Evidence map›Paper›PMID 29906573›Full record

ArticleNeurobiology of learning and memory2018

Store depletion-induced h-channel plasticity rescues a channelopathy linked to Alzheimer's disease.

Timothy F Musial, Elizabeth Molina-Campos, Linda A Bean, Natividad Ybarra, Ronen Borenstein, Matthew L Russo, Eric W Buss, Daniel Justus, Krystina M Neuman, Gelique D Ayala and 23 more

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of learning and memory, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  7. Article
  8. Article
  9. 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
  10. Review
  11. Review
  12. Cardiac and neuronal HCN channelopathies.Pflugers Archiv : European journal of physiology · 2020
    Review
  13. Review
  14. Review
  15. Review
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

33 authors at 3 institutions in 2 countries.

Timothy F MusialDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Elizabeth Molina-CamposDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Linda A BeanDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Natividad YbarraDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Ronen BorensteinDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Matthew L RussoDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Eric W BussDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Daniel JustusNeuronal Networks Group, Deutsches Zenstrum für Neurodegenerative Erkrankungen, Ludwig-Erhard-Allee 2, 53175 Bonn, Germany.
Krystina M NeumanDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Gelique D AyalaDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Sheila A MullenDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Yuliya VoskobiynykDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Christopher T TulisiakDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Jasmine A FelsDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Nicola J CorbettDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Gabriel CarballoDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Colette D KennedyDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Jelena PopovicDepartment of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Josefina Ramos-FrancoDepartment of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, IL 60612, USA.
Michael FillDepartment of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, IL 60612, USA.
Melissa R PergandeDepartment of Pathology, Rush University Medical Center, Chicago, IL 60612, USA.
Jeffrey A BorgiaDepartment of Pathology, Rush University Medical Center, Chicago, IL 60612, USA; Department of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
Grant T CorbettDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Kalipada PahanDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA.
Ye HanDavee Department of Neurology and Clinical Neurosciences, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Dane M ChetkovichDavee Department of Neurology and Clinical Neurosciences, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Robert J VassarDepartment of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Richard W ByrneDepartment of Neurosurgery, Rush University Medical Center, Chicago, IL 60612, USA.
M Matthew OhDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Travis R StoubDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA; Department of Neurosurgery, Rush University Medical Center, Chicago, IL 60612, USA.
Stefan RemyNeuronal Networks Group, Deutsches Zenstrum für Neurodegenerative Erkrankungen, Ludwig-Erhard-Allee 2, 53175 Bonn, Germany; Department of Epileptology, University of Bonn Medical Center, Sigmund-Freud-Straβe 25, 53125 Bonn, Germany.
John F DisterhoftDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: jdisterhoft@northwestern.edu.
Daniel A NicholsonDepartment of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA. Electronic address: dan_nicholson@rush.edu.
Rush University Medical Center · USGerman Center for Neurodegenerative Diseases · DENorthwestern University · US

Funding

SYNAPTIC SUBSTRATES OF AGE-DEPENDENT MEMORY DEFICITSR01AG017139 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DISTERHOFT, JOHN F · 1999 to 2013
$4.6M
Synaptic substrates of age-dependent memory deficitsRF1AG017139 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DISTERHOFT, JOHN F, NICHOLSON, DANIEL A · 2016 to 2016
$2.9M
Proteomic reconstructive microscopy of healthy and diseased dendritesR01AG047073 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI NICHOLSON, DANIEL A · 2013 to 2016
$1.3M
Synaptic dysregulation in a mouse model of Alzheimer's diseaseR00AG031574 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI NICHOLSON, DANIEL A · 2009 to 2011
$671k
Computational neurobiology of hippocampal dendritesK02AG050767 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI NICHOLSON, DANIEL A · 2015 to 2019
$603k
Synaptic Substrates of Age-Dependent Memory DeficitsR56AG017139 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GEINISMAN, YURI · 2008 to 2008
$500k
Synaptic dysregulation in a mouse model of Alzheimer's diseaseK99AG031574 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI NICHOLSON, DANIEL A · 2008 to 2009
$180k
NIA NIH HHS K02 AG050767NIA NIH HHS K99 AG031574NIA NIH HHS R00 AG031574NIA NIH HHS R01 AG017139NIA NIH HHS R01 AG047073NIA NIH HHS R56 AG017139NIA NIH HHS RF1 AG017139
6 · The paper itself

Abstract

Voltage-gated ion channels are critical for neuronal integration. Some of these channels, however, are misregulated in several neurological disorders, causing both gain- and loss-of-function channelopathies in neurons. Using several transgenic mouse models of Alzheimer's disease (AD), we find that sub-threshold voltage signals strongly influenced by hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels progressively deteriorate over chronological aging in hippocampal CA1 pyramidal neurons. The degraded signaling via HCN channels in the transgenic mice is accompanied by an age-related global loss of their non-uniform dendritic expression. Both the aberrant signaling via HCN channels and their mislocalization could be restored using a variety of pharmacological agents that target the endoplasmic reticulum (ER). Our rescue of the HCN channelopathy helps provide molecular details into the favorable outcomes of ER-targeting drugs on the pathogenesis and synaptic/cognitive deficits in AD mouse models, and implies that they might have beneficial effects on neurological disorders linked to HCN channelopathies.

Indexed as

Neuronal PlasticityAction PotentialsAgingAlzheimer DiseaseAnimalsCA1 Region, HippocampalChannelopathiesDisease Models, AnimalEndoplasmic ReticulumFemaleHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMaleMice, TransgenicPyramidal CellsHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsArray tomographyCarvedilolElectron microscopyEndoplasmic reticulumHCN channelPatch-clampTRIP8b

Identifiers

PMID29906573
PMCPMC6434702
OpenAlexW2808224242

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.