Evidence map›Paper›PMID 31671574›Full record

SynthesisInternational journal of molecular sciences2019

Meta-Analysis of Gene Expression Changes in the Blood of Patients with Mild Cognitive Impairment and Alzheimer's Disease Dementia.

Virginie Bottero, Judith A Potashkin

Abstract readMeta-Analysis
In one paragraph

Synthesis in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Meta-Analysis of Transcriptomic Studies of Blood and Six Brain Regions Identifies a Consensus of 15 Cross-Tissue Mechanisms in Alzheimer's Disease and Suggests an Origin of Cross-Study Heterogeneity.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2025
    Pooled it
  2. Pooled it
  3. Review
  4. Resistance of E2F4DN to p38Scientific reports · 2026
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  10. Cytosolic calcium: Judge, jury and executioner of neurodegeneration in Alzheimer's disease and beyond.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    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

2 authors.

Virginie BotteroCenter for Neurodegenerative Disease and Therapeutics, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA. virginie.bottero@rosalindfranklin.edu.
Judith A PotashkinCenter for Neurodegenerative Disease and Therapeutics, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA. judy.potashkin@rosalindfranklin.edu.

Funding

Network analysis for identifying disease mechanisms and therapeutic targets for dementiaR01AG062176 · NIA · ROSALIND FRANKLIN UNIV OF MEDICINE & SCI · PI POTASHKIN, JUDITH ANN · 2018 to 2019
$624k
NIA NIH HHS R01 AG062176NIA NIH HHS R01AG062176
6 · The paper itself

Abstract

backgroundDementia is a major public health concern affecting approximately 47 million people worldwide. Mild cognitive impairment (MCI) is one form of dementia that affects an individual's memory with or without affecting their daily life. Alzheimer's disease dementia (ADD) is a more severe form of dementia that usually affects elderly individuals. It remains unclear whether MCI is a distinct disorder from or an early stage of ADD.

methodsGene expression data from blood were analyzed to identify potential biomarkers that may be useful for distinguishing between these two forms of dementia.

resultsA meta-analysis revealed 91 genes dysregulated in individuals with MCI and 387 genes dysregulated in ADD. Pathway analysis identified seven pathways shared between MCI and ADD and nine ADD-specific pathways. Fifteen transcription factors were associated with MCI and ADD, whereas seven transcription factors were specific for ADD. Mir-335-5p was specific for ADD, suggesting that it may be useful as a biomarker. Diseases that are associated with MCI and ADD included developmental delays, cognition impairment, and movement disorders.

conclusionThese results provide a better molecular understanding of peripheral changes that occur in MCI and ADD patients and may be useful in the identification of diagnostic and prognostic biomarkers.

Indexed as

Alzheimer DiseaseBiomarkersCognitive DysfunctionFemaleGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHumansMaleMicroRNAsBiomarkersMicroRNAsMIRN335 microRNA, humanAlzheimer’s diseasedementiagene expressionmild cognitive impairmentnetwork analysis

Identifiers

PMID31671574
PMCPMC6862214

What Socratic 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 Socratic graph.