimer's disease (AD), subcortical small-vessel disease (SSVD) and mixed AD/SSVD. The International Working Group (IWG) for New Research Criteria for the Diagnosis of AD has proposed a conceptual framework for guiding diagnosis by biomarker analysis. In short, patients with typical AD and mixed AD/SSVD should display decreased amyloid-β (Aβ) 1-42 together with increased total tau or phosphorylated tau in cerebrospinal fluid (CSF).</p></div><div><h3>Methods</h3><p>In this project, we used the IWG-2 criteria to help the exploration of preclinical CSF biomarkers for SSVD. To this end, we investigated the odds of SCI and MCI patients with and without AD pathology converting to SSVD. Moreover, we investigated how CSF biomarker levels at baseline affected risk of converting to SSVD. The applied cut-offs for AD pathology were Aβ-42 &lt; 530 ng/L, t-tau&gt;350 ng/L and p-tau181&gt;59 ng/L. The study cohort consisted of 29 SCI with AD pathology and 173 SCI without AD pathology, and 98 MCI with AD pathology and 203 MCI without AD pathology. CSF biomarkers Aβ-38, Aβ-40 and Aβ-42, and soluble amyloid precursor protein (sAPP) alpha and beta were analyzed at baseline.</p></div><div><h3>Results</h3><p>While SCI and MCI patients with pathological AD biomarkers were 30 times more likely to convert to AD and 15 times more likely to convert to mixed AD/SSVD, pathological AD biomarkers did not predict conversion to SSVD. Using Cox regression analysis, we found that higher levels of sAPP-α and sAPP-β at baseline were associated with lower risk of converting to SSVD. Moreover, Kaplan- Meier estimations showed that when preclinical subjects were stratified according to baseline levels of sAPP-α or Aβ-40, those with the lower levels of the proteins had increased probability of converting to SSVD. No other biomarkers were associated with conversion to SSVD.</p></div><div><h3>Discussion</h3><p>sAPP-α/-β and Aβ-40 could be used as potential biomarkers to evaluate progression to SSVD.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100301"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024001028/pdfft?md5=82f0f4a80ce5b6c91d1ed94ab6a1b443&pid=1-s2.0-S2666245024001028-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122046","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":"METABOLIC SYNDROME IS ASSOCIATED WITH POOR COGNITION: A POPULATION-BASED STUDY OF 70-YEAR-OLDS WITHOUT DEMENTIA","authors":"Anna Marseglia ,&nbsp;Alexander Darin-Mattsson ,&nbsp;Johan Skoog ,&nbsp;Lina Rydén ,&nbsp;Timothy Hadarsson-Bodin ,&nbsp;Silke Kern ,&nbsp;Therese Rydberg Sterner ,&nbsp;Ying Shang ,&nbsp;Anna Zettergren ,&nbsp;Eric Westman ,&nbsp;Ingmar Skoog","doi":"10.1016/j.cccb.2022.100095","DOIUrl":"https://doi.org/10.1016/j.cccb.2022.100095","url":null,"abstract":"","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100095"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245022000605/pdfft?md5=ef07743ea3b39b9d0df732d07d0ec663&pid=1-s2.0-S2666245022000605-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141478824","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":"SMALL AND LARGE MRI-VISIBLE PERIVASCULAR SPACES IN THE BASAL GANGLIA OF PARKINSON'S DISEASE PATIENTS","authors":"Stephanie Berberian ,&nbsp;Joel Ramirez ,&nbsp;David P. Breen ,&nbsp;Anne Rowling ,&nbsp;Tiago A. Mestre ,&nbsp;Connie Marras ,&nbsp;Donna Kwan ,&nbsp;Sean Symons ,&nbsp;Mario Masellis ,&nbsp;Sandra E. Black ,&nbsp;Anthony E. Lang","doi":"10.1016/j.cccb.2022.100096","DOIUrl":"https://doi.org/10.1016/j.cccb.2022.100096","url":null,"abstract":"","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100096"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245022000617/pdfft?md5=294b8b5723eccd0988808110c9e0afbb&pid=1-s2.0-S2666245022000617-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141480274","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":"The protocol for an observational Australian cohort study of CADASIL: The AusCADASIL study","authors":"Danit G. Saks ,&nbsp;Beata Bajorek ,&nbsp;Vibeke S. Catts ,&nbsp;Adam C. Bentvelzen ,&nbsp;Jiyang Jiang ,&nbsp;Wei Wen ,&nbsp;Karen A. Mather ,&nbsp;Anbupalam Thalamuthu ,&nbsp;Jessie Huang-Lung ,&nbsp;Lisa Nivison-Smith ,&nbsp;Lyn R. Griffiths ,&nbsp;Robert A. Smith ,&nbsp;Adrienne Sexton ,&nbsp;Paul James ,&nbsp;Tharusha Jayasena ,&nbsp;Anne Poljak ,&nbsp;Gurpreet K. Hansra ,&nbsp;Satoshi Hosoki ,&nbsp;Ashley Park ,&nbsp;Claudia M. Hillenbrand ,&nbsp;Perminder S. Sachdev","doi":"10.1016/j.cccb.2024.100225","DOIUrl":"https://doi.org/10.1016/j.cccb.2024.100225","url":null,"abstract":"<div><h3>Introduction</h3><p>Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a rare genetic condition with a broad phenotypic presentation. This study aims to establish the first Australian cohort of individuals affected by CADASIL (AusCADASIL) and examine its clinical features and longitudinal course, and to investigate neuroimaging and blood biomarkers to assist in early diagnosis and identify disease progression.</p></div><div><h3>Methods</h3><p>Participants will be recruited from six study centres across Australia for an observational study of CADASIL. We aim to recruit 150 participants with diagnosed CADASIL, family history of CADASIL or suspected CADASIL symptoms, and 150 cognitively normal <em>NOTCH3</em> negative individuals as controls. Participants will complete: 1) online questionnaires on medical and family history, mental health, and wellbeing; 2) neuropsychological evaluation; 3) neurological examination and brain MRI; 4) ocular examination and 5) blood sample donation. Participants will have annual follow-up for 4 years to assess their progression and will be asked to invite a study partner to corroborate their self-reported cognitive and functional abilities.</p><p>Primary outcomes include cognitive function and neuroimaging abnormalities. Secondary outcomes include investigation of genetics and blood and ocular biomarkers. Data from the cohort will contribute to an international consortium, and cohort participants will be invited to access future treatment/health intervention trials.</p></div><div><h3>Discussion</h3><p>AusCADASIL will be the first study of an Australian cohort of individuals with CADASIL. The study will identify common pathogenic variants in this cohort, and characterise the pattern of clinical presentation and longitudinal progression, including imaging features, blood and ocular biomarkers and cognitive profile.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100225"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000266/pdfft?md5=d13da543f8720e9a466517825ffaa5e8&pid=1-s2.0-S2666245024000266-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141239334","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":"FIBRINOGEN ACTIVATES MICROGLIA AND DRIVES EXTRACELLULAR VESICLE MEDIATED PROPAGATION OF PRO-INFLAMMATORY SIGNALING","authors":"Austyn Roseborough,&nbsp;Yunxu Zhu,&nbsp;Lin Zhao,&nbsp;Shawn Whitehead","doi":"10.1016/j.cccb.2022.100073","DOIUrl":"https://doi.org/10.1016/j.cccb.2022.100073","url":null,"abstract":"","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100073"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245022000381/pdfft?md5=5bec3d929599919620a921d54c2d7c97&pid=1-s2.0-S2666245022000381-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141479197","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":"Correlates of axonal content in healthy adult span: Age, sex, myelin, and metabolic health","authors":"Agnieszka Z Burzynska ,&nbsp;Charles Anderson ,&nbsp;David B. Arciniegas ,&nbsp;Vince Calhoun ,&nbsp;In-Young Choi ,&nbsp;Andrea Mendez Colmenares ,&nbsp;Arthur F Kramer ,&nbsp;Kaigang Li ,&nbsp;Jongho Lee ,&nbsp;Phil Lee ,&nbsp;Michael L Thomas","doi":"10.1016/j.cccb.2024.100203","DOIUrl":"https://doi.org/10.1016/j.cccb.2024.100203","url":null,"abstract":"<div><p>As the emerging treatments that target grey matter pathology in Alzheimer's Disease have limited effectiveness, there is a critical need to identify new neural targets for treatments. White matter's (WM) metabolic vulnerability makes it a promising candidate for new interventions. This study examined the age and sex differences in estimates of axonal content, as well the associations of with highly prevalent modifiable health risk factors such as metabolic syndrome and adiposity. We estimated intra-axonal volume fraction (ICVF) using the Neurite Orientation Dispersion and Density Imaging (NODDI) in a sample of 89 cognitively and neurologically healthy adults (20–79 years). We showed that ICVF correlated positively with age and estimates of myelin content. The ICVF was also lower in women than men, across all ages, which difference was accounted for by intracranial volume. Finally, we found no association of metabolic risk or adiposity scores with the current estimates of ICVF. In addition, the previously observed adiposity-myelin associations (Burzynska et al., 2023) were independent of ICVF. Although our findings confirm the vulnerability of axons to aging, they suggest that metabolic dysfunction may selectively affect myelin content, at least in cognitively and neurologically healthy adults with low metabolic risk, and when using the specific MRI techniques. Future studies need to revisit our findings using larger samples and different MRI approaches, and identify modifiable factors that accelerate axonal deterioration as well as mechanisms linking peripheral metabolism with the health of myelin.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100203"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000047/pdfft?md5=f1904373d769d3ad4b2aba8267134510&pid=1-s2.0-S2666245024000047-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139473511","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":"Standing middle cerebral artery velocity predicts cognitive function and gait speed in older adults with cognitive impairment, and is impacted by sex differences","authors":"Laura K Fitzgibbon-Collins ,&nbsp;Geoff B Coombs ,&nbsp;Mamiko Noguchi ,&nbsp;Shashankdhwaj Parihar ,&nbsp;Richard L Hughson ,&nbsp;Michael Borrie ,&nbsp;Sue Peters ,&nbsp;J Kevin Shoemaker ,&nbsp;Jaspreet Bhangu","doi":"10.1016/j.cccb.2023.100198","DOIUrl":"https://doi.org/10.1016/j.cccb.2023.100198","url":null,"abstract":"<div><p>Upright posture challenges the cerebrovascular system, leading to changes in middle cerebral artery velocity (MCAv) dynamics which are less evident at supine rest. Chronic alterations in MCAv have been linked to hypoperfusion states and the effect that this may have on cognition remains unclear. This study aimed to determine if MCAv and oscillatory metrics of MCAv (ex. pulsatility index, PI) during upright posture are i) associated with cognitive function and gait speed (GS) to a greater extent than during supine rest, and ii) are different between sexes.</p><p>Beat-by-beat MCAv (transcranial Doppler ultrasound) and mean arterial pressure (MAP, plethysmography) were averaged for 30-seconds during supine-rest through a transition to standing for 53 participants (73±6yrs, 17 females). While controlling for age, multiple linear regressions predicting MoCA scores and GS from age, supine MCAv metrics, and standing MCAv metrics, were completed. Simple linear regressions predicting Montreal Cognitive Assessment (MoCA) score and GS from MCAv metrics were performed separately for females and males. Significance was set to <em>p</em>&lt;0.05.</p><p>Lower standing diastolic MCAv was a significant (<em>p</em> = 0.017) predictor of lower MoCA scores in participants with mild cognitive impairment, and this relationship only remained significant for males. Lower standing PI was associated with slower GS (<em>p</em> = 0.027, <em>r</em>=-0.306) in both sexes. Our results indicate a relationship between blunted MCAv and altered oscillatory flow profiles during standing, with lower MoCA scores and GS. These relationships were not observed in the supine position, indicating a unique relationship between standing measures of MCAv with cognitive and physical functions.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100198"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245023000429/pdfft?md5=f91d374e99f31e53a9a484e25388be84&pid=1-s2.0-S2666245023000429-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139479978","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":"What matters to people and families affected by cerebral small vessel disease (SVD)? A qualitative grounded theory investigation","authors":"Sophia Wong Ching Hwai ,&nbsp;Joanna M. Wardlaw ,&nbsp;Anna Williams ,&nbsp;Fergus N. Doubal","doi":"10.1016/j.cccb.2024.100202","DOIUrl":"10.1016/j.cccb.2024.100202","url":null,"abstract":"<div><h3>Background</h3><p>Cerebral small vessel disease (SVD) is a common neurological disorder contributing to stroke, dementia, and disability. No treatment options exist although clinical trials are ongoing. We aimed to understand what matters to people and families affected by SVD to inform future research.</p></div><div><h3>Methods</h3><p>We thematically analysed unsolicited correspondences from members of the public addressed to members of the Edinburgh SVD Research Group on a variety of subjects related to SVD. We used inductive thematic codes, categorised under concerns, requests, emotions, and contributions, to form a grounded theory that categorised and ranked concerns raised.</p></div><div><h3>Results</h3><p>101 correspondents expressed 346 concerns between August 2015 and February 2021, mostly via email. 60 correspondents (59.4 %) disclosed a SVD diagnosis, 39 (38.6 %) disclosed a previous stroke or TIA, and 40 (39.6 %) were family of people living with SVD. Primary concerns related to cognitive problems (number of correspondents (n)=43 (42.6 %)), lack of support or information from healthcare services (<em>n</em> = 41 (40.6 %)), prognosis (<em>n</em> = 37 (36.6 %)), sensory disturbances (<em>n</em> = 27 (26.7 %)), functional problems (<em>n</em> = 24, (23.8 %)), impact on daily life (<em>n</em> = 24 (23.8 %)), and causes of SVD (<em>n</em> = 19 (18.8 %)). 57 correspondents (56.4 %) expressed support for research, 43 (42.6 %) expressed an eagerness to understand SVD, 35 (34.7 %) expressed helplessness, and 19 (18.8 %) expressed frustration.</p></div><div><h3>Conclusions</h3><p>Cognitive decline was the main concern for people and families living with SVD who corresponded with the Edinburgh SVD research group. These findings also indicate a need for more accessible services and better information about SVD for patients and families.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100202"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000035/pdfft?md5=b2f3385ad243f9fe6cf33fe58bc0f2f5&pid=1-s2.0-S2666245024000035-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139634784","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}