Cerebral circulation - cognition and behavior最新文献

{"title":"Neuropsychological assessment in vascular cognitive impairment: A call to lay the quest for the best test to rest","authors":"Geert Jan Biessels, GJ Biessels","doi":"10.1016/j.cccb.2024.100219","DOIUrl":"https://doi.org/10.1016/j.cccb.2024.100219","url":null,"abstract":"","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100219"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000205/pdfft?md5=73d5ea6667ac63d1b600b976a1851ee4&pid=1-s2.0-S2666245024000205-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140296721","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 is brain health?","authors":"Philip B. Gorelick,&nbsp;Farzaneh A. Sorond","doi":"10.1016/j.cccb.2023.100190","DOIUrl":"10.1016/j.cccb.2023.100190","url":null,"abstract":"<div><p>The call to optimize brain health is now a local, regional and global priority. Organizations such as the World Health Organization, Centers for Disease Control and Prevention and Alzheimer's Association, American Academy of Neurology, World Federation of Neurology, and others have developed recommendations for the maintenance of brain health. Brain health definitions range from broad to narrow in scope and may focus on cognition or encompass broader core components such as cerebral, mental and social domains. In this manuscript we will explore various definitions of brain health and its core components, the importance of cognitive and functional domains, and briefly introduce the concept of cognitive medicine in the context of brain health.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100190"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266624502300034X/pdfft?md5=291223c05f9be0d0c5c9ca7d4a964f05&pid=1-s2.0-S266624502300034X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136093158","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":"Associations between metabolic syndrome and markers of brain pathology: the role of sex- differences","authors":"Anna Marseglia ,&nbsp;Alexandra Cooper ,&nbsp;Lina Ryden ,&nbsp;Silke Kern ,&nbsp;Sara Shams ,&nbsp;Olof Lindberg ,&nbsp;Kaj Blennow ,&nbsp;Henrik Zetterberg ,&nbsp;Anna Zettergren ,&nbsp;Ingmar Skoog ,&nbsp;Eric Westman ,&nbsp;Henrik Zetterberg ,&nbsp;Anna Zettergren ,&nbsp;Ingmar Skoog ,&nbsp;Eric Westman","doi":"10.1016/j.cccb.2024.100241","DOIUrl":"10.1016/j.cccb.2024.100241","url":null,"abstract":"<div><h3>Introduction</h3><p>Cardiovascular and metabolic disorders rarely occur alone in old age but often cluster together in the so-called metabolic syndrome (MetS). While individual components of MetS, such as obesity, hypertension, and diabetes, have been linked to dementia and brain atrophy, their combined impact on cognitive and brain aging remains poorly explored. Our current study aims to investigate the relationship between MetS and markers of neurodegenerative and cerebrovascular pathologies while also considering potential differences between sexes.</p></div><div><h3>Methods</h3><p>We included 741 cognitively intact septuagenarians from the Gothenburg H70-Birth cohort 1944 with available brain MRI (286 had cerebrospinal fluid [CSF] sampling). MetS was defined by standard criteria (at least three among adiposity, raised blood pressure, blood glucose, reduced HDL-cholesterol, elevated triglycerides). MRI markers of brain pathology included overall (mean cortical thickness) and Alzheimer's disease (AD; average cortical thickness in signature areas) neurodegeneration, cerebral small vessel disease (SVD; markers such as white matter hyperintensity, lacunes, microbleeds, and perivascular spaces, and SVD score) and DTI's white- matter microstructural changes (fractional anisotropy). CSF biomarkers included t-tau, neurofilament light, neurogranin (overall neurodegeneration), Aβ42 and p-tau (AD), and CSF/serum albumin ratio (blood-brain barrier integrity). Analyses included regression models and stratification by sex.</p></div><div><h3>Results</h3><p>Overall, 410 participants (53%, n=196 women) had MetS. MetS was associated with increased odds of overall (OR=2.0, 95%CI 1.4–2.9) and AD-related (OR=1.8, 95%CI 1.4–2.6) neurodegeneration, high SVD burden (presence of ≥3 SVD compared to none: OR=2.1, 95%CI 1.1–4.3), and white-matter microstructural changes. Within the SVD markers, MetS was particularly related to white matter hyperintensities, lacunes, and perivascular spaces in basal ganglia. Furthermore, MetS was associated with alterations of blood-brain barrier integrity in the CSF subsample. Sex differences showed increased SVD burden in men with MetS, especially enlarged perivascular spaces (OR=2.9, 95%CI 1.7–5.0), while no differences were observed in women. No associations were detected with amyloid and tau.</p></div><div><h3>Discussion</h3><p>MetS in late life is linked to neurodegenerative and cerebrovascular pathologies, with SVD more prominent in men with MetS, but not in women.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100241"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000424/pdfft?md5=dd4e4c9de92b887cf5a511a0b8ec59d2&pid=1-s2.0-S2666245024000424-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142121669","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":"Diabetes and Dementia in 3 H-70 cohorts in Gothenburg","authors":"Roland Haase ,&nbsp;Xin Xin Guo ,&nbsp;Valter Sundh ,&nbsp;Ingmar Skoog","doi":"10.1016/j.cccb.2024.100317","DOIUrl":"10.1016/j.cccb.2024.100317","url":null,"abstract":"<div><p>A total number of 2498 individuals 70 years old were randomly elicited in Gothenburg, n=966 in 1971, n=1028 in 1976 and n=504 in 2000. Blood glucose levels in the 3 cohorts were 5.53 mmol/l for 1971 cohort, 5.30 mmol/l for 1976 and 5.83 mmol/l for 2000. Blood glucose levels declined when the cohorts were examined again with 75 years and 79 years. Looking at DM individuals, blood glucose levels at age 70 for the cohort 1971 was 8,90 mmol/l (n=54), for cohort 1976 of 8,91 mmol/l (n=64) and for cohort 1930 of 8,45 mmol/l (n=57). A strong correlation between Diabetes mellitus (DM) and body mass index (BMI) existed: BMI &lt;25 had a frequency of DM in 6,0%, for BMI =25&lt;30 had 6,4% DM, for BMI =30&lt;35 had 10,6% and BMI &gt;=35 had 23,1% DM. HbA1c mean was 40,68 (median 38,0) for all participants and 53,12 (median 51,0) in DM. The correlation of HbA1c with BMI did not reach statistical significance (p=0,09). In 2009 in DM individuals HbA1c was considerably higher in cerebrovascular dementia (62,3 mmol/l) than in DM with Alzheimer dementia (52,3 mmol/l) or in non-dementia (52,5 mmol/l) but numbers were too small for significance (rank test pooled 0,14; Satterthwaite 0,22). The proportion of DM was higher in the cerebrovascular group (8 of 18; 44%) than in the Alzheimer dementia (9 of 38; 27%) or in non-dementia (83 of 600; 13,8%). This prospective study showed an association between DM with cerebrovascular dementia, whereas the association with Alzheimer dementia was weaker.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100317"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024001181/pdfft?md5=2e21e99c85afcc3254f2a97a5297c183&pid=1-s2.0-S2666245024001181-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142121692","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":"TREM2-regulated microglial reactivity confers resilience against vascular contributions to white matter injury and cognitive decline","authors":"Stefan Szymkowiak ,&nbsp;Mila Redzic ,&nbsp;Anirudh Patir ,&nbsp;Clare Latta ,&nbsp;Michael Daniels ,&nbsp;Jack Barrington ,&nbsp;Katie Askew ,&nbsp;Jessica Duncombe ,&nbsp;Karen Horsburgh ,&nbsp;Barry McColl","doi":"10.1016/j.cccb.2024.100318","DOIUrl":"10.1016/j.cccb.2024.100318","url":null,"abstract":"<div><p>Cerebrovascular disease is a major contributor to subcortical white matter pathology, vascular cognitive impairment (VCI) and dementia. Although the precise pathophysiological mechanisms remain unclear, it is increasingly evident that microglial responses may be critical to the development and progression of cerebrovascular disease and its cognitive consequences. To investigate this further, we assessed microglial reactivity in white matter regions of human post- mortem tissue with pathologically confirmed cerebrovascular injury. In parallel, we implemented a mouse model of VCI induced by bilateral carotid artery stenosis (BCAS) and determined the impact of genetically deleting the microglial immunoreceptor triggering receptor expressed on myeloid cells 2 (TREM2), a key regulator of microglial homeostatic and reactive functions. Using immunohistochemistry (IHC) and quantitative polymerase chain reaction (QPCR) we observed increased microglial reactivity and TREM2 expression in our human cohort implicating TREM2 signalling in microglial responses to cerebrovascular. In mice, IHC and flow cytometric analysis revealed Trem2 deficiency blunted microglial reactivity following BCAS (1 month). Transcriptomic analysis of Trem2-/- microglia also demonstrated attenuated induction of gene expression modules associated with inflammation, lysosomal function, lipid processing and metabolic reprogramming following BCAS (data not shown). Importantly, this was associated with greater white matter injury compared to wildtype (WT) counterparts in the absence of overt cognitive changes. Following longer durations of BCAS (6 months), Trem2-/- mice exhibited additional parenchymal and vascular pathologies associated with impairments in spatial learning and memory whilst such changes were largely absent in WT mice. Interestingly, assessment of microglia by IHC demonstrated reduced interaction with white matter cerebrovasculature in Trem2-/- mice. Taken together, these data support a role for microglia in cerebrovascular contributions to cognitive decline and dementia. Therefore, targeting regulators of microglia reactivity may provide means to influence cerebrovascular disease trajectory and associated cognitive changes. While further work is required to delineate the precise function of microglia in this context, our preclinical data suggest TREM2-regulated microglial responses to cerebrovascular insult are important for maintenance of brain health and cognitive resilience. Future work will continue to decipher how TREM2 mediates such resilience with particular focus on interaction with other cell types within the neurogliovascular unit.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100318"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024001193/pdfft?md5=f38710d7ba93681190ddec3dec12c2b7&pid=1-s2.0-S2666245024001193-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142121694","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":"Diabetes and MRI Infarction in the Hispanic Community Health Study, Study of Latinos","authors":"Vincent Chen ,&nbsp;Ariana Stickel ,&nbsp;Wassim Tarraf ,&nbsp;Kevin Gonzalez ,&nbsp;Donglin Zeng ,&nbsp;Jianwen Cai ,&nbsp;Carmen Isasi ,&nbsp;Robert Kaplan ,&nbsp;Richard Lipton ,&nbsp;Martha Daviglus ,&nbsp;Fernando Testai ,&nbsp;Melissa Lamar ,&nbsp;Linda Gallo ,&nbsp;Gregory Talavera ,&nbsp;Vladimir Ivanovic ,&nbsp;Stephan Seiler ,&nbsp;Hector Gonzalez ,&nbsp;Charles DeCarli","doi":"10.1016/j.cccb.2024.100289","DOIUrl":"10.1016/j.cccb.2024.100289","url":null,"abstract":"<div><h3>Introduction</h3><p>HCHS/SOL is a representative study of Hispanic/Latinos living in the US. HCHS/SOL participants have a high prevalence of diabetes (1) and diabetic associated cognitive decline (2). Previous studies of predominantly non-Hispanic White populations indicate that silent brain infarcts are associated with incident dementia (3). Given that diabetes is prevalent in HCHS/SOL and associated with cognitive decline, we examined whether diabetes may also lead to infarction on MRI.</p></div><div><h3>Methods</h3><p>SOL-INCA-MRI consists of 2668 individuals of Hispanic/Latino Heritage from 4 centers across the US. Demographics of the cohort are summarized in the Table. The presence or absence of infarction on MRI was determined from review of high resolution T1, T2 and FLAIR imaging as well as gradient echo imaging by a neuroradiologist and a stroke neurologist with a high level of agreement (ICC &gt;0.90). Desperate readings were adjudicated by a neurologist with experience in vascular brain injury. Diabetes based on American Diabetes Association definition of normal, prediabetic and diabetic. This definition used measures serum glucose levels adjusted for fasting time and, if available, post-OGTT glucose levels, A1C percentages, and scanned/transcribed anti- diabetic medication use. General linear model was used to test the associated between the presence or absence of MRI and diabetes adjusting for age, gender, heritage, and center.</p></div><div><h3>Results</h3><p>Subjects were 62.3 + 9.2 years of age at MRI range [35-86], 67% were female and the prevalence of MRI infarction was 7% (Table). Pre-diabetes was present in 45% and diabetes in 22%. Stroke prevalence increased with age ranging from &lt;1% at age 40 to 18% at age 80 (Figure 1). Diabetes or pre-diabetes prevalence also increased with age being 10% at 40 and over 60% at age 80 (Figure 2). Adjusting for age, men were 2 times more likely to be diabetic. In the full model, age, gender, and diabetes were significantly associated with infarction seen on MRI with the likelihood of infarction 1.9 times greater in persons with diabetes.</p></div><div><h3>Discussion</h3><p>These results indicate that the presence of diabetes is strongly associated with infarction on MRI in Hispanic/Latinos in the US. This association may explain, in part, the association between diabetes and cognitive decline.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100289"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000904/pdfft?md5=f537124251def64cd9c846fc95353e0e&pid=1-s2.0-S2666245024000904-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122117","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":"Modes of covariation between vascular risk factors and cognition in cohorts with cultural and geographical variations","authors":"Bonnie Yin Ka Lam ,&nbsp;Vincent Hui ,&nbsp;Huijing Zheng ,&nbsp;Yuan Cai ,&nbsp;Ludovica Griffanti ,&nbsp;Sana Suri ,&nbsp;Klaus P. Ebmeier ,&nbsp;Thomas E. Nichols ,&nbsp;Vincent C.T. Mok ,&nbsp;Heidi Johansen-Berg ,&nbsp;Piergiorgio Salvan","doi":"10.1016/j.cccb.2024.100296","DOIUrl":"10.1016/j.cccb.2024.100296","url":null,"abstract":"<div><h3>Introduction</h3><p>The number of people living with dementia worldwide is growing. Devising and implementing preventive strategies that are globally applicable is of paramount importance. However, previous studies have largely been limited to cohorts that are geographically and culturally homogenous. It is not known whether the associations between demographics, vascular risk factors (VRFs), and cognitive changes are consistent across cohorts with cultural and geographical variations.</p></div><div><h3>Methods</h3><p>Data were analysed retrospectively from 6 community-dwelling cohorts (&gt; 60 years old) with cultural and geographical variations (British = 536; Hong Kong Chinese = 494; Australian = 302; Singaporean Chinese = 108; German = 102; Swedish = 94). Clinical demographics, VRFs, longitudinal cognitive changes, and MRI data (including T1, FLAIR, and diffusion images) were analysed from all 6 cohorts. First, across all cohorts, a grand canonical correlation analysis (n=1636) was used to establish common modes of covariation between demographics and VRFs on one side, and cognitive changes on the other side. Second, separately for each cohort, mediation analysis was used to investigate the mediating role of normalised total grey matter volume, microstructural integrity, white matter hyperintensity, and hippocampal structural network in the association mentioned above. Then the mediation outputs will be used in the meta- analysis to assess the indirect effect estimates and variance of each significant brain mediator.</p></div><div><h3>Results</h3><p>We identified three modes of covariation between dementia risk and cognition across all cohorts (p&lt; 0.01). The strongest mode linked younger age and higher levels of education with better cognition at baseline and follow-up (Figure 1). Meta-analysis showed that, across cohorts, normalised total grey matter volume (Indirect effect = 0.02, Z = 3.13, p &lt; 0.001, I² = 0%) was a significant mediator between demographics, VRFs, and cognitive decline after Bonferroni correction (Figure 2). The hippocampal structural network did not survive Bonferroni correlation while other brain mediators were not significant in the meta-analyses.</p></div><div><h3>Discussion</h3><p>This study investigated the complex relationship between demographics, VRFs, brain health, and cognition. Cohorts with cultural and demographic variations shared a common relationship between age, education, and cognition. However, individual cohort differences are detected in the contribution of different neuroimaging metrics.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100296"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000977/pdfft?md5=886bf63c637d9c622cb4749bb6387460&pid=1-s2.0-S2666245024000977-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122124","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":"Role of neurovascular uncoupling in cognitive decline induced by metabolic disturbances: vascular explorations in a mice model","authors":"Manon Haas ,&nbsp;Maud Pétrault ,&nbsp;Thavarak Ouk ,&nbsp;Patrick Gelé ,&nbsp;Olivier Pétrault ,&nbsp;Michèle Bastide","doi":"10.1016/j.cccb.2024.100247","DOIUrl":"10.1016/j.cccb.2024.100247","url":null,"abstract":"<div><h3>Introduction</h3><p>A link between vascular risk factors caused by metabolic disorders in mid-life and the onset of cognitive impairments has been evidenced. Our team has demonstrated that, in a mice model, a cognitive decline occurred after 6 months of high-fat diet (HFD). The cognitive impairment onset was concomitant to that of metabolic disorders and a dysfunction in cerebrovascular relaxation in regions involved in the altered cognitive tasks. This could be caused by a neurovascular coupling dysfunction, which allows the adjustment of cerebral blood flow to neuronal activity. Glutamate, both an excitative neurotransmitter and potent vasodilator, could be involved. When released, glutamate can activate a neuronal pathway involving nNOS and COX2 and/or an astrocytic pathway involving COX1. Those enzymes then produce vasodilatory agents. Our aim is to investigate potential neurovascular alterations induced by metabolic disorders by focusing on the role of vasoactive enzymes.</p></div><div><h3>Methods</h3><p>Male C57Bl6/J mice are fed with HFD or normal diet for 12 months. Vasomotricity of basilar artery and neurovascular coupling assessments are performed with Halpern's arteriograph and with an ex-vivo brain slice model using pharmacological modulation.</p></div><div><h3>Results</h3><p>Mice fed with HFD demonstrate a significantly decreased myogenic tone of the basilar artery, that is conversely correlated with weight gain. The vasodilatory response to glutamate was decreased in intraparenchymal arterioles of the animals in the HFD group compared to that of the control group. Specific inhibition of the enzymes involved in the glutamatergic pathways may demonstrate a different pattern of involvement of each of these enzymes in the vasodilatory response to glutamate of the HFD-fed mice, pointing to a greater participation of the neuronal pathway enzymes (nNOS and COX2).</p></div><div><h3>Discussion</h3><p>These results indicate that HFD could modify the basal functioning of cerebral arteries as well as their interaction with neurons and astrocytes, indicating a potential neurovascular uncoupling in our model. The reduced vasodilatory effect of glutamate in HFD-mice seems to be related to a decreased activation of COX1 to the profit of the glutamatergic neuronal pathway, notably of COX 2, whose expression is known to be increased in neuroinflammation, a recurrent occurrence in metabolic syndrome models as ours.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100247"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000485/pdfft?md5=fd82b3d2456703a17ede0c3be9855600&pid=1-s2.0-S2666245024000485-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122288","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":"Cerebral microbleeds are associated with slowed processing speed in middle-aged adults with type 1 diabetes","authors":"Iiris Kyläheiko ,&nbsp;Aleksi Tarkkonen ,&nbsp;Juha Martola ,&nbsp;Teemu Paajanen ,&nbsp;Jussi Virkkala ,&nbsp;Per-Henrik Groop ,&nbsp;Lena M. Thorn ,&nbsp;Jukka Putaala ,&nbsp;Daniel Gordin ,&nbsp;Hanna Jokinen ,&nbsp;FinnDiane Study Group","doi":"10.1016/j.cccb.2024.100276","DOIUrl":"10.1016/j.cccb.2024.100276","url":null,"abstract":"<div><h3>Introduction</h3><p>Type 1 diabetes (T1D) is an important risk factor for cerebral small vessel disease (SVD). Cerebral microbleeds (CMB) and white matter hyperintensities (WMH) can already be observed in early midlife in individuals with T1D, even though generally, this pathology is seen decades later in those without diabetes. Whether these changes affect cognitive functions, remains unclear. We investigated the associations of CMB and WMH with processing speed and attention in adults with T1D without major neurological symptoms.</p></div><div><h3>Methods</h3><p>As part of an ongoing FinnDiane sub-study, brain magnetic resonance imaging, and extensive clinical and neuropsychological examinations were done for 142 participants with T1D (age 47.2±7.6 years, diabetes duration 31.6±11.0 years). CMB and WMH were evaluated visually by an experienced neuroradiologist and categorized according to number and severity (CMB: 0 vs 1-2 vs ≥3; WMH: Fazekas score 0 vs ≥1). The assessment of processing speed and attention included the Wechsler Adult Intelligence Scale-IV (WAIS-IV) Coding and Symbol search subtests, the Stroop test, and the computerized Flexible Attention Test (FAT) Simple Visuomotor Speed, Numbers and Number-Letter subtasks.</p></div><div><h3>Results</h3><p>CMB (≥3) and mild WMH were associated with poorer performance in WAIS-IV Coding and Symbol Search, and Stroop and FAT subtasks (p&lt;0.05) in univariate linear regression analyses. After controlling for age and years of education, the associations of CMB with Coding (stand. β=-0.17, p=0.038), FAT Simple Visuomotor Speed (stand. β=0.16, p=0.048) and Stroop color- incongruent part (stand. β=0.18, p=0.038) remained significant, whereas WMH were no longer related to cognitive performance. When CMB and WMH were entered together in multiple linear regression models adjusted for age and education, CMB had independent negative contributions to Coding (stand. β=-0.17, p=0.045). The effect sizes of the significant associations were small (Cohen's f2=0.04) (Fig. 1).</p></div><div><h3>Discussion</h3><p>CMB were related to a subtle decline in processing speed and attention in middle-aged adults with T1D. The associations were only partly explained by age. Effect sizes on a group level were small indicating minor clinical significance. However, our results provide insight into the development of SVD-related cognitive changes already in midlife and suggest an increased risk of cognitive decline in individuals with T1D.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100276"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024000771/pdfft?md5=2d6f7ad47617253ace745cdd6a6e439f&pid=1-s2.0-S2666245024000771-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122303","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 predictors and clinical outcomes of incident infarcts in the year after a mild stroke","authors":"Una Clancy ,&nbsp;Carmen Arteaga ,&nbsp;Daniela Jaime Garcia ,&nbsp;Will Hewins ,&nbsp;Rachel Locherty ,&nbsp;Maria Valdes-Hernandez ,&nbsp;Stewart Wiseman ,&nbsp;Michael Stringer ,&nbsp;Michael J Thrippleton ,&nbsp;Agniete Kampaite ,&nbsp;Olivia KL Hamilton ,&nbsp;Francesca M Chappell ,&nbsp;Angela CC Jochems ,&nbsp;Salvatore Rudilosso ,&nbsp;Xiaodi Liu ,&nbsp;Yajun Cheng ,&nbsp;Junfang Zhang ,&nbsp;Rosalind Brown ,&nbsp;Mark E Bastin ,&nbsp;Susana Munoz Maniega ,&nbsp;Joanna M Wardlaw","doi":"10.1016/j.cccb.2024.100331","DOIUrl":"10.1016/j.cccb.2024.100331","url":null,"abstract":"<div><h3>Introduction</h3><p>Factors associated with incident infarcts after stroke are unclear. We aimed to determine whether subsequent incident infarcts continue to develop one year post-stroke and how incident infarcts relate to baseline imaging features, vascular risks, and cognitive outcomes.</p></div><div><h3>Methods</h3><p>We recruited patients with non-disabling stroke. After diagnostic MRI, we repeated MRI at 3-6 monthly intervals for 12 months, visually assessing incident infarcts on DWI or FLAIR. We used logistic regression to determine associations with incident infarcts, including baseline vascular risks, SVD score, and index stroke subtype. We quantified 7-level ordinal cognitive outcome status at one year, using MoCA/telephone MoCA and modified Rankin Scale.[1,2] We used ordinal regression to determine whether cognitive outcomes associated with incident infarcts and baseline age, mRS, MoCA, and WMH volume.</p></div><div><h3>Results</h3><p>We recruited 229 participants, mean age 65.9 (SD 11.1) years; 77/229 (33.6%) female; 130/229 (56.8%) index lacunar stroke. From baseline to one-year MRI, we detected 117 incident infarcts in n=57/229 participants at 80 visits. Most were small subcortical infarcts: 86/117 (73.5%) infarcts in n=38/57 (66%). N=39 participants had incident infarcts at one visit; n=14 at two visits; n=3 at three visits, and n=1 at four visits. Nineteen participants had multiple incident infarcts at a single visit. Baseline summary SVD score was the strongest predictor of incident infarcts (aOR 1.74, 95%CI 1.29-2.41, Figure 1). At one year, 10/218 (4.6%) participants met criteria for single-domain and 62/218 (28.4%) for multi-domain neurocognitive disorder; 15/218 (6.8%) for mild dementia; 2/218 (0.9%) for moderate dementia; none severe; 3/229 (1.3%) had died. Participants’ odds of impaired one-year cognition increased for every one-unit increment in baseline mRS (aOR=2.03 [1.30-3.10]) and decreased for every one-unit increment in baseline MoCA (aOR=0.78 [0.71-0.85]). For participants with incident small subcortical infarcts, the odds of impaired cognition were 23% higher than for incident cortical infarcts, though not statistically significant (aOR 1.23 [0.55-2.1])(Figure 2).</p></div><div><h3>Discussion</h3><p>In a mild stroke population, incident infarcts, mostly small subcortical, occur in one quarter and associate with worse baseline SVD. Minor neurocognitive disorder occurs in one third and associates with baseline mRS, MoCA, and trends towards incident small subcortical rather than cortical infarcts.</p></div>","PeriodicalId":72549,"journal":{"name":"Cerebral circulation - cognition and behavior","volume":"6 ","pages":"Article 100331"},"PeriodicalIF":1.9,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666245024001326/pdfft?md5=86852cb873b4b5a5cb8aed7352dec199&pid=1-s2.0-S2666245024001326-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142122306","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}