Evidence map›Paper›PMID 39034389›Full record

ArticleAlzheimer's research & therapy2024

Hormone therapy is associated with lower Alzheimer's disease tau biomarkers in post-menopausal females -evidence from two independent cohorts.

Yi-Ting Wang, Joseph Therriault, Cécile Tissot, Stijn Servaes, Nesrine Rahmouni, Arthur Cassa Macedo, Jaime Fernandez-Arias, Sulantha S Mathotaarachchi, Jenna Stevenson, Firoza Z Lussier and 7 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Trial
  2. Article
  3. Loss of ovarian function and estrogen therapy remodel the brain's synaptic and metabolic proteome.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Article
  4. Women's midlife: the front line of Alzheimer prevention.The Journal of clinical investigation · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Yi-Ting WangTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Joseph TherriaultTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Cécile TissotTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Stijn ServaesTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Nesrine RahmouniTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Arthur Cassa MacedoTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Jaime Fernandez-AriasTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Sulantha S MathotaarachchiTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Jenna StevensonTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Firoza Z LussierDepartment of Neurology and Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, USA.
Andréa L BenedetDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Tharick A PascoalDepartment of Neurology and Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, USA.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden.
Serge GauthierTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada.
Pedro Rosa-NetoTranslational Neuroimaging Laboratory, McGill Research Centre for Studies in Aging, Montreal, Canada. pedro.rosa@mcgill.ca.

Funding

Alzheimer's Association [NIRG-12-92090, NIRP-12-259245]Canadian Consortium of Neurodegeneration and Aging (CCNA) [MOP-11-51-31 -team 1]Canadian Institutes of Health Research (CIHR) [MOP-11-51-31; RFN 152985, 159815, 162303]Fondation Brain Canada CFI Project 34874; 33397Fonds de Recherche du Québec - Santé (FRQS) Chercheur Boursier 2020-VICO-279314
6 · The paper itself

Abstract

backgroundFemales represent approximately 70% of the Alzheimer's disease (AD) cases and the literature has proposed a connection between the decreased estrogen levels during menopause and an increased AD risk. Previous investigations have predominantly focused on assessing how hormone therapy (HT) affects the likelihood of AD development and cognitive deterioration. However, as the research framework has shifted toward a biomarker-defined AD and alterations in specific biomarkers could take place years before cognitive decline becomes discernible, it is crucial to examine how HT influences AD biomarkers. The main goal of this study was to evaluate the impact of HT on AD biomarker-informed pathophysiology in both cognitively unimpaired (CU) and cognitively impaired (CI) post-menopausal females across the aging and AD spectrum.

methodsThis cross-sectional study included post-menopausal females without HT history (HT-) and with HT (HT+) at the time of PET imaging assessment from two cohorts: the Translational Biomarkers in Aging and Dementia (TRIAD) cohort, and the Alzheimer's Disease Neuroimaging Initiative (ADNI). Participants underwent magnetic resonance imaging (MRI), positron emission tomography (PET) and biofluid collection. Voxel-based t-tests were performed to assess the differences in amyloid-β (Aβ) and tau neurofibrillary tangles (NFTs) loads between HT- and HT + females. Linear regression models with interaction terms were also conducted to examine the interactive effects of HT and Aβ-PET on regional tau-PET.

resultsHT + females demonstrated significantly lower tau-PET standardized uptake value ratio (SUVR) in Braak I-II ROIs (P < 0.05, Hedges' g = 0.73), Braak III-IV ROIs (P < 0.0001, Hedges' g = 0.74) and Braak V-VI ROIs (P < 0.0001, Hedges' g = 0.69) compared to HT- females. HT + females also showed significantly lower CSF p-tau

conclusionsOverall, findings from this observational study suggest that HT is associated with lower tau neuroimaging and fluid biomarkers in postmenopausal females. Due to the close link between tau and cognition, this study highlights the need for large randomized controlled trials designed to systemically study the influences of HT on AD biomarkers and disease progression.

Indexed as

Alzheimer DiseaseBiomarkersPostmenopausetau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBrainCognitive DysfunctionCohort StudiesCross-Sectional StudiesEstrogen Replacement TherapyFemaleHumansMiddle AgedPositron-Emission TomographyAmyloid beta-PeptidesBiomarkersMAPT protein, humantau Proteins

Identifiers

PMID39034389
PMCPMC11265084

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.