Evidence map›Paper›PMID 30768754›Full record

ReviewAging cell2019

Accelerated bio-cognitive aging in Down syndrome: State of the art and possible deceleration strategies.

Claudio Franceschi, Paolo Garagnani, Noémie Gensous, Maria Giulia Bacalini, Maria Conte, Stefano Salvioli

Open access · goldAbstract readReview
In one paragraph

Review in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 2 pooled it
9.8field-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.

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

38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 82 citations in OpenAlex.

  1. Pooled it
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  12. Aging, Cancer, and Inflammation: The Telomerase Connection.International journal of molecular sciences · 2024
    Review
  13. Transcranial photobiomodulation for neurodevelopmental disorders: a narrative review.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2024
    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

6 authors at 3 institutions in 3 countries.

Claudio FranceschiIRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
Paolo GaragnaniDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy.
Noémie GensousDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy.ORCID 0000-0002-8428-616X
Maria Giulia BacaliniIRCCS Istituto delle Scienze Neurologiche di Bologna, Bologna, Italy.
Maria ConteDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy.
Stefano SalvioliDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy.
University of Bologna · ITIstituto delle Scienze Neurologiche di Bologna · ITKarolinska University Hospital · SE

Funding

EU FP7 "HUMAN" 602757EU H2020 Propag-ageing 634821EU H2020 research and innovation programme (PANINI) 675003EU JPND "ADAGE"Roberto and Cornelia Pallotti legacy for cancer researchRussian Federation megagrant DPM-Ageing 2017-220-06-4741
6 · The paper itself

Abstract

Down syndrome (DS) has been proposed by George Martin as a segmental progeroid syndrome since 1978. In fact, DS persons suffer from several age-associated disorders much earlier than euploid persons. Furthermore, a series of recent studies have found that DS persons display elevated levels of age biomarkers, thus supporting the notion that DS is a progeroid trait. Nowadays, due to the progressive advancements in social inclusion processes and medical assistance, DS persons live much longer than in the past; therefore, the early-onset health problems of these persons are becoming an urgent and largely unmet social and medical burden. In particular, the most important ailment of DS persons is the accelerated cognitive decline that starts when they reach about 40 years of age. This decline can be at least in part counteracted by multi-systemic approaches including early-onset cognitive training, physical activity, and psychosocial assistance. However, no pharmacological treatment is approved to counteract this decline. According to the most advanced conceptualization of Geroscience, tackling the molecular mechanisms underpinning the aging process should be a smart/feasible strategy to combat and/or delay the great majority of age-related diseases, including cognitive decline. We think that a debate is needed urgently on if (and how) this strategy could be integrated in protocols to face DS-associated dementia and overall unhealthy aging. In particular we propose that, on the basis of data obtained in different clinical settings, metformin is a promising candidate that could be exploited to counteract cognitive decline in DS.

Indexed as

Cognitive AgingAnimalsDown SyndromeHumansaccelerated aginganti-aging strategiescognitive impairmentDown syndromemetformin

Identifiers

PMID30768754
PMCPMC6516152
OpenAlexW2911884234

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.