Evidence map›Paper›PMID 38610055›Full record

SynthesisAlzheimer's research & therapy2024

Risk of conversion to mild cognitive impairment or dementia among subjects with amyloid and tau pathology: a systematic review and meta-analysis.

Zsolt Huszár, Marie Anne Engh, Márk Pavlekovics, Tomoya Sato, Yalea Steenkamp, Bernard Hanseeuw, Tamás Terebessy, Zsolt Molnár, Péter Hegyi, Gábor Csukly

Registry-linked trialOpen access · goldAbstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07651787 (Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment), which is not on this map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
8.1field-weighted citation impact, top 2% of its field
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.

NCT07651787 narecruitingnot on this mapstarted 2025, after this paper: background citation

Neurovascular and Mitochondrial Mechanisms of Transcranial Photobiomodulation in Vascular Mild Cognitive Impairment

TypeinterventionalSponsorUniversity of OklahomaRan2025 to 2026Enrolled40ConditionsMild Cognitive Impairment (MCI), Amyloid PathologyArmsActive Vielight Neuro RX-Duo device -Active transcranial photobiomodulation, Sham Vielight Neuro RX-Duo device -Sham transcranial photobiomodulation
3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

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  10. Emergent neuropsychiatric symptoms as preclinical flags of cognitive decline: Clinical implications.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  11. Moderating effects of plasma glial fibrillary acidic protein along the Alzheimer's disease continuum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

10 authors at 2 institutions in 4 countries.

Zsolt HuszárCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Marie Anne EnghCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Márk PavlekovicsCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Tomoya SatoCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Yalea SteenkampCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Bernard HanseeuwDepartment of Neurology and Institute of Neuroscience, Cliniques Universitaires Saint-Luc, Université Catholique de Louvain, Brussels, 1200, Belgium.
Tamás TerebessyCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Zsolt MolnárCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Péter HegyiCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary.
Gábor CsuklyCentre for Translational Medicine, Semmelweis University, Üllői út 26, Budapest, 1085, Hungary. csukly.gabor@semmelweis.hu.
Semmelweis University · HUCliniques Universitaires Saint-Luc · BE

Funding

EU Joint Programme - Neurodegenerative Disease Research 2019-2.1.7-ERA-NET-2020-00006European Regional Development Fund GINOP-2.3.4-15-2020-00008National Research, Development and Innovation Office NKFI/OTKA FK 138385
6 · The paper itself

Abstract

backgroundMeasurement of beta-amyloid (Aβ) and phosphorylated tau (p-tau) levels offers the potential for early detection of neurocognitive impairment. Still, the probability of developing a clinical syndrome in the presence of these protein changes (A+ and T+) remains unclear. By performing a systematic review and meta-analysis, we investigated the risk of mild cognitive impairment (MCI) or dementia in the non-demented population with A+ and A- alone and in combination with T+ and T- as confirmed by PET or cerebrospinal fluid examination.

methodsA systematic search of prospective and retrospective studies investigating the association of Aβ and p-tau with cognitive decline was performed in three databases (MEDLINE via PubMed, EMBASE, and CENTRAL) on January 9, 2024. The risk of bias was assessed using the Cochrane QUIPS tool. Odds ratios (OR) and Hazard Ratios (HR) were pooled using a random-effects model. The effect of neurodegeneration was not studied due to its non-specific nature.

resultsA total of 18,162 records were found, and at the end of the selection process, data from 36 cohorts were pooled (n= 7,793). Compared to the unexposed group, the odds ratio (OR) for conversion to dementia in A+ MCI patients was 5.18 [95% CI 3.93; 6.81]. In A+ CU subjects, the OR for conversion to MCI or dementia was 5.79 [95% CI 2.88; 11.64]. Cerebrospinal fluid Aβ42 or Aβ42/40 analysis and amyloid PET imaging showed consistent results. The OR for conversion in A+T+ MCI subjects (11.60 [95% CI 7.96; 16.91]) was significantly higher than in A+T- subjects (2.73 [95% CI 1.65; 4.52]). The OR for A-T+ MCI subjects was non-significant (1.47 [95% CI 0.55; 3.92]). CU subjects with A+T+ status had a significantly higher OR for conversion (13.46 [95% CI 3.69; 49.11]) than A+T- subjects (2.04 [95% CI 0.70; 5.97]). Meta-regression showed that the ORs for Aβ exposure decreased with age in MCI. (beta = -0.04 [95% CI -0.03 to -0.083]).

conclusionsIdentifying Aβ-positive individuals, irrespective of the measurement technique employed (CSF or PET), enables the detection of the most at-risk population before disease onset, or at least at a mild stage. The inclusion of tau status in addition to Aβ, especially in A+T+ cases, further refines the risk assessment. Notably, the higher odds ratio associated with Aβ decreases with age.

trial registrationThe study was registered in PROSPERO (ID: CRD42021288100).

Indexed as

Cognitive DysfunctionDementiaAmyloidogenic ProteinsHumansProspective StudiesRetrospective StudiesAmyloidogenic ProteinsAlzheimer’s diseaseBeta-amyloidDementiaMild cognitive impairmentPhosphorylated tau

Identifiers

PMID38610055
PMCPMC11015617
OpenAlexW4394767360

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.