Evidence map›Paper›PMID 25948650›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2016

From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.

Chris G Dulla, Douglas A Coulter, Jokubas Ziburkus

Open access · greenAbstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  7. Flexibility ofFrontiers in cellular neuroscience · 2022
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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

3 authors at 3 institutions in 1 country.

Chris G DullaDepartment of Neuroscience, Tufts University School of Medicine, Boston, MA, USA chris.dulla@tufts.edu.
Douglas A CoulterDepartment of Pediatrics and Neuroscience, University of Pennsylvania Perleman School of Medicine, Philadelphia, PA, USA Division of Neurology and the Research Institute of Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Jokubas ZiburkusDepartment of Biology and Biochemistry, University of Houston, Houston, TX, USA.
Tufts University · USUniversity of Houston · USUniversity of Pennsylvania · US

Funding

Neuronal Circuit Mechanisms of EpileptogenesisR01NS038572 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI COULTER, DOUGLAS A · 1999 to 2022
$8.0M
Normal and Pathological Function of the Dentate GyrusR01NS082046 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI Hajime Takano · 2012 to 2026
$6.1M
Impact of Astrocytic Glutamate Transport on Epilepsy Associated with DevelopmentaR01NS076885 · NINDS · TUFTS UNIVERSITY BOSTON · PI DULLA, CHRIS G · 2012 to 2016
$1.8M
The Role of Glutamate Signaling in Developmental Cortical MalformationsR56NS076885 · NINDS · TUFTS UNIVERSITY BOSTON · PI DULLA, CHRIS G · 2017 to 2017
$491k
NINDS NIH HHS R01 NS038572NINDS NIH HHS R01 NS076885NINDS NIH HHS R01 NS082046NINDS NIH HHS R56 NS076885
6 · The paper itself

Abstract

Complex circuitry with feed-forward and feed-back systems regulate neuronal activity throughout the brain. Cell biological, electrical, and neurotransmitter systems enable neural networks to process and drive the entire spectrum of cognitive, behavioral, and motor functions. Simultaneous orchestration of distinct cells and interconnected neural circuits relies on hundreds, if not thousands, of unique molecular interactions. Even single molecule dysfunctions can be disrupting to neural circuit activity, leading to neurological pathology. Here, we sample our current understanding of how molecular aberrations lead to disruptions in networks using three neurological pathologies as exemplars: epilepsy, traumatic brain injury (TBI), and Alzheimer's disease (AD). Epilepsy provides a window into how total destabilization of network balance can occur. TBI is an abrupt physical disruption that manifests in both acute and chronic neurological deficits. Last, in AD progressive cell loss leads to devastating cognitive consequences. Interestingly, all three of these neurological diseases are interrelated. The goal of this review, therefore, is to identify molecular changes that may lead to network dysfunction, elaborate on how altered network activity and circuit structure can contribute to neurological disease, and suggest common threads that may lie at the heart of molecular circuit dysfunction.

Indexed as

Alzheimer DiseaseAnimalsBrainBrain Injuries, TraumaticCerebral CortexEpilepsygamma-Aminobutyric AcidGlutamic AcidHippocampusHumansIon ChannelsNeural PathwaysNeuronstau ProteinsThalamusTOR Serine-Threonine Kinasesgamma-Aminobutyric AcidGlutamic AcidIon Channelstau ProteinsTOR Serine-Threonine KinasesAlzheimer’s diseasecircuitsepilepsymolecular dysfunctiontraumatic brain injury

Identifiers

PMID25948650
PMCPMC4641826
OpenAlexW2282875368

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.