Hypertension acts together with Aβ pathology in late-life to promote memory loss - 23/05/26

Doi : 10.1016/j.tjpad.2026.100579

Lucas U Da Ros ^a,^j,^{^{1
Contributed equally as the first author.}}, João Pedro Ferrari-Souza ^b,^j,^{^{1
Contributed equally as the first author.}}, Marco Antônio de Bastiani ^a, Lucas A. Hauschild ^c, Bruna Bellaver ^d, Pamela C.L. Ferreira ^d, Douglas Teixeira Leffa ^d, Guilherme Povala ^d, Firoza Z. Lussier ^d, Mira Chamoun ^e,^f, Gleb Bezgin ^e,^f, Andrea L. Benedet ^g, Nesrine Rahmouni ^e,^f, Arthur C. Macedo ^e,^f, Kaj Blennow ^g,^h,^o,^p, Nicholas Ashton ^g,^m,ⁿ, Henrik Zetterberg ^g,^h,^q,^r,^s,^t, Wyllians Vendramini Borelli ^a,^b,ⁱ, Diogo O. Souza ^b, Tharick A. Pascoal ^d,^l, Pedro Rosa-Neto ^e,^f,^u,^v, Eduardo R. Zimmer ^a,^b,^j,^k,^⁎
for the
Alzheimer’s Disease Neuroimaging Initiative ^²
Data used in the preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in the analysis or writing of this report. A complete listing of ADNI investigators can be found at: ADNI_Acknowledgement_List.pdf .

^a Graduate Program in Biological Sciences: Pharmacology and Therapeuctis, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

^b Graduate Program in Biological Sciences: Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

^c Hospital de Clínicas de Porto Alegre, Porto Alegre, RS, Brazil

^d Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA

^e Translational Neuroimaging Laboratory, McGill Centre for Studies in Aging, McGill University, Montreal, QC, Canada

^f Department of Neurology and Neurosurgery, McGill University, Montreal, QC, Canada

^g Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden

^h Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Gothenburg, Sweden

ⁱ Memory Center, Hospital Moinhos de Vento, Porto Alegre, RS, Brazil

^j Neuroscience Unit, Hospital Moinhos de Vento, Porto Alegre, RS, Brazil

^k Department of Pharmacology, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

^l Department of Neurology, University of Pittsburgh, Pittsburgh, PA, USA

^m Banner Alzheimer's Institute and University of Arizona, Phoenix, AZ, USA

ⁿ Banner Sun Health Research Institute, Sun City, AZ, USA

^o Paris Brain Institute, ICM, Pitié-Salpêtrière Hospital, Sorbonne University, Paris, France

^p Neurodegenerative Disorder Research Center, Division of Life Sciences and Medicine, and Department of Neurology, Institute on Aging and Brain Disorders, University of Science and Technology of China and First Affiliated Hospital of USTC, Hefei, PR China

^q Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK

^r UK Dementia Research Institute at UCL, London, UK

^s Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China

^t Wisconsin Alzheimer’s Disease Research Center, School of Medicine and Public Health, University of Wisconsin, Madison, WI, USA

^u McConnel Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada

^v Peter O'donnell Jr Brain Institute, The University of Texas Southwestern Medical center, Dallas, TX, USA

^⁎ Corresponding author to Neuroscience Unit, Hospital Moinhos de Vento, Porto Alegre, RS, Brazil. Graduate Program in Biological Sciences: Pharmacology and Therapeuctis Universidade Federal do Rio Grande do Sul Porto Alegre RS Brazil

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Highlights

•	Although midlife hypertension (HTN) is a known risk factor for dementia and Alzheimer's Disease (AD), the impact of late-life HTN on concomitant cognitive decline remains controversial, with inconsistent evidence in the literature.
•	This is the first study to investigate the effect of HTN and biologically determined AD on different cognitive domains in late-life, addressing a significant gap in current knowledge.
•	Our results demonstrate that individuals already at risk for cognitive decline due to AD are the most susceptible to the deleterious effects of HTN on cognition, with memory being the most affected domain.
•	The study utilized well-established biomarkers to determine AD, accounted for important covariates (age, sex, APOE ε4 status), and replicated findings in two independent cohorts.
•	The evidence suggests that HTN is a critical modifiable risk factor, and assessing specific memory outcomes can enhance the understanding of its impact on cognition in the elderly, aiding in the development of more precise prevention strategies.

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Abstract

Midlife hypertension (HTN) contributes to cognitive decline in Alzheimer's disease (AD). However, the exact effect of late-life HTN on the AD pathology and on cognitive decline is still controversial. Here, we aimed to assess the impact of HTN and AD pathology in cognitively unimpaired (CU) individuals over 65 years of age on longitudinal cognitive decline. We evaluated 637 CU individuals from two independent cohorts (475 CU individuals from the ADNI cohort; and 162 CU individuals from the TRIAD cohort), with a follow-up of up to 6 years. Linear mixed-effects models showed that HTN and Aβ acted together to promote longitudinal cognitive decline, especially memory loss, in a synergistic way, with a dose-dependent association of blood pressure and Aβ pathology. Hence, HTN in late-life confers additional risk for cognitive decline, particularly for memory loss, in CU individuals at risk of developing dementia due to AD and is a potential modifiable risk factor even at older age.

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Keywords : Hypertension, Alzheimer's disease, Modifiable risk factor

Plan

Introduction

Methods

Cohorts

Participants and clinical assessment:

Cognitive assessment:

Biomarkers assessment:

Statistical analysis:

Results

HTN in late-life and aβ pathology acted jointly to promote memory loss

Greater risk of conversion into cognitive impairment in hypertensive aβ+ individuals

HTN in late-life had no impact on AD pathology

Validation of findings in an independent cohort

Discussion

Funding

Data availability

Declaration of generative AI and AI-assisted technologies in the writing process

Conflict of interest

CRediT authorship contribution statement

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Vol 13 - N° 7

Article 100579- août 2026 Retour au numéro

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Hypertension acts together with Aβ pathology in late-life to promote memory loss - 23/05/26

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