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Deficits in memory performance have been linked to a wide range of neurological and neuropsychiatric conditions. While many studies have assessed the memory impacts of individual conditions, this study considers a broader perspective by evaluating how memory recall is differentially associated with nine common neuropsychiatric conditions using data drawn from 55 international studies, aggregating 15,883 unique participants aged 15-90. The effects of dementia, mild cognitive impairment, Parkinson's disease, traumatic brain injury, stroke, depression, attention-deficit/hyperactivity disorder (ADHD), schizophrenia, and bipolar disorder on immediate, short-, and long-delay verbal learning and memory (VLM) scores were estimated relative to matched healthy individuals. Random forest models identified age, years of education, and site as important VLM covariates. A Bayesian harmonization approach was used to isolate and remove site effects. Regression estimated the adjusted association of each clinical group with VLM scores. Memory deficits were strongly associated with dementia and schizophrenia (p < 0.001), while neither depression nor ADHD showed consistent associations with VLM scores (p > 0.05). Differences associated with clinical conditions were larger for longer delayed recall duration items. By comparing VLM across clinical conditions, this study provides a foundation for enhanced diagnostic precision and offers new insights into disease management of comorbid disorders.
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INTRODUCTION: Regular aerobic exercise is associated with improved cognitive function, implicating it as a strategy to reduce dementia risk. This is reinforced by the association between greater cardiorespiratory fitness and larger brain volume, superior cognitive performance and lower dementia risk. However, the optimal aerobic exercise dose, namely the intensity and mode of delivery, to improve brain health and lower dementia risk has received less attention. We aim to determine the effect of different doses of aerobic exercise training on markers of brain health in sedentary middle-aged adults, hypothesising that high-intensity interval training (HIIT) will be more beneficial than moderate-intensity continuous training (MICT). METHODS AND ANALYSIS: In this two-group parallel, open-label blinded endpoint randomised trial, 70 sedentary middle-aged (45-65 years) adults will be randomly allocated to one of two 12-week aerobic exercise training interventions matched for total exercise training volume: (1) MICT (n=35) or HIIT (n=35). Participants will perform ~50 min exercise training sessions, 3 days per week, for 12 weeks. The primary outcome will be measured as between-group difference in cardiorespiratory fitness (peak oxygen uptake) change from baseline to the end of training. Secondary outcomes include between-group differences in cognitive function and ultra-high field MRI (7T) measured markers of brain health (brain blood flow, cerebrovascular function, brain volume, white matter microstructural integrity and resting state functional brain activity) changes from baseline to the end of training. ETHICS AND DISSEMINATION: The Victoria University Human Research Ethics Committee (VUHREC) has approved this study (HRE20178), and all protocol modifications will be communicated to the relevant parties (eg, VUHREC, trial registry). Findings from this study will be disseminated via peer-review publications, conference presentations, clinical communications and both mainstream and social media. TRIAL REGISTRATION NUMBER: ANZCTR12621000144819.
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Demência , Substância Branca , Pessoa de Meia-Idade , Adulto , Humanos , Encéfalo/diagnóstico por imagem , Cognição , Exercício FísicoRESUMO
Investigators in neuroscience have turned to Big Data to address replication and reliability issues by increasing sample sizes, statistical power, and representativeness of data. These efforts unveil new questions about integrating data arising from distinct sources and instruments. We focus on the most frequently assessed cognitive domain - memory testing - and demonstrate a process for reliable data harmonization across three common measures. We aggregated global raw data from 53 studies totaling N = 10,505 individuals. A mega-analysis was conducted using empirical bayes harmonization to remove site effects, followed by linear models adjusting for common covariates. A continuous item response theory (IRT) model estimated each individual's latent verbal learning ability while accounting for item difficulties. Harmonization significantly reduced inter-site variance while preserving covariate effects, and our conversion tool is freely available online. This demonstrates that large-scale data sharing and harmonization initiatives can address reproducibility and integration challenges across the behavioral sciences.
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BACKGROUND: Type 2 diabetes (T2DM) is recognised as a major contributor to cognitive decline. People with T2DM demonstrate abnormalities on MRI compared to control individuals. The aim of this analysis was to investigate differences in cognitive performance and brain volume between individuals with T2DM participating in the Diabetes-and-Dementia (D2) study and a group of healthy controls (HC) part of the Cognition And Neocortical Volume After Stroke (CANVAS) study. METHOD: One hundred and fifty individuals with T2DM and 36 cognitively-normal participants completed neuropsychological assessments and a 3T-MRI scan. FreeSurfer was used to estimate total brain volume (TBV), mean cortical thickness and subcortical volumes, including the thalami and caudate nuclei. Averages between left and right volumes were calculated for subcortical structures. WMH volumes were estimated manually using FLAIR MRI. Five cognitive domains, including attention, visuospatial skills, memory, language and executive function were computed using z-scores. These domains were used to compare cognitive performance between individuals with and without T2DM. Demographic and clinical comparisons were completed in MATLAB using Two-Sample t-test (age), Fisher Exact test (education, sex, APOE-e4), and Wilcoxon Rank Sum test (BMI). A linear regression model was used to compare cognitive performance between the two groups with correction for age, sex and education level (more/less than 12 years), as well as total intracranial volume for comparing brain volumes. RESULT: Participants with T2DM were significantly younger, with a higher BMI, had reduced cortical thickness, significantly smaller TBV and smaller subcortical volumes including thalamic, brainstem, amygdala, accumbens area and choroid plexus. Individuals with T2DM exhibited a poorer cognitive performance on tests of language, memory, attention, and visuospatial skills compared to the HC group. There were no significant differences between the two groups in terms of sex, education level, APOE-e4 carriage, WMH, hippocampal volume (see Table 1). CONCLUSION: T2DM is associated with accelerated structural brain aging, manifesting as cerebral atrophy and poorer cognitive function.
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Encéfalo , Diabetes Mellitus Tipo 2 , Imageamento por Ressonância Magnética , Testes Neuropsicológicos , Humanos , Masculino , Feminino , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/patologia , Idoso , Encéfalo/patologia , Encéfalo/diagnóstico por imagem , Testes Neuropsicológicos/estatística & dados numéricos , Pessoa de Meia-Idade , Disfunção Cognitiva/patologia , Tamanho do Órgão , Cognição/fisiologiaRESUMO
Cortical thinning has been described in many neurodegenerative diseases and used for both diagnosis and disease monitoring. The imaging signatures of post-stroke vascular cognitive impairment have not been well described. We investigated the trajectory of cortical thickness over 3 years following ischaemic stroke compared to healthy stroke-free age- and sex-matched controls. We also compared cortical thickness between cognitively normal and impaired stroke survivors, and between APOE É4 carriers and non-carriers. T1-weighted MRI and cognitive data for 90 stroke survivors and 36 controls from the Cognition And Neocortical Volume After Stroke (CANVAS) study were used. Cortical thickness was estimated using FreeSurfer volumetric reconstruction according to the Desikan-Killiany parcellation atlas. Segmentation inaccuracies were manually corrected and infarcted ipsilesional vertices in cortical thickness maps were identified and excluded using stroke lesion masks traced a-priori. Mixed-effects regression was used to compare cortical thickness cross-sectionally between groups and longitudinally between timepoints. Healthy control and stroke groups did not differ on demographics and most clinical characteristics, though controls were less likely to have atrial fibrillation. Age was negatively associated with global mean cortical thickness independent of sex or group, with women in both groups having significantly thicker cortex. Three months post-stroke, cortical thinning was limited and focal. From 3 months to 3 years, the rate of cortical thinning in stroke was faster compared to that in healthy controls. However, this difference in cortical thinning rate could not survive family-wise correction for multiple comparisons. Yet, cortical thinning at 3 years was found more spread especially in ipsilesional hemispheres in regions implicated in motor, sensory, and memory processing and recovery. The cognitively impaired stroke survivors showed greater cortical thinning, compared to controls, than those who were cognitively normal at 3 years. Also, carriers of the APOE É4 allele in stroke exhibited greater cortical thinning independent of cognitive status. The temporal changes of cortical thickness in both healthy and stroke cohorts followed previously reported patterns of cortical thickness asymmetry loss across the human adult life. However, this loss of thickness asymmetry was amplified in stroke. The post-stroke trajectories of cortical thickness reported in this study may contribute to our understanding of imaging signatures of vascular cognitive impairment.
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Afinamento Cortical Cerebral , Disfunção Cognitiva , AVC Isquêmico , Adulto , Feminino , Humanos , Isquemia Encefálica/complicações , Isquemia Encefálica/diagnóstico por imagem , Isquemia Encefálica/patologia , Córtex Cerebral/patologia , Afinamento Cortical Cerebral/patologia , Disfunção Cognitiva/etiologia , Disfunção Cognitiva/genética , AVC Isquêmico/complicações , AVC Isquêmico/diagnóstico por imagem , AVC Isquêmico/patologia , Imageamento por Ressonância Magnética/métodos , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/diagnóstico por imagem , Acidente Vascular Cerebral/patologia , Apolipoproteína E4/genética , Apolipoproteína E4/metabolismoRESUMO
Dynamic whole-brain changes occur following stroke, and not just in association with recovery. We tested the hypothesis that the presence of a specific behavioural deficit after stroke would be associated with structural decline (atrophy) in the brain regions supporting the affected function, by examining language deficits post-stroke. We quantified whole-brain structural volume changes longitudinally (3-12 months) in stroke participants with (N = 32) and without aphasia (N = 59) as assessed by the Token Test at 3 months post-stroke, compared with a healthy control group (N = 29). While no significant difference in language decline rates (change in Token Test scores from 3 to 12 months) was observed between groups and some participants in the aphasic group improved their scores, stroke participants with aphasia symptoms at 3 months showed significant atrophy (>2%, P = 0.0001) of the left inferior frontal gyrus not observed in either healthy control or non-aphasic groups over the 3-12 months period. We found significant group differences in the inferior frontal gyrus volume, accounting for age, sex, stroke severity at baseline, education and total intracranial volume (Bonferroni-corrected P = 0.0003). In a subset of participants (aphasic N = 14, non-aphasic N = 36, and healthy control N = 25) with available diffusion-weighted imaging data, we found significant atrophy in the corpus callosum and the left superior longitudinal fasciculus in the aphasic compared with the healthy control group. Language deficits at 3 months post-stroke are associated with accelerated structural decline specific to the left inferior frontal gyrus, highlighting that known functional brain reorganization underlying behavioural improvement may occur in parallel with atrophy of brain regions supporting the language function.
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PURPOSE: White matter hyperintensities (WMHs) are associated with poststroke cognitive decline and mortality. Physical activity (PA) may decrease WMH risk by reducing vascular risk factors and promoting cerebral perfusion. However, the association between poststroke PA and WMH progression remains unclear. We examined the association between PA and WMH volume 12 months after stroke, and between PA and change in WMH volume between 3 and 12 months after stroke. METHODS: We included ischemic stroke survivors from the Cognition And Neocortical Volume After Stroke cohort with available brain magnetic resonance imaging and objective PA data. Total, periventricular, and deep WMH volumes (in milliliters) were estimated with manually edited, automated segmentations (Wisconsin White Matter Hyperintensities Segmentation toolbox). Moderate-to-vigorous intensity PA (MVPA) was estimated using the SenseWear® Armband. Participants with MVPA ≥30 min·d -1 were classified as "meeting PA guidelines." We used quantile regression to estimate the associations between PA (MVPA and meeting PA guidelines) with WMH volume at 12 months and change in WMH volume between 3 and 12 months after stroke. RESULTS: A total of 100 participants were included (median National Institutes of Health Stroke Scale 2; interquartile range, 1-4). MVPA was not associated with WMH volume. In univariable analysis, meeting PA guidelines was associated with lower total, periventricular, and deep WMH volumes by 3.0 mL (95% confidence interval (CI), 0.5-9.7 mL), 2.8 mL (95% CI, 0.5-7.1 mL), and 0.9 mL (95% CI, 0.1-3.0 mL), respectively. However, in multivariable analysis, meeting PA guidelines was not associated with WMH volume, and older age was associated with greater WMH volume at 12 months. PA was not associated with change in WMH volume. CONCLUSIONS: Meeting PA guidelines was associated with lower WMH volume at 12 months in univariable analysis, but not in multivariable analysis. Age consistently predicted greater WMH volume.
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Acidente Vascular Cerebral , Substância Branca , Encéfalo/diagnóstico por imagem , Cognição , Exercício Físico , Humanos , Imageamento por Ressonância Magnética/métodos , Acidente Vascular Cerebral/diagnóstico por imagem , Substância Branca/diagnóstico por imagem , Substância Branca/patologiaRESUMO
OBJECTIVES: Cognitive and mood dysfunction are major contributors to post-stroke disability. The longer-term trajectories of mood and cognition post-stroke remain unclear, as do which cognitive domains decline, improve, or remain stable after stroke, and in which patients. We aimed to characterize the cognitive trajectories of mild ischemic stroke survivors over one year compared to stroke-free controls, and to investigate whether symptoms of anxiety and depression were associated with cognitive function. MATERIALS AND METHODS: All participants were tested with a neuropsychological test battery at 3-months and 12-months post-stroke, assessing attention/processing speed, memory, visuospatial function, executive function, and language. Anxiety and depression symptomatology were also assessed at both timepoints. RESULTS: Stroke participants (N=126, mean age 68.44 years ±11.83, 87 males, median [Q1, Q3] admission NIHSS=2 [1, 4]) performed worse on cognitive tests and endorsed significantly higher depression and anxiety symptomatology than controls (N=40, mean age=68.82 years ±6.33, 25 males) at both timepoints. Mood scores were not correlated with cognitive performance. Stroke participants' scores trended higher across cognitive domains from 3- to 12-months but statistically significant improvement was only observed on executive function tasks. CONCLUSION: Stroke participants performed significantly worse than controls on all cognitive domains following mild ischemic stroke. Stroke participants only exhibited statistically significant improvement on executive function tasks between 3- and 12- months. Whilst anxiety and depression symptoms were higher in stroke participants, this was not correlated with cognitive performance. Further studies are needed to understand factors underlying cognitive recovery and decline after stroke.
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Disfunção Cognitiva , AVC Isquêmico , Acidente Vascular Cerebral , Afeto , Idoso , Cognição , Disfunção Cognitiva/complicações , Disfunção Cognitiva/etiologia , Função Executiva , Humanos , Masculino , Testes Neuropsicológicos , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/diagnósticoRESUMO
BACKGROUND: The structural integrity of hippocampal subfields has been investigated in many neurological disorders and was shown to be better associated with cognitive performance than whole hippocampus. In stroke, hippocampal atrophy is linked to cognitive impairment, but it is unknown whether the hippocampal subfields atrophy differently. PURPOSE: To evaluate longitudinal hippocampal subfield atrophy in first year poststroke, in comparison with atrophy in healthy individuals. STUDY TYPE: Cohort. SUBJECTS: A total of 92 ischemic stroke (age: 67 ± 12 years, 63 men) and 39 healthy participants (age: 69 ± 7 years, 24 men). FIELD STRENGTH/SEQUENCE: A3 T/T1-MPRAGE, T2-SPACE, and T2-FLAIR. ASSESSMENT: FreeSurfer (6.0) was used to delineate 12 hippocampal subfields. Whole hippocampal volume was computed as sum of subfield volumes excluding hippocampal fissure volume. Separate assessments were completed for contralesional and ipsilesional hippocampi. STATISTICAL TESTS: A mixed-effect regression model was used to compare subfield volumes cross-sectionally between healthy and stroke groups and longitudinally between 3-month and 12-month timepoints. False discovery rate at 0.05 significance level was used to correct for multiple comparisons. Also, a receiver operating characteristic (ROC) curve analysis was performed to assess differentiation between healthy and stroke participants based on subfield volumes. RESULTS: There were no volume differences between groups at 3 months, but there was a significant difference (P = 0.027) in whole hippocampal volume reduction over time between control and stroke ipsilesionally. Thus, the ipsilesional whole hippocampal volume in stroke became significantly smaller (P = 0.035) at 12 months. The hippocampal tail was the highest single-region contributor (22.7%) to ipsilesional hippocampal atrophy (1.19%) over 9 months. The cornu ammonis areas (CA1) subfield volume reduction was minimal in controls and stroke contralesionally but significant ipsilesionally (P = 0.007). CA1 volume significantly outperformed whole hippocampal volume (P < 0.01) in discriminating between stroke participants and healthy controls in ROC curve analysis. DATA CONCLUSION: Greater stroke-induced effects were observed in the ipsilesional hippocampus anteriorly in CA1 and posteriorly in the hippocampal tail. Atrophy of CA1 and hippocampal tail may provide a better link to cognitive impairment than whole hippocampal atrophy. LEVEL OF EVIDENCE: 2 TECHNICAL EFFICACY STAGE: 3.
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Disfunção Cognitiva , AVC Isquêmico , Idoso , Atrofia/patologia , Disfunção Cognitiva/patologia , Hipocampo/diagnóstico por imagem , Hipocampo/patologia , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-IdadeRESUMO
Introduction: Coronavirus (COVID-19) instigated unprecedented global effects on healthcare systems, economies, employment, education, travel, and social lives. In addition to increased mental health challenges, pandemic restrictions have triggered emerging cognitive concerns. University students are at particularly high risk of adverse lockdown-related effects, yet despite the substantial adaptions to learning necessitated by COVID-19, limited research has so far focused on the cognitive consequences of the pandemic among university students. This study aimed to comprehensively examine the nature, prevalence, and correlates of subjective cognitive concerns among 972 students (Median age = 22âyears, 70% female) enrolled at Monash University, Australia, in December 2020. Methods: Students completed the online THRIVE@Monash survey, 5âweeks following prolonged lockdown in Melbourne. Using group comparisons and hierarchical binary logistic regression analyses, we examined associations between demographic and enrolment characteristics, COVID-19-related experiences and impacts (author-developed questions), self-reported anxiety and depression symptoms (PROMIS Anxiety and Depression scales), and students' perceived changes in everyday cognitive functions (author-developed questions). Results: Over 60% of students reported subjective cognitive concerns (SCCs). After controlling for anxiety and depression symptoms, students reporting more SCCs were more likely to be younger, from White/European ethnic backgrounds, and in their first year of undergraduate study. No differences in SCCs were found between male and female students. Greater worry, anxiety, or stress related to COVID-19 (e.g., infection, leaving the house, hygiene and exposure prevention, impact on physical and mental health), and time spent reading or talking about COVID-19, were generally not associated with SCCs after controlling for anxiety and depression symptoms. Discussion: These findings highlight vulnerable subgroups of students who might benefit from regular monitoring, education, and interventions to support their cognitive health during the pandemic and beyond. In addition, cognitive concerns may provide additional insight into mental health problems among students, and emphasize the importance of understanding factors that impact students' long-term academic and career success.
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Background: Stroke survivors are at high risk of dementia, associated with increasing age and vascular burden and with pre-existing cognitive impairment, older age. Brain atrophy patterns are recognised as signatures of neurodegenerative conditions, but the natural history of brain atrophy after stroke remains poorly described. We sought to determine whether stroke survivors who were cognitively normal at time of stroke had greater total brain (TBV) and hippocampal volume (HV) loss over 3 years than controls. We examined whether stroke survivors who were cognitively impaired (CI) at 3 months following their stroke had greater brain volume loss than cognitively normal (CN) stroke participants over the next 3 years. Methods: Cognition And Neocortical Volume After Stroke (CANVAS) study is a multi-centre cohort study of first-ever or recurrent adult ischaemic stroke participants compared to age- and sex-matched community controls. Participants were followed with MRI and cognitive assessments over 3 years and were free of a history of cognitive impairment or decline at inclusion. Our primary outcome measure was TBV change between 3 months and 3 years; secondary outcomes were TBV and HV change comparing CI and CN participants. We investigated associations between group status and brain volume change using a baseline-volume adjusted linear regression model with robust standard error. Results: Ninety-three stroke (26 women, 66.7 ± 12 years) and 39 control participants (15 women, 68.7 ± 7 years) were available at 3 years. TBV loss in stroke patients was greater than controls: stroke mean (M) = 20.3 cm3 ± SD 14.8 cm3; controls M = 14.2 cm3 ± SD 13.2 cm3; [adjusted mean difference 7.88 95%CI (2.84, 12.91) p-value = 0.002]. TBV decline was greater in those stroke participants who were cognitively impaired (M = 30.7 cm3; SD = 14.2 cm3) at 3 months (M = 19.6 cm3; SD = 13.8 cm3); [adjusted mean difference 10.42; 95%CI (3.04, 17.80), p-value = 0.006]. No statistically significant differences in HV change were observed. Conclusions: Ischaemic stroke survivors exhibit greater neurodegeneration compared to stroke-free controls. Brain atrophy is greater in stroke participants who were cognitively impaired early after their stroke. Early cognitive impairment was associated greater subsequent atrophy, reflecting the combined impacts of stroke and vascular brain burden. Atrophy rates could serve as a useful biomarker for trials testing interventions to reduce post-stroke secondary neurodegeneration. Clinical Trail Registration: http://www.clinicaltrials.gov, identifier: NCT02205424.
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INTRODUCTION: Hippocampal subfield volumes are more closely associated with cognitive impairment than whole hippocampal volume in many diseases. Both memory and whole hippocampal volume decline after stroke. Understanding the subfields' temporal evolution could reveal valuable information about post-stroke memory. METHODS: We sampled 120 participants (38 control, 82 stroke), with cognitive testing and 3T-MRI available at 3 months and 3 years, from the Cognition and Neocortical Volume after Stroke (CANVAS) study. Verbal memory was assessed using the Hopkins Verbal Learning Test-Revised. Subfields were delineated using FreeSurfer. We used partial Pearson's correlation to assess the associations between subfield volumes and verbal memory scores, adjusting for years of education, sex, and stroke side. RESULTS: The left cornu ammonis areas 2/3 and hippocampal tail volumes were significantly associated with verbal memory 3-month post-stroke. At 3 years, the associations became stronger and involved more subfields. DISCUSSION: Hippocampal subfield volumes may be a useful biomarker for post-stroke cognitive impairment.
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Hippocampal atrophy is seen in many neurodegenerative disorders and may be a cardinal feature of vascular neurodegeneration. We examined hippocampal volume (HV) in a group of ischemic stroke survivors with amyloid 18F-NAV4694 PET imaging three years after stroke. We compared HV between the amyloid-positive (nâ=â4) and amyloid-negative (nâ=â29) groups, and associations with co-morbidities using Charlson Comorbidity Indices and multi-way ANOVA. Amyloid status was not associated with verbal or visual delayed free recall memory indices or cognitive impairment. We found no association between amyloid status and HV in this group of ischemic stroke survivors.
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Amiloide/metabolismo , Hipocampo/diagnóstico por imagem , AVC Isquêmico/diagnóstico por imagem , AVC Isquêmico/metabolismo , Atrofia , Transtornos Cognitivos/metabolismo , Transtornos Cognitivos/psicologia , Estudos de Coortes , Comorbidade , Hipocampo/patologia , Imageamento por Ressonância Magnética , Transtornos da Memória/metabolismo , Transtornos da Memória/psicologia , Rememoração Mental , Testes Neuropsicológicos , Projetos Piloto , Tomografia por Emissão de Pósitrons , Comportamento VerbalRESUMO
BACKGROUND AND PURPOSE: Brain atrophy can be regarded as an end-organ effect of cumulative cardiovascular risk factors. Accelerated brain atrophy is described following ischemic stroke, but it is not known whether atrophy rates vary over the poststroke period. Examining rates of brain atrophy allows the identification of potential therapeutic windows for interventions to prevent poststroke brain atrophy. METHODS: We charted total and regional brain volume and cortical thickness trajectories, comparing atrophy rates over 2 time periods in the first year after ischemic stroke: within 3 months (early period) and between 3 and 12 months (later period). Patients with first-ever or recurrent ischemic stroke were recruited from 3 Melbourne hospitals at 1 of 2 poststroke time points: within 6 weeks (baseline) or 3 months. Whole-brain 3T magnetic resonance imaging was performed at 3 time points: baseline, 3 months, and 12 months. Eighty-six stroke participants completed testing at baseline; 125 at 3 months (76 baseline follow-up plus 49 delayed recruitment); and 113 participants at 12 months. Their data were compared with 40 healthy control participants with identical testing. We examined 5 brain measures: hippocampal volume, thalamic volume, total brain and hemispheric brain volume, and cortical thickness. We tested whether brain atrophy rates differed between time points and groups. A linear mixed-effect model was used to compare brain structural changes, including age, sex, years of education, a composite cerebrovascular risk factor score, and total intracranial volume as covariates. RESULTS: Atrophy rates were greater in stroke than control participants. Ipsilesional hemispheric, hippocampal, and thalamic atrophy rates were 2 to 4 times greater in the early versus later period. CONCLUSIONS: Regional atrophy rates vary over the first year after stroke. Rapid brain volume loss in the first 3 months after stroke may represent a potential window for intervention. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT02205424.
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Atrofia , Isquemia Encefálica/patologia , Encéfalo/patologia , Acidente Vascular Cerebral/patologia , Adulto , Fatores Etários , Idoso , Encéfalo/diagnóstico por imagem , Isquemia Encefálica/diagnóstico por imagem , Córtex Cerebral/diagnóstico por imagem , Progressão da Doença , Feminino , Hipocampo/diagnóstico por imagem , Hipocampo/patologia , Humanos , Processamento de Imagem Assistida por Computador , Modelos Lineares , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Recidiva , Fatores Sexuais , Acidente Vascular Cerebral/diagnóstico por imagem , Tálamo/diagnóstico por imagem , Tálamo/patologia , Resultado do TratamentoRESUMO
BACKGROUND: The apolipoprotein E (APOE) gene É4 allele is a risk factor for Alzheimer's disease and cardiovascular disease. However, its relationship with cognition and brain volume after stroke is not clear. OBJECTIVE: We compared cognition and medial temporal lobe volumes in APOEÉ4 carriers and non-carriers in the first year after ischemic stroke. METHODS: We sampled 20 APOEÉ4 carriers and 20 non-carriers from a larger cohort of 135 ischemic stroke participants in the longitudinal CANVAS study. Participants were matched on a range of demographic and stroke characteristics. We used linear mixed-effect models to compare cognitive domain z-scores (attention, processing speed, executive function, verbal and visual memory, language, visuospatial function) and regional medial temporal lobe volumes (hippocampal, entorhinal cortex) between groups at each time-point (3, 12-months post-stroke), and within groups across time-points. APOE gene single nucleotide polymorphisms (SNPs; rs7412, rs429358) were genotyped on venous blood. RESULTS: APOEÉ4 carriers and non-carriers did not differ on any demographic, clinical, or stroke variable. Carriers performed worse than non-carriers in verbal memory at 3 months post-stroke (pâ=â0.046), but were better in executive function at 12 months (pâ=â0.035). Carriers demonstrated a significant improvement in verbal memory (pâ=â0.012) and executive function (pâ=â0.015) between time-points. Non-carriers demonstrated a significant improvement in visual memory (pâ=â0.0005). Carriers had smaller bilateral entorhinal cortex volumes (pâ<â0.05), and larger right sided and contralesional hippocampal volumes, at both time-points (pâ<â0.05). CONCLUSION: APOE É4 is associated with delayed recovery of verbal memory function and reduced entorhinal cortex volumes in the first year after ischemic stroke.
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Apolipoproteína E4/genética , Isquemia Encefálica/complicações , Córtex Entorrinal/patologia , Acidente Vascular Cerebral/complicações , Aprendizagem Verbal , Idoso , Idoso de 80 Anos ou mais , Isquemia Encefálica/patologia , Isquemia Encefálica/psicologia , Estudos de Casos e Controles , Córtex Entorrinal/diagnóstico por imagem , Feminino , Heterozigoto , Humanos , Estudos Longitudinais , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Neuroimagem , Tamanho do Órgão , Estudos Prospectivos , Recuperação de Função Fisiológica , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/psicologiaRESUMO
Focal epilepsy is a unilateral brain network disorder, providing an ideal neuropathological model with which to study the effects of focal neural disruption on a range of cognitive processes. While language and memory functions have been extensively investigated in focal epilepsy, music cognition has received less attention, particularly in patients with music training or expertise. This represents a critical gap in the literature. A better understanding of the effects of epilepsy on music cognition may provide greater insight into the mechanisms behind disease- and training-related neuroplasticity, which may have implications for clinical practice. In this cross-sectional study, we comprehensively profiled music and non-music cognition in 107 participants; musicians with focal epilepsy (n = 35), non-musicians with focal epilepsy (n = 39), and healthy control musicians and non-musicians (n = 33). Parametric group comparisons revealed a specific impairment in verbal cognition in non-musicians with epilepsy but not musicians with epilepsy, compared to healthy musicians and non-musicians (P = 0.029). This suggests a possible neuroprotective effect of music training against the cognitive sequelae of focal epilepsy, and implicates potential training-related cognitive transfer that may be underpinned by enhancement of auditory processes primarily supported by temporo-frontal networks. Furthermore, our results showed that musicians with an earlier age of onset of music training performed better on a composite score of melodic learning and memory compared to non-musicians (P = 0.037), while late-onset musicians did not differ from non-musicians. For most composite scores of music cognition, although no significant group differences were observed, a similar trend was apparent. We discuss these key findings in the context of a proposed model of three interacting dimensions (disease status, music expertise, and cognitive domain), and their implications for clinical practice, music education, and music neuroscience research.