Evidence map›Paper›PMID 39462394›Full record

ArticleAlzheimer's research & therapy2024

Association of modifiable risk factors with progression to dementia in relation to amyloid and tau pathology.

Zsolt Huszár, Alina Solomon, Marie Anne Engh, Vanda Koszovácz, Tamás Terebessy, Zsolt Molnár, Péter Hegyi, András Horváth, Francesca Mangialasche, Miia Kivipelto and 1 more

Abstract read
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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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

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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

11 authors.

Zsolt HuszárCentre for Translational Medicine, Semmelweis University, Üllői Út 26, Budapest, Hungary.
Alina SolomonInstitute of Clinical Medicine/Neurology, University of Eastern Finland, Kuopio, Finland.
Marie Anne EnghCentre for Translational Medicine, Semmelweis University, Üllői Út 26, Budapest, Hungary.
Vanda KoszováczDepartment of Psychiatry and Psychotherapy, Semmelweis University, Balassa U. 6, Budapest, 1083, Hungary.
Tamás TerebessyCentre for Translational Medicine, Semmelweis University, Üllői Út 26, Budapest, Hungary.
Zsolt MolnárCentre for Translational Medicine, Semmelweis University, Üllői Út 26, Budapest, Hungary.
Péter HegyiCentre for Translational Medicine, Semmelweis University, Üllői Út 26, Budapest, Hungary.
András HorváthCentre for Translational Medicine, Semmelweis University, Üllői Út 26, Budapest, Hungary.
Francesca MangialascheInstitute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Miia KivipeltoDivision of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Gábor CsuklyCentre for Translational Medicine, Semmelweis University, Üllői Út 26, Budapest, Hungary. csukly.gabor@semmelweis.hu.

Funding

EU Joint Programme - Neurodegenerative Disease Research 2019-2.1.7-ERA-NET-2020-00006European Research Council 804371Hungarian Scientific Research Fund 138385
6 · The paper itself

Abstract

backgroundDementia preventive interventions targeting multiple modifiable risk factors are a promising approach. However, the impact of modifiable risk factors in the presence of beta-amyloid or phosphorylated-tau (p-tau) pathology is unclear.

methodsThe objective of the study was to examine the role of modifiable risk factors (vascular factors, depression, and smoking) in the progression to mild cognitive impairment (MCI) or dementia among 434 cognitively unimpaired (CU) and 611 individuals with MCI from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Vascular risk factors were summarized with the Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) score, dichotomized into higher versus lower risk. Depression and smoking (yes/no) were categorised according to medical history or current symptoms. Analyses were stratified by beta-amyloid negative (A-) and positive (A +), p-tau negative (T-) and positive (T +), or beta-amyloid and p-tau negative (A-T-) and positive (A + T +) biomarker status. Cox proportional hazard models were adjusted for age, sex, education, baseline MMSE score, baseline hippocampal volume and ApoE4 carrier status.

resultsHigher CAIDE score was associated with increased risk of progression to all-cause dementia in most MCI subgroups: adjusted hazard ratios (aHR) [95% CI] were 3.1 [1.43; 6.53] in the A- subgroup, 1.7 [1.20-2.27] in T + , 2.6 [1.06-6.59] in A-T-, and 1.6 [1.15-2.22] in the A + T + subgroup. Smoking (yes/no) was associated with increased dementia aHR in the A + MCI subgroup: 1.6 [1.07-2.34]. Depression increased dementia aHR in the T + MCI subgroup: 1.5 [1.06-2.02]. No significant associations were found in the CU biomarker subgroups.

conclusionAddressing modifiable risk factors carries an important potential for reducing the risk of dementia even after the onset of Alzheimer's pathology. Knowledge of biomarker status can further optimize prevention strategies.

Indexed as

Amyloid beta-PeptidesCognitive DysfunctionDementiaDisease Progressiontau ProteinsAgedAged, 80 and overBiomarkersDepressionFemaleHumansMaleMiddle AgedRisk FactorsAmyloid beta-PeptidesBiomarkerstau ProteinsAmyloidCAIDEDepressionMCIModifiable risk factorsSmokingTau

Identifiers

PMID39462394
PMCPMC11515263

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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.