Evidence map›Paper›PMID 31161490›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2019

Molecular Signatures of the Aging Brain: Finding the Links Between Genes and Phenotypes.

Giuseppe Lupo, Silvana Gaetani, Emanuele Cacci, Stefano Biagioni, Rodolfo Negri

Abstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–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

28 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Effects ofFrontiers in pharmacology · 2025
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Role of Senescent Astrocytes in Health and Disease.International journal of molecular sciences · 2023
    Review
  18. Article
  19. Article
  20. 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

5 authors.

Giuseppe LupoDepartment of Chemistry, Sapienza University of Rome, Piazzale A. Moro, 00185, Rome, Italy. giuseppe.lupo@uniroma1.it.ORCID 0000-0001-7218-4003
Silvana GaetaniDepartment of Physiology and Farmacology "V. Erspamer", Sapienza University of Rome, Piazzale A. Moro, 00185, Rome, Italy.
Emanuele CacciDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Piazzale A. Moro, 00185, Rome, Italy.
Stefano BiagioniDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Piazzale A. Moro, 00185, Rome, Italy.
Rodolfo NegriDepartment of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, Piazzale A. Moro, 00185, Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is associated with cognitive decline and increased vulnerability to neurodegenerative diseases. The progressive extension of the average human lifespan is bound to lead to a corresponding increase in the fraction of cognitively impaired elderly individuals among the human population, with an enormous societal and economic burden. At the cellular and tissue levels, cognitive decline is linked to a reduction in specific neuronal subpopulations, a widespread decrease in synaptic plasticity and an increase in neuroinflammation due to an enhanced activation of astrocytes and microglia, but the molecular mechanisms underlying these functional changes during normal aging and in neuropathological conditions remain poorly understood. In this review, we summarize very recent and outstanding progress in elucidating the molecular changes associated with cognitive decline through the genome-wide profiling of aging brain cells at different molecular levels (genomic, epigenomic, transcriptomic, proteomic). We discuss how the correlation of different molecular and phenotypic traits driven by mathematical and computational analyses of large datasets has led to the prediction of key molecular nodes of neurodegenerative pathways, and provide a few examples of candidate regulators of cognitive decline identified with these approaches. Furthermore, we highlight the dysregulation of the synaptic transcriptome in neuronal cells and of the inflammatory transcriptome in glial cells as some of the key events during normal and neuropathological human brain aging.

Indexed as

Genetic Association StudiesAgingAnimalsBrainCognitive AgingEpigenomicsGene Expression ProfilingHumansNeurodegenerative DiseasesAgingBrainCognitive declineDNA methylationGene expressionHistone acetylation

Identifiers

PMID31161490
PMCPMC6694319

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.