2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T663,It is unknown if ocular migraine patients have an increased risk of cerebrovascular disease. This study aimed to determine if cerebrovascular and cardiovascular events were elevated among those with ocular migraine compared to controls. This cohort study utilised a platform of aggregate, de-identified electronic health record data to identify patients with a diagnostic code for ocular migraine based on ICD codes (n = 21,949). Ocular migraine patients were compared to ophthalmology (n = 1,492,348), migraine with aura (MA) (n = 129,099) and migraine without aura (MO) controls. Cohorts were propensity score matched on current age, sex, race/ethnicity, diabetes, essential hypertension, lipoprotein disorders, atherosclerosis and body mass index. Risk ratios and 95% confidence intervals were calculated. A risk ratio between 0.9 and 1.1 was considered not significant. Compared with ophthalmology controls ≥ 50 years old, patients with a diagnostic code ocular migraine had an increased risk of all outcomes, with a risk ratio of 1.48 (95% CI 1.33, 1.64), transient ischemic stroke 2.68 (2.20, 3.27) and cerebral infarct 1.81 (1.55, 2.10). These findings continued to be significant among the ≥ 65 years old cases and controls. Compared to patients with MA or MO, patients had a comparable risk of all outcomes (p > 0.05). Patients with a diagnostic code for ocular migraine ≥ 50 years old had a 48% increased risk of cerebrovascular and cardiovascular outcomes, compared to ophthalmology controls. Future retrospective and prospective cohort analyses are needed to further verify these findings.31:Ta5e,Abstract Background It is unknown if ocular migraine patients have an increased risk of cerebrovascular disease. This study aimed to determine if cerebrovascular and cardiovascular events were elevated among those with ocular migraine compared to controls. Methods This cohort study utilised a platform of aggregate, de-identified electronic health record data to identify patients with a diagnostic code for ocular migraine based on ICD codes ( n = 21,949). Ocular migraine patients were compared to ophthalmology ( n = 1,492,348), migraine with aura (MA) ( n = 129,099) and migraine without aura (MO) controls. Cohorts were propensity score matched on current age, sex, race/ethnicity, diabetes, essential hypertension, lipoprotein disorders, atherosclerosis and body mass index. Risk ratios and 95% confidence intervals were calculated. A risk ratio between 0.9 and 1.1 was considered not significant. Results Compared with ophthalmology controls ≥ 50 years old, patients with a diagnostic code ocular migraine had an increased risk of all outcomes, with a risk ratio of 1.48 (95% CI 1.33, 1.64), transient ischemic stroke 2.68 (2.20, 3.27) and cerebral infarct 1.81 (1.55, 2.10). These findings continued to be significant among the ≥ 65 years old cases and controls. Compared to patients with MA or MO, patients had a comparable risk of all outcomes ( p > 0.05). Conclusion Patients with a diagnostic code for ocular migraine ≥ 50 years old had a 48% increased risk of cerebrovascular and cardiovascular outcomes, compared to ophthalmology controls. Future retrospective and prospective cohort analyses are needed to further verify these findings. 32:T45b,The concepts of brain health (ie, optimal functioning of the brain across cognitive, emotional, and behavioral domains throughout life) and cognitive resilience (ie, the ability of the brain to recover after an insult) have become increasingly important as the population ages. Previous research has called attention to vascular risk factors underlying cerebrovascular disease, as well as modifiable variables that contribute to premature aging and cognitive dysfunction. In this scientific statement, we focus on the role of nonvascular physical and psychologic variables that affect brain health across the life span. We provide a broad overview of influences such as chronic medical conditions, inflammation, environmental exposures, and socioeconomic drivers that affect the developing brain, along with factors including sleep quality, the gut microbiome, and mental health that contribute to neurodegeneration. We also review the varying strength of evidence supporting biologic mechanisms and mitigating strategies that may help optimize resilience, with the goal of providing a framework for future studies.33:T4cb, The concepts of brain health (ie, optimal functioning of the brain across cognitive, emotional, and behavioral domains throughout life) and cognitive resilience (ie, the ability of the brain to recover after an insult) have become increasingly important as the population ages. Previous research has called attention to vascular risk factors underlying cerebrovascular disease, as well as modifiable variables that contribute to premature aging and cognitive dysfunction. In this scientific statement, we focus on the role of nonvascular physical and psychologic variables that affect brain health across the life span. We provide a broad overview of influences such as chronic medical conditions, inflammation, environmental exposures, and socioeconomic drivers that affect the developing brain, along with factors including sleep quality, the gut microbiome, and mental health that contribute to neurodegeneration. We also review the varying strength of evidence supporting biologic mechanisms and mitigating strategies that may help optimize resilience, with the goal of providing a framework for future studies. 25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Cerebrovascular Disease: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Cerebrovascular Disease (condition). 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clinical applicability is not assessed.","value_numeric":null},{"paper_doi":"10.1177/0271678x261490246","tag_type":"warning","value":"This is a narrative review with no original data or quantitative synthesis; conclusions on modality superiority reflect expert opinion rather than meta-analytic evidence.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates preclinical in-vivo cerebrovascular imaging techniques used in rodent models of Alzheimer's disease (AD), comparing modalities including two-photon microscopy, multi-exposure speckle imaging, optical coherence tomography, MRI, PET, contrast-enhanced ultrasound, and ultrafast ultrasound localisation microscopy (ULM) for assessing cerebral microvascular flow.","key_result":"No single modality meets all needs; ultrafast ultrasound localisation microscopy is identified as the best-positioned technique for standardised, longitudinal, multiscale cerebral microvascular imaging in rodents, offering a favourable balance of resolution, sensitivity, depth, and non-invasiveness.","limitations":"- Review is preclinical and rodent-specific; direct translation to human imaging is not addressed.\n- No systematic meta-analysis or quantitative comparison of modalities is performed.\n- Anaesthetic and methodological variability across studies limits cross-study comparability, a problem acknowledged but not resolved by this review.","practice_takeaway":"When designing preclinical AD studies requiring longitudinal cerebrovascular imaging, ultrafast ultrasound localisation microscopy offers the strongest combination of resolution, depth, and non-invasiveness. Researchers should standardise anaesthetic protocols and modality selection criteria using the framework provided to improve cross-study comparability."}},{"doi":"10.1093/brain/awag287","pmid":"42634961","title":"Diabetes and neurodegeneration in cognitively unimpaired older adults: implications for cognition","journal_title":"Brain","journal_issn":"0006-8950","published_at":"2026-08-24T00:00:00.000Z","url":"https://doi.org/10.1093/brain/awag287","source_score":27,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-29T06:19:15.320Z","updated_at":"2026-08-29T06:19:15.320Z","tags":[{"paper_doi":"10.1093/brain/awag287","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"category","value":"Clinical Neurology","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"category","value":"Neurosciences","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"condition","value":"Alzheimer's Disease","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"condition","value":"Neurodegeneration","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"condition","value":"Type 2 Diabetes Mellitus","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"generic","value":"hemoglobin A1c","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"modality","value":"Glycemic Control","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"sample_size","value":"n=1298","value_numeric":1298},{"paper_doi":"10.1093/brain/awag287","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"study_design","value":"Longitudinal Cohort Study","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"warning","value":"The cohort (HABS-HD) is focused on health disparities and may skew toward specific ethnic/socioeconomic groups; generalizability to broader populations should be assessed.","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — the mediation effect is modest (~13%) and the study is observational; clinical translation requires further confirmation.","value_numeric":null},{"paper_doi":"10.1093/brain/awag287","tag_type":"warning","value":"The study labels participants as 'cognitively unimpaired' at baseline, but formal diagnostic criteria used are not detailed in the abstract.","value_numeric":null}],"summaries":{"what_studied":"This longitudinal study examined regional cortical thinning associated with type 2 diabetes and glycemic control (HbA1c) over ~3 years in 1,298 cognitively unimpaired older adults (305 diabetic), controlling for amyloid-PET, tau-PET, white matter hyperintensities, and APOE ε4 status. It also tested whether diabetes-related cortical thinning mediated cognitive decline.","key_result":"Diabetic participants showed faster cortical thinning in 7 frontal, parietal, and occipital regions (βs −0.060 to −0.046, corrected p<0.017), independent of Alzheimer's and cerebrovascular pathology. Higher baseline HbA1c predicted faster thinning in these regions (corrected p<0.032). Cortical thinning mediated ~13% of the effect of diabetes on processing speed decline (indirect effect β=−0.034, p=0.019).","limitations":"- Sample is from a single cohort (HABS-HD), which may limit generalizability.\n- Mediation analysis explained only ~13% of the diabetes–processing speed relationship, leaving most of the effect unexplained.\n- Causality cannot be established from an observational design; reverse causation cannot be ruled out.","practice_takeaway":"Chronic poor glycemic control (elevated baseline HbA1c) appears to drive regional brain atrophy and accelerated cognitive decline in cognitively normal older adults, independent of Alzheimer's or vascular pathology. Optimizing long-term glycemic control in midlife and older adult patients may be a meaningful lever for reducing neurodegeneration risk, even before cognitive symptoms appear."}},{"doi":"10.1038/s41541-026-01528-3","pmid":"42472854","title":"Multiorgan Outcomes Following BNT162b2 mRNA Vaccination vs SARS-CoV-2 Infection: A 30-Million-Person Real-World Cohort Analysis","journal_title":"npj Vaccines","journal_issn":"2059-0105","published_at":"2026-07-19T00:00:00.000Z","url":"https://doi.org/10.1038/s41541-026-01528-3","source_score":17,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-24T13:38:12.350Z","updated_at":"2026-07-24T13:38:12.350Z","tags":[{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"brand","value":"Comirnaty","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"condition","value":"COVID-19","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"condition","value":"Major Adverse Cardiovascular Events","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"condition","value":"Myocarditis","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"condition","value":"Pericarditis","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"condition","value":"Pulmonary Embolism","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"generic","value":"BNT162b2","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"modality","value":"mRNA Vaccine","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"sample_size","value":"n=30300000","value_numeric":30300000},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"warning","value":"Biological sex was used as the stratification variable; gender identity data were not available.","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"warning","value":"The >9-month window for vaccinated-only groups shows elevated mortality vs. controls (males RR 1.22, females RR 1.40), likely reflecting survivorship bias and healthy vaccinee effect reversal over time—this should not be interpreted as vaccine-caused late mortality.","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"warning","value":"The study is limited to BNT162b2 (Pfizer-BioNTech) and excludes Moderna, Janssen, AstraZeneca, and Novavax recipients, limiting generalizability across vaccine platforms.","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"warning","value":"Total cohort size of 30.3 million is reported in the abstract, but individual group sizes across supplemental tables sum to a smaller overlapping network; the effective denominators per comparison vary substantially.","value_numeric":null},{"paper_doi":"10.1038/s41541-026-01528-3","tag_type":"warning","value":"TriNetX suppresses event counts below 10 and reports them as '10' for de-identification, which may meaningfully inflate relative risks for rare outcomes (e.g., thrombosis with thrombocytopenia, ECMO use).","value_numeric":null}],"summaries":{"what_studied":"This retrospective cohort study used the TriNetX US network (Dec 2020–Dec 2024) to compare 50 cardiovascular, cerebrovascular, and mortality outcomes across four mutually exclusive groups: unvaccinated/uninfected controls (n≈27M), SARS-CoV-2 infected/unvaccinated, BNT162b2-vaccinated only, and hybrid immunity (infected + vaccinated). Outcomes were tracked over four time windows (0–3, 3–6, 6–9, and >9 months), stratified by biological sex.","key_result":"SARS-CoV-2 infection drove 3- to 5-fold acute cardiovascular risk increases vs. controls, including myocarditis (males RR 4.44, females RR 5.59) and all-cause mortality (males RR 4.53), with elevated risk persisting beyond 9 months. BNT162b2 vaccination reduced MACE by 65–76% in the acute phase vs. controls. Completing the two-dose primary series cut mortality by 77% and myocarditis by 62% vs. one dose. Hybrid immunity added a 36–38% MACE reduction vs. infection alone; however, males with hybrid immunity showed late pericarditis elevation beyond 9 months (RR 1.80).","limitations":"- Observational design using EHR claims data prevents causal inference and is subject to residual confounding (e.g., unmeasured comorbidities, healthcare-seeking behavior).\n- TriNetX privacy threshold suppresses counts below 10, potentially inflating relative risks for rare events.\n- Study is BNT162b2-specific and limited to a US population; results may not generalize to other vaccines or settings.","practice_takeaway":"For patients weighing COVID-19 vaccination risks and benefits: infection carries far greater and more sustained cardiovascular harm than BNT162b2 vaccination across all sex and age groups. Completing the full two-dose primary series provides substantially more protection than a single dose—clinicians should continue to prioritize vaccination completion."}},{"doi":"10.1016/j.ajog.2026.07.017","pmid":"42468866","title":"Association of Hormone Therapy with Long-Term Outcomes After Chemoradiation for Locally Advanced Cervical Cancer","journal_title":"American Journal of Obstetrics and Gynecology","journal_issn":"0002-9378","published_at":"2026-07-17T00:00:00.000Z","url":"https://doi.org/10.1016/j.ajog.2026.07.017","source_score":7,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-25T13:57:45.679Z","updated_at":"2026-07-25T13:57:45.679Z","tags":[{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"category","value":"Obstetrics & Gynecology","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"condition","value":"Locally Advanced Cervical Cancer","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"condition","value":"Osteoporosis","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"condition","value":"Premature Menopause","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"condition","value":"Type 2 Diabetes Mellitus","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"modality","value":"Chemoradiotherapy","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"modality","value":"Hormone Therapy","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"sample_size","value":"n=4656","value_numeric":4656},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"warning","value":"The 1-year landmark design reduces immortal time bias but assumes uniform treatment initiation timing, which may not reflect real-world variability.","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"warning","value":"The study is retrospective and observational; despite propensity score matching, unmeasured confounders (e.g., physician preference, patient health-seeking behavior) may have influenced both HT uptake and outcomes.","value_numeric":null},{"paper_doi":"10.1016/j.ajog.2026.07.017","tag_type":"warning","value":"The TriNetX platform provides aggregate EHR data; HT formulation (e.g., estrogen-only vs. combined), route of administration, and duration could not be characterized, limiting dose-response or subgroup interpretation.","value_numeric":null}],"summaries":{"what_studied":"This retrospective multinational cohort study (TriNetX) evaluated whether initiating estrogen-based hormone therapy (HT) within 1 year of chemoradiotherapy was associated with better long-term metabolic, skeletal, cardiovascular, oncologic, and survival outcomes in women <45 years with FIGO 2018 stage IIB–IVA cervical cancer; median follow-up ~11–12 years.","key_result":"After propensity score matching (n=4,656), HT was associated with lower risk of type 2 diabetes (5.3% vs. 9.8%; HR 0.59), cerebrovascular events (5.1% vs. 8.9%; HR 0.71), and compression fractures (3.1% vs. 7.4%; HR 0.69), improved overall survival (HR 0.81), and no increased risk of thromboembolism, breast cancer, or colorectal cancer.","limitations":"- Retrospective EHR-based design limits causal inference; cumulative HT dose, formulation, and discontinuation rates were not quantifiable.\n- Crossover contamination: 4.8% of non-HT patients later received HT, likely biasing results toward the null.\n- Residual confounding cannot be excluded despite propensity score matching.","practice_takeaway":"Clinicians treating young patients with locally advanced cervical cancer should strongly consider offering estrogen-based HT after chemoradiotherapy, as it appears safe oncologically and may meaningfully reduce metabolic, skeletal, and cerebrovascular morbidity while improving survival. Persistent hesitation based on cancer-recurrence fears is not supported by this large, long-term dataset."}},{"doi":"10.1002/alz.71582","pmid":"42429220","title":"Associations of distinct sedentary behaviors with cortical, subcortical, and white matter hyperintensity volumes: Evidence from the ARIC study","journal_title":"Alzheimer's & Dementia","journal_issn":"1552-5260","published_at":"2026-07-10T00:00:00.000Z","url":"https://doi.org/10.1002/alz.71582","source_score":18,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-12T13:19:38.382Z","updated_at":"2026-07-12T13:19:38.382Z","tags":[{"paper_doi":"10.1002/alz.71582","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"category","value":"Clinical Neurology","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"condition","value":"Alzheimer's Disease","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"condition","value":"Dementia","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"condition","value":"White Matter Hyperintensities","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"modality","value":"Behavioral Intervention / Lifestyle Modification","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"sample_size","value":"n=1712","value_numeric":1712},{"paper_doi":"10.1002/alz.71582","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"study_design","value":"Prospective Cohort Study","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"warning","value":"Sex-specific findings (associations mainly in males) may partly reflect differential exposure patterns rather than true biological sex differences; this warrants cautious interpretation.","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"warning","value":"The mean age at baseline was 53 years, but the table footnote states mean age at visit 5 was 76 years (SD 5.2); the abstract's '53(5.2) years' refers to visit 1 age. Readers should note the long lag between exposure and outcome measurement (~22 years).","value_numeric":null},{"paper_doi":"10.1002/alz.71582","tag_type":"warning","value":"The 'practice_changing' impact flag reflects the novel finding that sedentary behavior context (passive vs. cognitively active) differentially predicts brain outcomes independent of physical activity — but the observational design limits causal claims. Clinicians should interpret this as hypothesis-generating.","value_numeric":null}],"summaries":{"what_studied":"This prospective cohort study (ARIC, n=1,712 non-demented adults, 57% women, mean age 53 at baseline) examined whether context-specific sedentary behaviors (TV watching vs. occupational sitting) assessed in 1987–1989 were associated with cortical, subcortical, and white matter hyperintensity (WMH) volumes on 3T MRI ~22 years later (2011–2013).","key_result":"Watching TV very often was linked to higher WMH volume (β=0.52; 95% CI: 0.30–0.74) and lower frontal (β=−0.25), occipital (β=−0.21), and AD-signature region (β=−0.24) cortical volumes. In contrast, always sitting at work was associated with lower WMH (β=−0.26; 95% CI: −0.41, −0.10) and larger parietal (β=0.19), occipital (β=0.22), and frontal (β=0.14) volumes. Sex-stratified analyses showed these associations were largely driven by males; no significant associations were found in females. Results held after adjusting for physical activity.","limitations":"- Sedentary behavior was self-reported (frequency only, not duration in hours/day), introducing potential recall bias and preventing precise time-based dose thresholds.\n- SB was measured only at baseline (visits 1 and 3), not at the imaging visit, so changes in behavior over the 22-year interval cannot be fully captured.\n- Observational design precludes causal inference; despite multiple sensitivity analyses, residual confounding cannot be excluded.","practice_takeaway":"Not all sitting is equal — leisure TV watching (cognitively passive) is tied to worse brain structure and more white matter damage, while occupational sitting (cognitively active) appears protective. Clinicians counseling older adults on dementia risk should address the *type* of sedentary time, not just total sitting hours."}},{"doi":"10.1038/s41433-026-04680-1","pmid":"42365192","title":"Retinal ischemic perivascular lesions in cortical cerebral infarction: a comparison against controls","journal_title":"Eye","journal_issn":"0950-222X","published_at":"2026-06-27T00:00:00.000Z","url":"https://doi.org/10.1038/s41433-026-04680-1","source_score":3,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-03T13:38:47.648Z","updated_at":"2026-07-03T13:38:47.648Z","tags":[{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"category","value":"Ophthalmology","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"condition","value":"Cortical Cerebral Infarction","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"condition","value":"Retinal Ischemic Perivascular Lesions","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"modality","value":"Optical Coherence Tomography","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"sample_size","value":"n=129","value_numeric":129},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"study_design","value":"Retrospective Cross-Sectional Study","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"warning","value":"Several authors (JBB, HS, MD, RGM) hold a pending US patent on RIPLs; readers should weigh this potential conflict of interest.","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"warning","value":"Study design is cross-sectional and single-institution with a small sample; findings should be considered hypothesis-generating rather than definitive.","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"warning","value":"The control group was defined by CAC = 0 but likely included individuals with cardiovascular risk factors, which may have inflated baseline RIPL counts and reduced the ability to detect differences between groups.","value_numeric":null},{"paper_doi":"10.1038/s41433-026-04680-1","tag_type":"warning","value":"The pre-stroke and post-stroke groups were not mutually exclusive — 5 patients contributed to both groups, which could introduce overlap bias.","value_numeric":null}],"summaries":{"what_studied":"This retrospective, cross-sectional study compared retinal ischemic perivascular lesion (RIPL) counts on OCT imaging among 65 controls (CAC score = 0), 27 pre-stroke patients, and 37 post-stroke patients with cortical cerebral infarction at a single institution; it also examined whether RIPLs differed by stroke circulation (anterior vs. posterior) or laterality (ipsilateral vs. contralateral eye).","key_result":"Both pre-stroke (mean 3.39) and post-stroke (mean 3.62) patients had significantly higher RIPL counts than controls (mean 2.05; p = 0.03). However, after multivariate adjustment for cardiovascular covariates (HTN, CAS, CVD history, sex, BMI), the association was no longer significant (OR 1.12, 95% CI 0.92–1.37, p = 0.24). No RIPL differences were found between anterior vs. posterior circulation or ipsilateral vs. contralateral eyes.","limitations":"- Small sample size (n = 129) with cross-sectional design limits causal inference.\n- Controls were selected by CAC = 0 but likely had underlying disease (mean RIPL ~2), reducing contrast with stroke groups.\n- Authors and some graders hold a patent application on RIPLs, introducing potential conflict of interest.","practice_takeaway":"RIPLs on OCT are elevated in cortical stroke patients, but this reflects chronic systemic microvascular risk rather than acute stroke-specific injury — so RIPLs should not be used to distinguish acute cortical events from baseline vascular burden. Clinicians may find a high RIPL count (≥2) a useful prompt to intensify cardiovascular risk-factor management and screen for carotid stenosis or atrial fibrillation."}},{"doi":"10.1161/circulationaha.125.077394","pmid":"42323953","title":"Contrastive Machine Learning to Quantify Hypertensive Multiorgan Damage and Identify New Disease Phenotypes: A Multinational Multimodal Study","journal_title":"Circulation","journal_issn":"0009-7322","published_at":"2026-06-21T00:00:00.000Z","url":"https://doi.org/10.1161/circulationaha.125.077394","source_score":49,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-26T13:25:34.186Z","updated_at":"2026-06-26T13:25:34.186Z","tags":[{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"condition","value":"Chronic Kidney Disease","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"condition","value":"Hypertension","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"condition","value":"Hypertensive End-Organ Damage","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"modality","value":"Machine Learning / Artificial Intelligence","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"modality","value":"Multimodal Imaging","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"sample_size","value":"n=32606","value_numeric":32606},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"study_design","value":"Machine Learning / Observational Cohort Study","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"warning","value":"Level of evidence set to 3 (observational cohort) given the non-randomized, non-interventional design; the ML/prognostic framing could be argued as level 2 for prognostic studies.","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — the framework is not yet deployed in clinical settings and requires large-scale imaging infrastructure not yet widely available.","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"warning","value":"The study_design is a novel ML-based semisupervised framework applied to two observational cohorts — it does not fit neatly into standard RCT/cohort categories; labeled here as observational cohort with ML development.","value_numeric":null},{"paper_doi":"10.1161/circulationaha.125.077394","tag_type":"warning","value":"Total sample size of 32,606 combines UK Biobank (27,099) and ARIC (5,507) across two distinct cohorts with different roles (development vs. external validation).","value_numeric":null}],"summaries":{"what_studied":"A semisupervised contrastive trajectory inference (cTI) machine learning framework was developed using 566 multimodal imaging and non-imaging variables from 27,099 UK Biobank participants to quantify hypertension-associated multiorgan damage (heart, brain, kidneys, vasculature, lungs, liver, metabolic) and identify disease phenotypes; external validation was performed in 5,507 ARIC participants with up to 7-year follow-up.","key_result":"The global organ damage score (HyperScore) achieved an AUC of 0.964 (95% CI 0.941–0.987) for identifying severe end-organ disease, with survival odds differing significantly across HyperScore stages (P<0.001) while blood pressure stratification alone was nonsignificant; 6 distinct hypertensive phenotypes (HyperTrajectory) were identified, and external ARIC validation showed Jensen-Shannon distances as low as 0.10 with no significant deviation in damage progression (P>0.05).","limitations":"- Both cohorts (UK Biobank, ARIC) are observational and may not represent all hypertensive populations globally.\n- The pseudotemporal modeling infers disease progression rather than tracking true longitudinal change in individuals.\n- The 566-variable multimodal imaging framework may not be feasible in most routine clinical settings.","practice_takeaway":"A machine learning-derived multiorgan damage score (HyperScore) outperforms blood pressure alone in stratifying survival risk in hypertensive patients and identifies 6 distinct organ-damage phenotypes that could guide phenotype-specific treatment strategies. Clinicians should anticipate future tools that move beyond BP thresholds toward personalized, imaging-informed hypertension management."}},{"doi":"10.1038/s41593-026-02326-9","pmid":"42271045","title":"Cerebrovascular vulnerability and fibrosis in human brain aneurysms","journal_title":"Nature Neuroscience","journal_issn":"1097-6256","published_at":"2026-06-10T00:00:00.000Z","url":"https://doi.org/10.1038/s41593-026-02326-9","source_score":88,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-13T15:34:48.333Z","updated_at":"2026-06-13T15:34:48.333Z","tags":[{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"category","value":"Neurosciences","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"condition","value":"Intracranial Aneurysm","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"condition","value":"Subarachnoid Hemorrhage","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"modality","value":"Translational Genomics","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"sample_size","value":"n=227663","value_numeric":227663},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"study_design","value":"Cross-Sectional Transcriptomic Atlas (Single-Cell RNA Sequencing + Spatial Transcriptomics)","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"warning","value":"Level of evidence is assigned as 4 (mechanistic/translational human tissue study) given the absence of a clinical intervention or outcomes analysis.","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"warning","value":"Study design is cross-sectional; causal ordering of fibrotic vs. inflammatory events cannot be established from this data alone.","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"warning","value":"The 'practice_changing' impact flag reflects novelty of mechanistic insight (fibrosis + myeloid axis) rather than an immediate change in clinical management, as no therapeutic interventions were tested.","value_numeric":null},{"paper_doi":"10.1038/s41593-026-02326-9","tag_type":"warning","value":"The sample size is small (14 aneurysms, 11 controls) relative to the cellular atlas scale; donor-level conclusions should be interpreted cautiously.","value_numeric":null}],"summaries":{"what_studied":"This study profiled 227,663 neurovascular cells (including 52,946 aneurysmal cells) from 14 adult human brain aneurysms and 11 control vessels using single-cell RNA sequencing and cell-resolution spatial transcriptomics to map the cellular and molecular pathology of aneurysm formation and rupture.","key_result":"Brain aneurysms showed loss of structurally supportive smooth muscle cells and emergence of activated perivascular fibroblasts that re-populate the vascular wall and express multiple aneurysm-risk genes; specialized macrophages rarely seen in healthy cerebrovasculature also infiltrate the aneurysmal wall, expressing destabilizing vascular cell programs and engaging in fibroblast-myeloid signaling.","limitations":"Small sample size (14 aneurysms, 11 controls) limits statistical power; all samples are adult human tissue, so findings may not capture earlier or pediatric disease stages; the cross-sectional design prevents causal inference about the sequence of fibrotic and inflammatory changes.","practice_takeaway":"Activated perivascular fibroblasts and a specialized macrophage population are emerging as key cellular drivers of cerebrovascular remodeling in brain aneurysms — these cell types and their signaling pathways represent potential translational targets. Clinicians should watch for therapeutic strategies aimed at fibrotic and myeloid-inflammatory mechanisms rather than solely smooth muscle biology."}},{"doi":"10.1177/0271678x261448670","pmid":"42152599","title":"Mechanisms of neurovascular regulation in health and disease: Insights from experimental animal models","journal_title":"Journal of Cerebral Blood Flow & Metabolism","journal_issn":"0271-678X","published_at":"2026-05-18T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13186933/","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-27T15:43:14.556Z","updated_at":"2026-05-27T15:43:14.556Z","tags":[{"paper_doi":"10.1177/0271678x261448670","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"condition","value":"Alzheimer's Disease","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"condition","value":"Hypertension","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"modality","value":"Neurovascular Regulation","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"warning","value":"Level of evidence set to 7 (expert opinion/review) as no original experimental data are presented.","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"warning","value":"The 'mixed' age group tag reflects that animal models span various life stages; no specific human age groups are defined in the abstract.","value_numeric":null},{"paper_doi":"10.1177/0271678x261448670","tag_type":"warning","value":"This is a narrative review based primarily on preclinical (animal) evidence; no original human clinical data or effect sizes are reported.","value_numeric":null}],"summaries":{"what_studied":"This review examines the mechanisms of neurovascular regulation — including neurovascular coupling, cerebrovascular autoregulation, and endothelial control of vascular tone — with a focus on insights derived from experimental animal models and their relevance to cerebrovascular and neurodegenerative diseases such as hypertension and Alzheimer's disease.","key_result":"Animal models have been central to dissecting the molecular and cellular pathways of the neurovascular unit (NVU), revealing how disruption of blood-brain barrier integrity, vascular tone, and metabolic exchange contributes to hypertension-related cerebrovascular disease and Alzheimer's disease pathology.","limitations":"Findings are primarily preclinical; translation of animal model insights to human disease remains uncertain. The review does not report original experimental data or effect sizes.","practice_takeaway":"Clinicians managing hypertension or Alzheimer's disease should be aware that neurovascular dysregulation — not just neuronal loss — is a core driver of disease progression. Preserving NVU integrity may be an important therapeutic target, though clinical interventions based on these preclinical mechanisms are not yet established."}},{"doi":"10.1001/jamacardio.2026.0915","pmid":"42126857","title":"Maternal Diabetes and Risk of Early-Onset Cardiovascular Diseases in Offspring","journal_title":"JAMA Cardiology","journal_issn":"2380-6583","published_at":"2026-05-13T00:00:00.000Z","url":"https://pmc.ncbi.nlm.nih.gov/articles/PMC13173430/","source_score":44,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-15T13:26:05.140Z","updated_at":"2026-07-15T13:26:05.140Z","tags":[{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"category","value":"Cardiac & Cardiovascular Systems","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Atrial Fibrillation","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Cardiovascular Disease","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Congenital Heart Disease","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Gestational Diabetes","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Heart Failure","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Pregestational Diabetes","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"condition","value":"Venous Thromboembolism","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"sample_size","value":"n=4274414","value_numeric":4274414},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"study_design","value":"Population-Based Cohort Study","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"warning","value":"Full text is under embargo until May 13, 2027; summary is based solely on the abstract and results sections provided.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"warning","value":"Mediation percentages are estimates from causal mediation models and assume no unmeasured mediator–outcome confounding.","value_numeric":null},{"paper_doi":"10.1001/jamacardio.2026.0915","tag_type":"warning","value":"The cohort is exclusively Swedish, which may limit generalizability to populations with different genetic backgrounds, healthcare systems, or diabetes prevalence.","value_numeric":null}],"summaries":{"what_studied":"This nationwide Swedish cohort study examined whether maternal diabetes during pregnancy (gestational or pregestational type 1/2) was associated with long-term CVD risk in offspring born 1973–2014, with follow-up through 2023 (median 27.6 years). Mediation by congenital heart disease (CHD), preterm birth, and large for gestational age (LGA) was also assessed.","key_result":"Any maternal diabetes raised offspring CVD risk (HR 1.16; 95% CI 1.12–1.20), with pregestational diabetes carrying a higher risk (HR 1.29) than gestational diabetes (HR 1.11). Specific subtypes most affected were heart failure (HR 1.65), cerebrovascular disease (HR 1.31), atrial fibrillation (HR 1.27), and venous thromboembolism (HR 1.20). CHD, preterm birth, and LGA mediated 31.87%, 16.06%, and 14.18% of the association, respectively.","limitations":"- Follow-up ends at a mean age of ~27 years, so lifetime CVD burden in exposed offspring may be underestimated.\n- Observational design; residual confounding from unmeasured genetic or lifestyle factors cannot be excluded despite sibling analyses.\n- Diabetes type and severity rely on register data, which may introduce misclassification.","practice_takeaway":"Offspring of mothers with diabetes—especially pregestational diabetes—carry meaningfully elevated long-term CVD risk and may warrant earlier cardiovascular surveillance. Optimizing glycemic control in pregnancy and monitoring for CHD, preterm birth, and LGA may help reduce downstream CVD burden in these children."}},{"doi":"10.1111/dom.70842","pmid":"42108425","title":"Diabetic Peripheral Neuropathy May Be an Independent Risk Marker for Dementia and Cerebrovascular Disease","journal_title":"Diabetes, Obesity and Metabolism","journal_issn":"1462-8902","published_at":"2026-05-10T00:00:00.000Z","url":"https://doi.org/10.1111/dom.70842","source_score":8,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-22T13:22:24.809Z","updated_at":"2026-05-22T13:22:24.809Z","tags":[{"paper_doi":"10.1111/dom.70842","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"category","value":"Endocrinology & Metabolism","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"condition","value":"Dementia","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"condition","value":"Diabetic Peripheral Neuropathy","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"condition","value":"Type 1 Diabetes","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"condition","value":"Type 2 Diabetes","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"modality","value":"Vibration Perception Threshold Testing","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"sample_size","value":"n=15036","value_numeric":15036},{"paper_doi":"10.1111/dom.70842","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"study_design","value":"Register-Based Cohort Study","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"warning","value":"Sample size of 15,036 reflects the combined T1D (n=5,641) and T2D (n=9,395) cohorts; the two groups were analyzed separately with distinct baseline ages and sex distributions.","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"warning","value":"The dementia outcome in T1D had very few events, producing a wide confidence interval (0.75–3.48); this null finding may reflect insufficient statistical power rather than a true absence of association.","value_numeric":null},{"paper_doi":"10.1111/dom.70842","tag_type":"warning","value":"The 'practice_changing' impact flag is applied cautiously — the association is strong in T2D but the study is observational and cannot establish causality. Clinicians should interpret DPN as a risk marker, not a proven causal pathway.","value_numeric":null}],"summaries":{"what_studied":"This register-based cohort study (1998–2020) examined whether diabetic peripheral neuropathy (DPN), defined by vibration perception threshold (VPT), is independently associated with incident dementia and cerebrovascular disease in 5,641 adults with Type 1 diabetes (T1D) and 9,395 with Type 2 diabetes (T2D) from Denmark.","key_result":"In T2D, DPN (VPT >25 V) was associated with a 4.36-fold higher rate of dementia (IRR 4.36, 95% CI 2.07–9.16) and 1.45-fold higher rate of cerebrovascular disease (IRR 1.45, 95% CI 1.18–1.80); these associations persisted after adjusting for retinopathy and nephropathy. In T1D, DPN was associated with increased cerebrovascular disease (IRR 1.45, 95% CI 1.11–1.91) but not dementia (IRR 1.61, 95% CI 0.75–3.48), and the cerebrovascular signal was attenuated after adjustment for other microvascular complications.","limitations":"- Observational design limits causal inference; residual confounding cannot be excluded.\n- Single-center diabetes cohort (Steno Diabetes Center Copenhagen) may limit generalizability.\n- Dementia event counts in T1D were too few to yield a precise estimate (wide CI crossing 1.0).","practice_takeaway":"DPN screening with VPT may help identify T2D patients at markedly elevated risk for dementia and cerebrovascular disease — consider it a prompt for intensified vascular risk-factor management. In T1D, DPN signals elevated cerebrovascular risk independent of other microvascular complications."}},{"doi":"10.1038/s41433-026-04479-0","pmid":"42056483","title":"Risk of cerebrovascular and cardiovascular outcomes in patients with an ICD code for ocular migraine","journal_title":"Eye","journal_issn":"0950-222X","published_at":"2026-04-30T00:00:00.000Z","url":"https://doi.org/10.1038/s41433-026-04479-0","source_score":4,"is_retracted":false,"is_open_access":true,"raw_metadata":{"ooir":{"day":"2026-05-03","doi":"10.1038/s41433-026-04479-0","days":"14","issn":"0950-222X","rank":"7","field":"Clinical Medicine","score":"4","category":"Ophthalmology","categories":["Ophthalmology"],"_categories":["Ophthalmology"]},"pubmed":{"doi":"10.1038/s41433-026-04479-0","title":"Risk of cerebrovascular and cardiovascular outcomes in patients with an ICD code for ocular migraine.","journal":"Eye (London, England)","methods":"","results":"Compared with ophthalmology controls ≥ 50 years old, patients with a diagnostic code ocular migraine had an increased risk of all outcomes, with a risk ratio of 1.48 (95% CI 1.33, 1.64), transient ischemic stroke 2.68 (2.20, 3.27) and cerebral infarct 1.81 (1.55, 2.10). These findings continued to be significant among the ≥ 65 years old cases and controls. Compared to patients with MA or MO, patients had a comparable risk of all outcomes (p > 0.05).","abstract":"$30","keywords":[],"pubmed_id":"42056483","conclusions":"Patients with a diagnostic code for ocular migraine ≥ 50 years old had a 48% increased risk of cerebrovascular and cardiovascular outcomes, compared to ophthalmology controls. Future retrospective and prospective cohort analyses are needed to further verify these findings.","publication_date":"2026-04-30T00:00:00"},"crossref":{"DOI":"10.1038/s41433-026-04479-0","URL":"https://doi.org/10.1038/s41433-026-04479-0","ISSN":["0950-222X","1476-5454"],"link":[{"URL":"https://www.nature.com/articles/s41433-026-04479-0.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https://www.nature.com/articles/s41433-026-04479-0","content-type":"text/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https://www.nature.com/articles/s41433-026-04479-0.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":null,"score":1,"title":["Risk of cerebrovascular and cardiovascular outcomes in patients with an ICD code for ocular migraine"],"author":[{"given":"Jacqueline K.","family":"Shaia","sequence":"first","affiliation":[]},{"given":"Priya","family":"Shukla","sequence":"additional","affiliation":[]},{"given":"Hayden","family":"Reed","sequence":"additional","affiliation":[]},{"given":"David C.","family":"Kaelber","sequence":"additional","affiliation":[]},{"given":"Rishi P.","family":"Singh","sequence":"additional","affiliation":[]},{"given":"Katherine E.","family":"Talcott","sequence":"additional","affiliation":[]}],"funder":[{"id":[{"id":"10.13039/100000053","id-type":"DOI","asserted-by":"publisher"}],"DOI":"10.13039/100000053","name":"U.S. Department of Health & Human Services | NIH | National Eye Institute","award":["T32 EY024236"],"award-info":[{"award-number":["T32 EY024236"]}],"doi-asserted-by":"publisher"},{"id":[{"id":"10.13039/100001818","id-type":"DOI","asserted-by":"publisher"}],"DOI":"10.13039/100001818","name":"Research to Prevent Blindness","award":["P30EY025585(BA-A)"],"award-info":[{"award-number":["P30EY025585(BA-A)"]}],"doi-asserted-by":"publisher"},{"id":[{"id":"10.13039/100001818","id-type":"DOI","asserted-by":"publisher"}],"DOI":"10.13039/100001818","name":"Research to Prevent Blindness","award":["P30EY025585(BA-A)"],"award-info":[{"award-number":["P30EY025585(BA-A)"]}],"doi-asserted-by":"publisher"}],"issued":{"date-parts":[[2026,4,29]]},"member":"297","prefix":"10.1038","source":"Crossref","volume":null,"created":{"date-time":"2026-04-29T06:13:27Z","timestamp":1777443207000,"date-parts":[[2026,4,29]]},"indexed":{"date-time":"2026-05-01T12:39:36Z","timestamp":1777639176990,"date-parts":[[2026,5,1]]},"license":[{"URL":"https://creativecommons.org/licenses/by/4.0","start":{"date-time":"2026-04-29T00:00:00Z","timestamp":1777420800000,"date-parts":[[2026,4,29]]},"delay-in-days":0,"content-version":"tdm"},{"URL":"https://creativecommons.org/licenses/by/4.0","start":{"date-time":"2026-04-29T00:00:00Z","timestamp":1777420800000,"date-parts":[[2026,4,29]]},"delay-in-days":0,"content-version":"vor"}],"subject":[],"abstract":"$31","language":"en","relation":{},"resource":{"primary":{"URL":"https://www.nature.com/articles/s41433-026-04479-0"}},"subtitle":[],"assertion":[{"name":"received","group":{"name":"ArticleHistory","label":"Article History"},"label":"Received","order":1,"value":"17 March 2025"},{"name":"revised","group":{"name":"ArticleHistory","label":"Article History"},"label":"Revised","order":2,"value":"15 January 2026"},{"name":"accepted","group":{"name":"ArticleHistory","label":"Article History"},"label":"Accepted","order":3,"value":"14 April 2026"},{"name":"first_online","group":{"name":"ArticleHistory","label":"Article History"},"label":"First Online","order":4,"value":"29 April 2026"},{"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"},"order":1,"value":"RPS reports personal fees from Apellis, Iveric Bio, Eyepoint, Regenxbio, Genentech, Bausch and Lomb, Zeiss, Alcon, and Regeneron, and research grants from Janssen. KET: Alimera (consultant), AbbVie (consultant), Apellis (consultant), Astellas (Speaker’s bureau), Eyepoint (consultant), Genentech (consultant, speaker’s bureau), Outlook (consultant), Regeneron (consultant, research), Zeiss (speaker, research, consultant). JKS: Impact Education—Regeneron Pharmaceuticals, Inc. The authors declare no competing interests."}],"deposited":{"date-time":"2026-04-29T06:13:32Z","timestamp":1777443212000,"date-parts":[[2026,4,29]]},"issn-type":[{"type":"print","value":"0950-222X"},{"type":"electronic","value":"1476-5454"}],"published":{"date-parts":[[2026,4,29]]},"publisher":"Springer Science and Business Media LLC","reference":[{"DOI":null,"key":"4479_CR1","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":"Murphy SL, Kochanek KD, Xu J, Arias E. Mortality in the United States, 2014. Key findings, Data from the National Vital Statistics System, Mortality. Published online in 2014. 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recommendations within the statement vary in evidence strength.","value_numeric":null},{"paper_doi":"10.1161/str.0000000000000518","tag_type":"warning","value":"This is an AHA scientific statement, not a primary study or systematic review — no original data or pooled effect sizes are reported.","value_numeric":null}],"summaries":{"what_studied":"This AHA scientific statement reviews nonvascular physical and psychological variables that affect brain health and cognitive resilience across the life span, including chronic medical conditions, inflammation, environmental exposures, socioeconomic drivers, sleep quality, the gut microbiome, and mental health.","key_result":"The statement synthesizes evidence on multiple modifiable and nonmodifiable factors — from early brain development through neurodegeneration — that influence cognitive and emotional functioning, and identifies gaps where the strength of evidence for biological mechanisms and mitigating strategies remains variable.","limitations":"As a scientific statement rather than a systematic review or meta-analysis, it does not provide pooled effect estimates; the breadth of topics covered limits depth on any single factor; and causal directionality for many reviewed associations remains uncertain.","practice_takeaway":"Clinicians should consider a broad range of modifiable factors — including sleep, gut health, mental health, environmental exposures, and socioeconomic determinants — not just vascular risk factors, when counseling patients on brain health across all ages. Intervening early and across multiple domains offers the best opportunity to preserve cognitive resilience."}},{"doi":"10.1111/1471-0528.70251","pmid":"42017268","title":"Long‐Term Cardiovascular Impact of Postpartum Treatment After Hypertensive Disorders of Pregnancy: Population‐Based Cohort Study","journal_title":"BJOG: An International Journal of Obstetrics & Gynaecology","journal_issn":"1470-0328","published_at":"2026-04-22T00:00:00.000Z","url":"https://doi.org/10.1111/1471-0528.70251","source_score":7,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-07T22:50:49.189Z","updated_at":"2026-05-07T22:50:49.189Z","tags":[{"paper_doi":"10.1111/1471-0528.70251","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"category","value":"Obstetrics & Gynecology","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"condition","value":"Cerebrovascular Disease","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"condition","value":"Chronic Hypertension","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"condition","value":"Coronary Artery Disease","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"condition","value":"Heart Failure","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"condition","value":"Hypertensive Disorders of Pregnancy","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"condition","value":"Peripheral Artery Disease","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"modality","value":"Antihypertensive Agent","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"sample_size","value":"n=108,906","value_numeric":108906},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"sex","value":"female","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"study_design","value":"Population-Based Cohort Study","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"warning","value":"Results are from a French administrative database (2010–2014); generalizability to other health systems or more recent practice may be limited.","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"warning","value":"The higher cardiovascular risk in treated women likely reflects confounding by indication (i.e., more severe or persistent HDP), not a harmful effect of antihypertensive treatment itself — clinicians should not interpret this as a reason to withhold postpartum treatment.","value_numeric":null},{"paper_doi":"10.1111/1471-0528.70251","tag_type":"warning","value":"The study does not report which specific antihypertensive agents were used, limiting drug-level clinical applicability.","value_numeric":null}],"summaries":{"what_studied":"This nationwide population-based cohort study in France evaluated whether early postpartum antihypertensive treatment (within 1 month of delivery) influences long-term cardiovascular outcomes over 10 years in 108,906 women with hypertensive disorders of pregnancy (HDP), excluding those with pre-existing chronic hypertension, who delivered between 2010 and 2014.","key_result":"Women treated early postpartum had significantly higher 10-year cardiovascular risk vs. untreated women: new-onset chronic hypertension (CH) aHR 3.07 (44% vs. 18% absolute risk), composite event including CH aHR 3.03, and composite excluding CH aHR 1.45. Treated women also developed events earlier in the postpartum period.","limitations":"Observational design limits causal inference — treated women likely had more severe HDP at baseline, introducing residual confounding by indication. The study cannot distinguish whether treatment itself drives outcomes or merely marks higher-risk women. Postpartum follow-up data rely on administrative health records, which may miss clinical nuance.","practice_takeaway":"All women with HDP — not just those requiring postpartum antihypertensives — need structured long-term cardiovascular follow-up, as ~1 in 5 untreated women still developed chronic hypertension within 10 years. Clinicians should use HDP as a trigger for ongoing BP monitoring and cardiovascular risk reduction regardless of whether medication was prescribed postpartum."}}],"initialOffset":14,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Cerebrovascular Disease"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Cerebrovascular Disease"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Cerebrovascular Disease"}}}]]

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