Evidence map›Paper›PMID 31442579›Full record

ReviewNeurobiology of learning and memory2019

Regulation of intrinsic excitability: Roles for learning and memory, aging and Alzheimer's disease, and genetic diversity.

Amy R Dunn, Catherine C Kaczorowski

Open access · greenAbstract readReview
In one paragraph

Review in Neurobiology of learning and memory, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. [Analysis of nerve excitability in the dentate gyrus of the hippocampus in cerebral ischaemia-reperfusion mice].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2024
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Intrinsic plasticity and birdsong learning.Neurobiology of learning and memory · 2021
    Review
  16. Review
  17. Cognitive aging is associated with redistribution of synaptic weights in the hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Review
  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

2 authors at 1 institution in 1 country.

Amy R DunnThe Jackson Laboratory, Bar Harbor, ME 04609, USA.
Catherine C KaczorowskiThe Jackson Laboratory, Bar Harbor, ME 04609, USA.
Jackson Laboratory · US

Funding

Systems Genetics Analysis of Resilience to Alzheimers diseaseR01AG057914 · NIA · JACKSON LABORATORY · PI KACZOROWSKI, CATHERINE COOK · 2017 to 2021
$7.0M
Systems Control of Normal Aging and Alzheimer's DiseaseR01AG054180 · NIA · JACKSON LABORATORY · PI KACZOROWSKI, CATHERINE COOK · 2017 to 2021
$4.4M
NIA NIH HHS R01 AG054180NIA NIH HHS R01 AG057914
6 · The paper itself

Abstract

Plasticity of intrinsic neuronal excitability facilitates learning and memory across multiple species, with aberrant modulation of this process being linked to the development of neurological symptoms in models of cognitive aging and Alzheimer's disease. Learning-related increases in intrinsic excitability of neurons occurs in a variety of brain regions, and is generally thought to promote information processing and storage through enhancement of synaptic throughput and induction of synaptic plasticity. Experience-dependent changes in intrinsic neuronal excitability rely on activity-dependent gene expression patterns, which can be influenced by genetic and environmental factors, aging, and disease. Reductions in baseline intrinsic excitability, as well as aberrant plasticity of intrinsic neuronal excitability and in some cases pathological hyperexcitability, have been associated with cognitive deficits in animal models of both normal cognitive aging and Alzheimer's disease. Genetic factors that modulate plasticity of intrinsic excitability likely underlie individual differences in cognitive function and susceptibility to cognitive decline. Thus, targeting molecular mediators that either control baseline intrinsic neuronal excitability, subserve learning-related intrinsic neuronal plasticity, and/or promote resilience may be a promising therapeutic strategy for maintaining cognitive function in aging and disease. In this review, we discuss the complementary relationship between intrinsic excitability and learning, with a particular focus on how this relationship varies as a function of age, disease state, and genetic make-up, and how targeting these factors may help to further elucidate our understanding of the role of intrinsic excitability in cognitive function and cognitive decline.

Indexed as

AgingAlzheimer DiseaseAnimalsBrainHumansLearningMemoryNeuronal PlasticityNeuronsAgingAlzheimer’s diseaseGenetic diversityHippocampusIntrinsic excitabilityLearning and memory

Identifiers

PMID31442579
PMCPMC6752224
OpenAlexW2969952587

What OpenQuestion holds

Textmetadata
LicenceTDM
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.