Evidence map›Paper›PMID 27318137›Full record

ArticleNeurobiology of aging2016

Corticothalamic network dysfunction and behavioral deficits in a mouse model of Alzheimer's disease.

Anupam Hazra, Brian F Corbett, Jason C You, Suzan Aschmies, Lijuan Zhao, Ke Li, Angelo C Lepore, Eric D Marsh, Jeannie Chin

Abstract read
In one paragraph

Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Implication of the thalamus in sleep alterations observed in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  2. Kv4.2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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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

9 authors at 2 institutions in 1 country.

Anupam Hazra *Department of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Brian F Corbett *Department of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Jason C YouDepartment of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Suzan AschmiesDepartment of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Lijuan ZhaoDepartment of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Ke LiDepartment of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Angelo C LeporeDepartment of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Eric D MarshDepartments of Pediatrics and Neurology, Children's Hospital of Philadelphia and the Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104.
Jeannie ChinDepartment of Neuroscience, Thomas Jefferson University, Philadelphia, PA 19107.
Thomas Jefferson University · USUniversity of Pennsylvania · US

Funding

Training Program in Neurodevelopmental DisabilitiesT32NS007413 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI AMELIA J EISCH, ERIC D MARSH · 1998 to 2026
$8.9M
The Intellectual and Developmental Disabilities Research Center at CHOP/PennU54HD086984 · NICHD · CHILDREN'S HOSP OF PHILADELPHIA · PI PUTT, MARY E. · 2016 to 2020
$6.3M
Seizure generation and network excitability in Arx related Infantile SpasmsR01NS082761 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI MARSH, ERIC D · 2013 to 2017
$1.8M
NICHD NIH HHS U54 HD086984NINDS NIH HHS R01 NS082761NINDS NIH HHS T32 NS007413
6 · The paper itself

Abstract

Alzheimer's disease is associated with cognitive decline and seizures. Growing evidence indicates that seizures contribute to cognitive deficits early in disease, but how they develop and impact cognition are unclear. To investigate potential mechanisms, we studied a mouse model that overexpresses mutant human amyloid precursor protein with high levels of amyloid beta (Aβ). These mice develop generalized epileptiform activity, including nonconvulsive seizures, consistent with alterations in corticothalamic network activity. Amyloid precursor protein mice exhibited reduced activity marker expression in the reticular thalamic nucleus, a key inhibitory regulatory nucleus, and increased activity marker expression in downstream thalamic relay targets that project to cortex and limbic structures. Slice recordings revealed impaired cortical inputs to the reticular thalamic nucleus that may contribute to corticothalamic dysfunction. These results are consistent with our findings of impaired sleep maintenance in amyloid precursor protein mice. Finally, the severity of sleep impairments predicted the severity of deficits in Morris water maze, suggesting corticothalamic dysfunction may relate to hippocampal dysfunction, and may be a pathophysiological mechanism underlying multiple behavioral and cognitive alterations in Alzheimer's disease.

Indexed as

BehaviorAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBehavior, AnimalCerebral CortexCognitionDisease Models, AnimalFemaleHippocampusMaleMice, TransgenicNerve NetSleep DeprivationThalamic NucleiAmyloid beta-PeptidesAlzheimer's diseaseAmyloid precursor proteinCorticothalamicEpilepsyReticular thalamic nucleus (nRT)SeizureSleep fragmentation

Identifiers

PMID27318137
PMCPMC4943218
OpenAlexW2344567909

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.