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:T610,Heavy alcohol use (HAU) is a modifiable risk factor that may influence intracerebral hemorrhage (ICH) severity and cerebral small vessel disease (cSVD), but its role remains insufficiently understood. We aimed to investigate how HAU is associated with acute ICH characteristics and cSVD burden. In this cross-sectional study, we analyzed prospectively collected data from consecutive patients admitted with spontaneous, nontraumatic ICH to Massachusetts General Hospital between 2003 and 2019. HAU was defined as regular alcohol consumption of ≥3 drinks per day. Multivariable regression models assessed associations between HAU and acute ICH clinical and radiologic features and MRI markers of cSVD. Among 1,600 patients (851 male patients [53%]; median age 75 [interquartile range 64-82] years), 104 (7%) met criteria for HAU. Compared with the non-HAU cohort, patients with HAU were significantly younger at ICH onset (median 64 vs 75 years; HAU is associated with younger age at ICH onset, larger hematoma size, and imaging features consistent with more advanced hypertensive cSVD, including a greater burden of white matter hyperintensities. These findings suggest that HAU may exacerbate acute ICH severity and accelerate long-term cerebral small vessel pathology. Study limitations include the cross-sectional design, MRI availability restricted to a subset, and lack of detailed lifetime alcohol exposure. Future studies should clarify alcohol-related mechanisms underlying cSVD progression and ICH severity and inform prevention strategies.31:T62a,Neighborhood deprivation increases dementia risk, although mechanisms remain unclear. We tested a framework in which modifiable risk factors and cerebral small vessel disease (SVD) mediate the link between neighborhood deprivation and cognition. In 585 cognitively healthy midlife adults (ages 40-59), neighborhood deprivation was derived from postcodes, cognition was assessed using the COGNITO, lifestyle risk factors were measured using clinical assessments, and SVD (white matter hyperintensities, lacunes, microbleeds, perivascular spaces) was assessed on 3T magnetic resonance imaging. Multivariate analyses examined association pathways among these variables. Neighborhood deprivation was associated with poorer cognition (r = 0.36, p < 0.001), greater prevalence of modifiable risk factors (r = 0.36, p < 0.001), and greater SVD burden (β = 0.18, p = 0.008). Serial mediation showed that the effects of deprivation on cognition were indirect, possibly operating via lifestyle risk and SVD, explaining 20% of the total effect, whereas SVD alone explained 28%. Neighborhood disadvantage relates to poorer cognition, possibly mediated through vascular risk factors and cerebrovascular disease. Neighborhood deprivation linked to poorer cognition in healthy midlife adults Deprivation linked to small vessel disease (SVD) and modifiable risk factors (chiefly cardiovascular risk) Association between deprivation and cognition mediated by modifiable risk and SVD Mediation was exclusive to hypertensive SVD, but not cerebral amyloid angiopathy (CAA)-related SVD.32:Td8e,ABSTRACT INTRODUCTION Neighborhood deprivation increases dementia risk, although mechanisms remain unclear. We tested a framework in which modifiable risk factors and cerebral small vessel disease (SVD) mediate the link between neighborhood deprivation and cognition. METHODS In 585 cognitively healthy midlife adults (ages 40–59), neighborhood deprivation was derived from postcodes, cognition was assessed using the COGNITO, lifestyle risk factors were measured using clinical assessments, and SVD (white matter hyperintensities, lacunes, microbleeds, perivascular spaces) was assessed on 3T magnetic resonance imaging. Multivariate analyses examined association pathways among these variables. RESULTS Neighborhood deprivation was associated with poorer cognition ( r = 0.36, p < 0.001), greater prevalence of modifiable risk factors ( r = 0.36, p < 0.001), and greater SVD burden ( β = 0.18, p = 0.008). Serial mediation showed that the effects of deprivation on cognition were indirect, possibly operating via lifestyle risk and SVD, explaining 20% of the total effect, whereas SVD alone explained 28%. DISCUSSION Neighborhood disadvantage relates to poorer cognition, possibly mediated through vascular risk factors and cerebrovascular disease. Highlights

Neighborhood deprivation linked to poorer cognition in healthy midlife adults

Deprivation linked to small vessel disease (SVD) and modifiable risk factors (chiefly cardiovascular risk)

Association between deprivation and cognition mediated by modifiable risk and SVD

Mediation was exclusive to hypertensive SVD, but not cerebral amyloid angiopathy (CAA)‐related SVD

25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Cerebral Small Vessel Disease: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Cerebral Small Vessel Disease (condition). Clinician-written summaries and actionable practice insights. 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Clinicians should interpret the human genetic associations (observational, n=836) cautiously.","value_numeric":null}],"summaries":{"what_studied":"This study used AAV-BR1–delivered CRISPR/Cas9 to selectively delete *Col4a1* (collagen IV) in adult mouse brain microvessels, then tracked cerebral microbleed (CMB) formation, cognitive/motor decline, and brain pathology over 6 months; a parallel human genomic analysis examined TIMP2/MMP2 pathway variants and CMB burden in 836 participants from the BICWALZS biobank.","key_result":"CMBs appeared on T2*-weighted MRI within 3 months post-injection, increased progressively and dose-dependently over 6 months, and were paired with cognitive decline, motor incoordination, basement membrane thinning, and widespread astrocytic reactivity; in humans, four TIMP2 variants were significantly associated with CMB susceptibility (odds ratios 1.50–1.96).","limitations":"Mouse model uses transgenic Cas9 animals with retro-orbital AAV delivery, which may not fully replicate the gradual, multifactorial pathogenesis of sporadic human cerebral small vessel disease; the human genomic analysis is cross-sectional and observational (n=836), limiting causal inference; white matter changes—a hallmark of human small vessel disease—were absent in the mouse model.","practice_takeaway":"Collagen IV integrity in brain microvessel basement membranes appears critical to preventing CMBs; the TIMP2/MMP2 axis is a plausible genetic risk factor worth considering in patients with unexplained CMB burden, though clinical translation requires further validation."}},{"doi":"10.1212/wnl.0000000000214935","pmid":"42060877","title":"Association of 24-Hour Blood Pressure Variability With Cognition and Brain MRI Markers of Structural Change in Adults in Mid- to Late-Life","journal_title":"Neurology","journal_issn":"0028-3878","published_at":"2026-04-30T00:00:00.000Z","url":"https://doi.org/10.1212/wnl.0000000000214935","source_score":56,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-10T14:24:36.825Z","updated_at":"2026-06-10T14:24:36.825Z","tags":[{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"category","value":"Clinical Neurology","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"condition","value":"Blood-Brain Barrier Dysfunction","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"condition","value":"Cerebral Small Vessel Disease","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"condition","value":"Cognitive Impairment","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"condition","value":"Hypertension","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"modality","value":"Ambulatory Blood Pressure Monitoring","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"modality","value":"Brain MRI","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"sample_size","value":"n=225","value_numeric":225},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"study_design","value":"Cross-Sectional Study","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"warning","value":"APOE ε4 interaction with BPV and WMH is a subgroup finding; the paper does not report the size of the ε4 carrier subgroup, so these results may be underpowered.","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"warning","value":"Sample size tag reflects the primary BACH cohort (n=225); the combined total across both cohorts is approximately 301.","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214935","tag_type":"warning","value":"The HYPER replication cohort (n=76) is notably smaller and younger (age 27–73) than the primary BACH cohort, limiting the strength of replication. The two cohorts also used different cognitive assessment tools, reducing direct comparability.","value_numeric":null}],"summaries":{"what_studied":"Cross-sectional study examining whether 24-hour ambulatory blood pressure variability (BPV) is associated with cognition and multimodal brain MRI markers (including WMH, BBB integrity, cerebral blood flow, white matter changes) in dementia-free adults aged 55–80 (BACH study, n=225), with partial replication in a second cohort aged 27–73 (HYPER study, n=76); also tested whether APOE ε4 status modified associations.","key_result":"Higher 24-hour and awake BPV were independently linked to poorer global cognition (β = −0.152 to −0.158) and executive function (β = −0.168 to −0.174), and reduced blood-brain barrier water exchange rate (β = −0.180). Mean 24-hour BP — not BPV — drove WMH burden (β = 0.182); BPV raised WMH only in APOE ε4 carriers. Asleep BPV was negatively associated with fluid cognition in the HYPER replication cohort (β = −0.211).","limitations":"Cross-sectional design prevents causal inference. The HYPER replication cohort was small (n=76) and used a different cognitive assessment tool. APOE ε4 interaction findings were subset analyses and may be underpowered.","practice_takeaway":"In mid- to late-life adults, high 24-hour BP variability — not just elevated mean BP — is tied to worse cognition and impaired blood-brain barrier integrity, especially in APOE ε4 carriers. Clinicians may consider monitoring BPV via ambulatory BP recording as an additional brain health risk marker, particularly in genetically at-risk patients."}},{"doi":"10.1212/wnl.0000000000214803","pmid":"42030516","title":"Association of MRI-Visible Perivascular Spaces With Longitudinal Cognitive Decline Over a Decade","journal_title":"Neurology","journal_issn":"0028-3878","published_at":"2026-04-24T00:00:00.000Z","url":"https://doi.org/10.1212/wnl.0000000000214803","source_score":12,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-05T13:26:51.815Z","updated_at":"2026-06-05T13:26:51.815Z","tags":[{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"age_group","value":"older_adult","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"category","value":"Clinical Neurology","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"condition","value":"Cerebral Small Vessel Disease","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"condition","value":"Cognitive Decline","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"condition","value":"Mild Cognitive Impairment","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"modality","value":"Neuroimaging Biomarker","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"sample_size","value":"n=750","value_numeric":750},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"study_design","value":"Longitudinal Observational Cohort Study","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"warning","value":"Beta coefficients represent effect per theoretical 0–100% PVS volume fraction increase; actual observed PVS values are much smaller, so absolute clinical effect sizes per individual patient are proportionally smaller than the reported betas.","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"warning","value":"Data collection for the expansion cohort is ongoing; the 11-year follow-up had only 18 participants, so long-term estimates are based on sparse data at the latest time points.","value_numeric":null},{"paper_doi":"10.1212/wnl.0000000000214803","tag_type":"warning","value":"Level of evidence set to 2 (prospective cohort); no randomization or intervention was involved — this is observational only, causation cannot be established.","value_numeric":null}],"summaries":{"what_studied":"This longitudinal cohort study (Vanderbilt Memory and Aging Project) examined whether baseline MRI-visible perivascular space (PVS) burden — measured by deep learning on 3T MRI — independently predicts cognitive decline across multiple domains over up to 11 years (mean 4.9 ± 3.1 years) in 750 older adults (age 68 ± 9, 52% female) free of stroke or dementia, while accounting for other SVD markers (WMH, CMBs, lacunes).","key_result":"Higher basal ganglia PVS burden was independently associated with faster decline in executive function (β = −7.47; 95% CI −12.84 to −2.10) and visuospatial skills (Hooper Visual Organization Test β = −22.11; 95% CI −42.38 to −1.85) even after head-to-head adjustment for WMH, CMBs, and lacunes. White matter PVS showed no significant independent associations with longitudinal cognition.","limitations":"- The cohort excluded stroke, dementia, heart failure, and other major illnesses, making it healthier than average and limiting generalizability.\n- Attrition bias is likely, as sicker participants withdrew preferentially, potentially biasing results toward the null.\n- PVS quantification relied on T1-weighted images rather than preferred T2-weighted imaging, and the basal ganglia mask included ventricular regions.","practice_takeaway":"Clinicians reading brain MRIs in older adults should note basal ganglia PVS burden as a marker of future executive function and visuospatial decline, independent of white matter hyperintensities or microbleeds. Tracking PVS alongside other SVD markers may help identify patients at higher risk for domain-specific cognitive decline before symptoms are obvious."}},{"doi":"10.1212/wnl.0000000000214348","pmid":"41191856","title":"Effects of Heavy Alcohol Use on Acute Intracerebral Hemorrhage and Cerebral Small Vessel Disease","journal_title":"Neurology","journal_issn":"0028-3878","published_at":"2025-11-05T00:00:00.000Z","url":"https://doi.org/10.1212/wnl.0000000000214348","source_score":575,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2026-01-08","doi":"10.1212/wnl.0000000000214348","days":"30","issn":"0028-3878","rank":"3","field":"Clinical Medicine","score":"575","category":"Clinical Neurology","categories":["Clinical Neurology"],"_categories":["Clinical Neurology"]},"pubmed":{"doi":"10.1212/WNL.0000000000214348","title":"Effects of Heavy Alcohol Use on Acute Intracerebral Hemorrhage and Cerebral Small Vessel Disease.","journal":"Neurology","methods":"","results":"Among 1,600 patients (851 male patients [53%]; median age 75 [interquartile range 64-82] years), 104 (7%) met criteria for HAU. Compared with the non-HAU cohort, patients with HAU were significantly younger at ICH onset (median 64 vs 75 years; ","abstract":"$30","keywords":[],"pubmed_id":"41191856","conclusions":"","publication_date":"2025-11-05T00:00:00"},"crossref":{"DOI":"10.1212/wnl.0000000000214348","URL":"https://doi.org/10.1212/wnl.0000000000214348","ISSN":["0028-3878","1526-632X"],"link":[{"URL":"https://www.neurology.org/doi/pdfdirect/10.1212/WNL.0000000000214348","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":null,"type":"journal-article","issue":"11","score":1,"title":["Effects of Heavy Alcohol Use on Acute Intracerebral Hemorrhage and Cerebral Small Vessel Disease"],"author":[{"given":"Mette Foldager","family":"Hindsholm","sequence":"first","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Alvin S.","family":"Das","sequence":"additional","affiliation":[{"name":"Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA;"}]},{"given":"Elif","family":"Gokcal","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Andrea","family":"Morotti","sequence":"additional","affiliation":[{"name":"Department of Clinical and Experimental Sciences, Neurology Unit, University of Brescia, Italy;"}]},{"given":"Ofer","family":"Rotschild","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Claus Ziegler","family":"Simonsen","sequence":"additional","affiliation":[{"name":"Department of Neurology, Aarhus University Hospital, Department of Clinical Medicine, Aarhus University, Denmark; and"}]},{"given":"Zora","family":"Dipucchio","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Anand","family":"Viswanathan","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Steven M.","family":"Greenberg","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Christopher D.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Jonathan","family":"Rosand","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]},{"given":"Joshua N.","family":"Goldstein","sequence":"additional","affiliation":[{"name":"Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston."}]},{"given":"M. Edip","family":"Gurol","sequence":"additional","affiliation":[{"name":"Department of Neurology, Massachusetts General Brigham, Harvard Medical School, Boston;"}]}],"issued":{"date-parts":[[2025,12,9]]},"member":"276","prefix":"10.1212","source":"Crossref","volume":"105","created":{"date-time":"2025-11-05T21:00:16Z","timestamp":1762376416000,"date-parts":[[2025,11,5]]},"indexed":{"date-time":"2025-11-05T21:07:11Z","timestamp":1762376831824,"date-parts":[[2025,11,5]]},"subject":[],"abstract":null,"language":"en","relation":{},"resource":{"primary":{"URL":"https://www.neurology.org/doi/10.1212/WNL.0000000000214348"}},"subtitle":[],"assertion":[{"name":"received","group":{"name":"publication_history","label":"Publication History"},"label":"Received","order":0,"value":"2025-05-29"},{"name":"accepted","group":{"name":"publication_history","label":"Publication History"},"label":"Accepted","order":2,"value":"2025-09-19"},{"name":"published","group":{"name":"publication_history","label":"Publication History"},"label":"Published","order":3,"value":"2025-11-05"}],"deposited":{"date-time":"2025-11-05T21:00:19Z","timestamp":1762376419000,"date-parts":[[2025,11,5]]},"issn-type":[{"type":"print","value":"0028-3878"},{"type":"electronic","value":"1526-632X"}],"published":{"date-parts":[[2025,12,9]]},"publisher":"Ovid Technologies (Wolters Kluwer Health)","reference":[{"DOI":"10.1016/S1474-4422(09)70340-0","key":"e_1_3_6_2_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1016/S1474-4422(19)30079-1","key":"e_1_3_6_3_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1056/NEJM200105103441907","key":"e_1_3_6_4_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1177/17474930221144911","key":"e_1_3_6_5_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1016/S0140-6736(10)60834-3","key":"e_1_3_6_6_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.3390/life14030311","key":"e_1_3_6_7_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1161/01.STR.21.11.1529","key":"e_1_3_6_8_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1016/j.jstrokecerebrovasdis.2019.104630","key":"e_1_3_6_9_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1136/svn-2022-001653","key":"e_1_3_6_10_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1212/WNL.0000000000002362","key":"e_1_3_6_11_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1161/01.HYP.9.2.111","key":"e_1_3_6_12_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1212/WNL.0000000000003952","key":"e_1_3_6_13_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":"10.1093/ije/dyad099","key":"e_1_3_6_14_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":null,"article-title":null,"journal-title":null,"doi-asserted-by":"publisher"},{"DOI":null,"key":"e_1_3_6_15_2","year":null,"issue":null,"author":null,"volume":null,"first-page":null,"unstructured":"Understanding Alcohol Drinking Patterns. 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disease","updated":"2025-11-11T00:23:42+00:00","published_date":"2025-11-01","best_oa_location":{"url":"https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/alz.70756","pmh_id":null,"url_for_pdf":"https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/alz.70756","url_for_landing_page":"https://doi.org/10.1002/alz.70756"}}},"created_at":"2025-12-08T12:24:58.509Z","updated_at":"2025-12-08T12:24:58.509Z","tags":[{"paper_doi":"10.1002/alz.70756","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"category","value":"Clinical Neurology","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"condition","value":"Cerebral Small Vessel Disease","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"sample_size","value":"n=585","value_numeric":585},{"paper_doi":"10.1002/alz.70756","tag_type":"study_design","value":"Cross-Sectional","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"warning","value":"Associations and mediation are reported; causality cannot be inferred from the provided data.","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"warning","value":"Criteria for classifying hypertensive versus CAA-related SVD are not detailed in the excerpt.","value_numeric":null},{"paper_doi":"10.1002/alz.70756","tag_type":"warning","value":"Details of which specific modifiable risk factors were measured are not provided beyond a general description.","value_numeric":null}],"summaries":{"what_studied":"In 585 cognitively healthy adults ages 40–59, the study examined how neighborhood deprivation (from postcodes) relates to cognition (COGNITO), modifiable lifestyle/vascular risk factors (clinical assessments), and cerebral small vessel disease (3T MRI markers), using multivariate association and serial mediation analyses.","key_result":"Neighborhood deprivation correlated with poorer cognition (r=0.36, p<0.001), more modifiable risk factors (r=0.36, p<0.001), and higher SVD burden (β=0.18, p=0.008). Serial mediation suggested indirect effects via lifestyle risk and SVD accounted for 20% of the total effect, SVD alone for 28%, with mediation specific to hypertensive SVD and not CAA-related SVD.","practice_takeaway":"For midlife adults in deprived neighborhoods, addressing modifiable vascular risks may help limit SVD burden linked to worse cognition; the pathway appears driven by hypertensive SVD rather than CAA-related SVD."}}],"initialOffset":5,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Cerebral Small Vessel Disease"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Cerebral Small Vessel Disease"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Cerebral Small Vessel Disease"}}}]]

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