Evidence map›Paper›PMID 33918046›Full record

ArticleInternational journal of molecular sciences2021

Ilaria Palmieri, Marialuisa Valente, Lisa Maria Farina, Simone Gana, Brigida Minafra, Roberta Zangaglia, Orietta Pansarasa, Daisy Sproviero, Alfredo Costa, Claudio Pacchetti and 3 more

Open access · goldAbstract readCase Reports
In one paragraph

Article in International journal of molecular sciences, 2021. 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
0.7field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. The curious case of a heterozygous loss-of-functionMolecular neurodegeneration advances · 2025
    Article
  2. Review
  3. Article
  4. Article
  5. Genetics, Functions, and Clinical Impact of Presenilin-1 (PSEN1) Gene.International journal of molecular sciences · 2022
    Review
  6. 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

13 authors at 4 institutions in 1 country.

Ilaria PalmieriGenomic and Post-Genomic Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.ORCID 0000-0002-0304-7299
Marialuisa ValenteLaboratory of Clinical Pathology Microbiology and Genetics, SS. Annunziata Hospital, 74100 Taranto, Italy.
Lisa Maria FarinaAdvanced Imaging and Radiomics Center, Neuroradiology Department, IRCCS Mondino Foundation, 27100 Pavia, Italy.
Simone GanaMedical Genetics Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.
Brigida MinafraParkinson and Movement Disorders Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.
Roberta ZangagliaParkinson and Movement Disorders Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.
Orietta PansarasaGenomic and Post-Genomic Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.ORCID 0000-0002-3041-0612
Daisy SprovieroGenomic and Post-Genomic Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.ORCID 0000-0001-5061-683X
Alfredo CostaUnit of Behavioral Neurology, IRCCS Mondino Foundation, 27100 Pavia, Italy.
Claudio PacchettiParkinson and Movement Disorders Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.
Anna PichiecchioAdvanced Imaging and Radiomics Center, Neuroradiology Department, IRCCS Mondino Foundation, 27100 Pavia, Italy.ORCID 0000-0002-5654-4088
Stella GagliardiGenomic and Post-Genomic Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.ORCID 0000-0002-6589-6907
Cristina CeredaGenomic and Post-Genomic Unit, IRCCS Mondino Foundation, 27100 Pavia, Italy.ORCID 0000-0001-9571-0862
Italian institute for Genomic Medicine · ITUniversity of Pavia · ITFondazione Istituto Neurologico Nazionale Casimiro Mondino · ITOspedale SS. Annunziata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder caused by the deposition of amyloid beta-peptide (Aβ) aggregates. Aβ aggregates lead to vessel rupture and intracerebral hemorrhages, detected by magnetic resonance imaging (MRI). Presenile CAA is usually genetically determined by mutations in the amyloid precursor protein (

Indexed as

MutationAllelesBrainCerebral Amyloid AngiopathyCognitive DysfunctionDNA Mutational AnalysisGenetic Association StudiesGenetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingHumansMagnetic Resonance ImagingMaleMiddle AgedModels, MolecularPhenotypePresenilin-1Presenilin-1PSEN1 protein, humanCAAcerebral amyloid angiopathycompound heterozygous mutationsnext-generation sequencingNGSPSEN1splice variantstop-gain variant

Identifiers

PMID33918046
PMCPMC8069161
OpenAlexW3140700451

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.