Evidence map›Paper›PMID 28631188›Full record

ArticleMolecular neurobiology2018

Role of CLU, PICALM, and TNK1 Genotypes in Aging With and Without Alzheimer's Disease.

Davide Seripa, Francesco Panza, Giulia Paroni, Grazia D'Onofrio, Paola Bisceglia, Carolina Gravina, Maria Urbano, Madia Lozupone, Vincenzo Solfrizzi, Alessandra Bizzarro and 7 more

Abstract readMulticenter Study
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 17% 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

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

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Genetic Variants ofFrontiers in neurology · 2019
    Article
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 at 4 institutions in 1 country.

Davide SeripaComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy. dseripa@operapadrepio.it.
Francesco PanzaComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy. geriat.dot@uniba.it.ORCID http://orcid.org/0000-0002-7220-0656
Giulia ParoniComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy.
Grazia D'OnofrioComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy.
Paola BiscegliaComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy.
Carolina GravinaComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy.
Maria UrbanoComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy.
Madia LozuponeUnit of Neurodegenerative Disease, Department of Basic Medicine Sciences, Neuroscience, and Sense Organs, University of "BariAldo Moro", Bari, Italy.
Vincenzo SolfrizziGeriatric Medicine-Memory Unit and Rare Disease Centre, University of Bari Aldo Moro, Bari, Italy.
Alessandra BizzarroInstitute of Neurology, Catholic University of Sacred Heart, Rome, Italy.
Virginia BoccardiInstitute of Gerontology and Geriatrics, Department of Medicine, University of Perugia, Perugia, Italy.
Chiara PiccininniInstitute of Neurology, Catholic University of Sacred Heart, Rome, Italy.
Antonio DanieleInstitute of Neurology, Catholic University of Sacred Heart, Rome, Italy.
Giancarlo LogroscinoUnit of Neurodegenerative Disease, Department of Basic Medicine Sciences, Neuroscience, and Sense Organs, University of "BariAldo Moro", Bari, Italy.
Patrizia MecocciInstitute of Gerontology and Geriatrics, Department of Medicine, University of Perugia, Perugia, Italy.
Carlo MasulloInstitute of Neurology, Catholic University of Sacred Heart, Rome, Italy.
Antonio GrecoComplex Structure of Geriatrics, Research Laboratory, Department of Medical Sciences, I.R.C.C.S. Casa Sollievo della Sofferenza, Viale Cappuccini 1, 71013, San Giovanni Rotondo, Foggia, Italy.
Casa Sollievo della Sofferenza · ITUniversità Cattolica del Sacro Cuore · ITUniversity of Bari Aldo Moro · ITUniversity of Perugia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Healthy and impaired cognitive aging may be associated to different prevalences of single-nucleotide polymorphisms (SNPs). In a multicenter case-control association study, we studied the SNPs rs11136000 (clusterin, CLU), rs541458 (phosphatidylinositol binding clatrin assembly protein, PICALM), and rs1554948 (transcription factor A, and tyrosine kinase, non-receptor, 1, TNK1) according to the three age groups 50-65 years (group 1), 66-80 years (group 2), and 80+ years (group 3) in 569 older subjects without cognitive impairment (NoCI) and 520 Alzheimer's disease (AD) patients. In NoCI subjects, a regression analysis suggested a relationship between age and TNK1 genotypes, with the TNK1-A/A genotype frequency that increased with higher age, and resulting in a different distribution of the TNK1-A allele. In AD patients, a regression analysis suggested a relationship between age and PICALM genotypes and TNK1 genotypes, with the PICALM-T/C and TNK1-A/A genotype frequencies that decreased with increasing age. A resulting difference in the distribution of PICALM-C allele and TNK1-A allele was also observed. The TNK1-A allele was overrepresented in NoCI subjects than in AD patients in age groups 2 and 3. These results confirmed after adjustment for apolipoprotein E polymorphism, which suggested a different role of PICALM and TNK1 in healthy and impaired cognitive aging. More studies, however, are needed to confirm the observed associations.

Indexed as

Genetic Predisposition to DiseaseAgedAged, 80 and overAgingAllelesAlzheimer DiseaseClusterinCohort StudiesFemaleFetal ProteinsGene FrequencyHumansMaleMiddle AgedMonomeric Clathrin Assembly ProteinsPolymorphism, Single NucleotideCLU protein, humanClusterinFetal ProteinsMonomeric Clathrin Assembly ProteinsPICALM protein, humanProtein-Tyrosine KinasesTNK1 protein, humanAlzheimer’s diseaseBiogerontologyBrain agingCognitionDementiaGenetics

Identifiers

PMID28631188
OpenAlexW2645870360

What OpenQuestion holds

Textmetadata
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.