Evidence map›Paper›PMID 35250545›Full record

ArticleFrontiers in aging neuroscience2022

Identification of Genetic Networks Reveals Complex Associations and Risk Trajectory Linking Mild Cognitive Impairment to Alzheimer's Disease.

Claudia Strafella, Valerio Caputo, Andrea Termine, Carlo Fabrizio, Giulia Calvino, Domenica Megalizzi, Paola Ruffo, Elisa Toppi, Nerisa Banaj, Andrea Bassi and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

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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

15 authors at 2 institutions in 2 countries.

Claudia StrafellaGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Valerio CaputoGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Andrea TermineGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Carlo FabrizioGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Giulia CalvinoGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Domenica MegalizziGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Paola RuffoGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Elisa ToppiLaboratory of Experimental Neuropsychobiology, Department of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy.
Nerisa BanajLaboratory of Neuropsychiatry, Department of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy.
Andrea BassiLaboratory of Neuropsychiatry, Department of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy.
Paola BossùLaboratory of Experimental Neuropsychobiology, Department of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy.
Carlo CaltagironeDepartment of Clinical and Behavioral Neurology, IRCCS Fondazione Santa Lucia, Rome, Italy.
Gianfranco SpallettaLaboratory of Neuropsychiatry, Department of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy.
Emiliano GiardinaGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Raffaella CascellaGenomic Medicine Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy.
Fondazione Santa Lucia · ITUniversity of Rome Tor Vergata · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amnestic mild cognitive impairment (aMCI) and sporadic Alzheimer's disease (AD) are multifactorial conditions resulting from a complex crosstalk among multiple molecular and biological processes. The present study investigates the association of variants localized in genes and miRNAs with aMCI and AD, which may represent susceptibility, prognostic biomarkers or multi-target treatment options for such conditions. We included 371 patients (217 aMCI and 154 AD) and 503 healthy controls, which were genotyped for a panel of 120 single nucleotide polymorphisms (SNPs) and, subsequently, analyzed by statistical, bioinformatics and machine-learning approaches. As a result, 21 SNPs were associated with aMCI and 13 SNPs with sporadic AD. Interestingly, a set of variants shared between aMCI and AD displayed slightly higher Odd Ratios in AD with respect to aMCI, highlighting a specific risk trajectory linking aMCI to AD. Some of the associated genes and miRNAs were shown to interact within the signaling pathways of APP (Amyloid Precursor Protein), ACE2 (Angiotensin Converting Enzyme 2), miR-155 and PPARG (Peroxisome Proliferator Activated Receptor Gamma), which are known to contribute to neuroinflammation and neurodegeneration. Overall, results of this study increase insights concerning the genetic factors contributing to the neuroinflammatory and neurodegenerative mechanisms underlying aMCI and sporadic AD. They have to be exploited to develop personalized approaches based on the individual genetic make-up and multi-target treatments.

Indexed as

Alzheimer’s diseasebiomarkersgenetic risk variantsmild cognitive impairmenttherapeutic target

Identifiers

PMID35250545
PMCPMC8892382
OpenAlexW4213283682

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.