Complexities of cerebral small vessel disease, blood pressure, and dementia relationship: new insights from genetics

Authors

Muralidharan Sargurupremraj, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Aicha Soumare, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Joshua C. Bis, Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA, USA.
Ida Surakka, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Tuuli Jurgenson, Estonian Genome Centre, Institute of Genomics, University of Tartu.
Pierre Joly, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Maria J. Knol, Department of Epidemiology, Erasmus MC.
Ruiqi Wang, Boston University and the NHLBI's Framingham Heart Study, Boston, MA.
Qiong Yang, Boston University and the NHLBI's Framingham Heart Study, Boston, MA.
Claudia L. Satizabal, Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, TX.
Alexander Gudjonsson, Icelandic Heart Association, 201 Kopavogur,Iceland.
Aniket Mishra, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Vincent Bouteloup, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Chia-Ling Phuah, Department of Neurology, Washington University School of Medicine & Barnes-Jewish Hospital, St. Louis, Missouri, USA.
Cornelia M. van Duijn, Nuffield Department ofPopulation Health, University of Oxford, Oxford, UK.
Carlos Cruchaga, NeuroGenomics and Informatics Center, Washington University in St Louis, Missouri, USA.
Carole Dufouil, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Geneviève Chêne, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Oscar Lopez, Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Bruce M. Psaty, Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle, WA, USA.
Christophe Tzourio, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Philippe Amouyel, INSERM U1167, Lille, France.
Hieab H. Adams, Department of Epidemiology, Erasmus MC.
Hélène Jacqmin-Gadda, University of Bordeaux, Inserm, Bordeaux Population Health Research Center, UMR 1219, Bordeaux, France.
Mohammad Arfan Ikram, Department of Epidemiology, Erasmus MC.
Vilmundur Gudnason, Icelandic Heart Association, 201 Kopavogur,Iceland.
Lili Milani, Estonian Genome Centre, Institute of Genomics, University of Tartu.
Bendik S. Winsvold, Department of Research and Innovation, Division of Clinical Neuroscience, Oslo University Hospital, Oslo, Norway.
Kristian Hveem, K. G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Paul M. Matthews, Department of Brain Sciences, Imperial College London, UK.
W T. Longstreth, Department of Neurology, University of Washington, Seattle, Washington, USA.

Document Type

Article

Abstract

IMPORTANCE: There is increasing recognition that vascular disease, which can be treated, is a key contributor to dementia risk. However, the contribution of specific markers of vascular disease is unclear and, as a consequence, optimal prevention strategies remain unclear. OBJECTIVE: To disentangle the causal relation of several key vascular traits to dementia risk: (i) white matter hyperintensity (WMH) burden, a highly prevalent imaging marker of covert cerebral small vessel disease (cSVD); (ii) clinical stroke; and (iii) blood pressure (BP), the leading risk factor for cSVD and stroke, for which efficient therapies exist. To account for potential epidemiological biases inherent to late-onset conditions like dementia. DESIGN SETTING AND PARTICIPANTS: This study first explored the association of genetically determined WMH, BP levels and stroke risk with AD using summary-level data from large genome-wide association studies (GWASs) in a two-sample Mendelian randomization (MR) framework. Second, leveraging individual-level data from large longitudinal population-based cohorts and biobanks with prospective dementia surveillance, the association of weighted genetic risk scores (wGRSs) for WMH, BP, and stroke with incident all-cause-dementia was explored using Cox-proportional hazard and multi-state models. The data analysis was performed from July 26, 2020, through July 24, 2022. EXPOSURES: Genetically determined levels of WMH volume and BP (systolic, diastolic and pulse blood pressures) and genetic liability to stroke. MAIN OUTCOMES AND MEASURES: The summary-level MR analyses focused on the outcomes from GWAS of clinically diagnosed AD (n-cases=21,982) and GWAS additionally including self-reported parental history of dementia as a proxy for AD diagnosis (AD, n-cases=53,042). For the longitudinal analyses, individual-level data of 157,698 participants with 10,699 incident all-cause-dementia were studied, exploring AD, vascular or mixed dementia in secondary analyses. RESULTS: In the two-sample MR analyses, WMH showed strong evidence for a causal association with increased risk of AD (OR, 1.16; 95%CI:1.05-1.28; P=.003) and AD (OR, 1.28; 95%CI:1.07-1.53; P=.008), after accounting for genetically determined pulse pressure for the latter. Genetically predicted BP traits showed evidence for a protective association with both clinically defined AD and AD, with evidence for confounding by shared genetic instruments. In longitudinal analyses the wGRSs for WMH, but not BP or stroke, showed suggestive association with incident all-cause-dementia (HR, 1.02; 95%CI:1.00-1.04; P=.06). BP and stroke wGRSs were strongly associated with mortality but there was no evidence for selective survival bias during follow-up. In secondary analyses, polygenic scores with more liberal instrument definition showed association of both WMH and stroke with all-cause-dementia, AD, and vascular or mixed dementia; associations of stroke, but not WMH, with dementia outcomes were markedly attenuated after adjusting for interim stroke. CONCLUSION: These findings provide converging evidence that WMH is a leading vascular contributor to dementia risk, which may better capture the brain damage caused by BP (and other etiologies) than BP itself and should be targeted in priority for dementia prevention in the population.

Publication Date

8-13-2023

Publication Title

medRxiv : the preprint server for health sciences

PubMed ID

37790435

Digital Object Identifier (DOI)

10.1101/2023.08.08.23293761

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