Evidence map›Paper›PMID 25540218›Full record

ArticleJournal of neurophysiology2015

Impaired firing properties of dentate granule neurons in an Alzheimer's disease animal model are rescued by PPARγ agonism.

Miroslav N Nenov, Filippo Tempia, Larry Denner, Kelly T Dineley, Fernanda Laezza

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Miroslav N NenovDepartment of Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, Texas;
Filippo TempiaDepartment of Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, Texas;ORCID http://orcid.org/0000-0003-2778-0943
Larry DennerDepartment of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas; Center for Addiction Research, The University of Texas Medical Branch, Galveston, Texas; Mitchell Center for Neurodegenerative Diseases, The University of Texas Medical Branch, Galveston, Texas; and.
Kelly T DineleyDepartment of Neurology, The University of Texas Medical Branch, Galveston, Texas; Center for Addiction Research, The University of Texas Medical Branch, Galveston, Texas; Mitchell Center for Neurodegenerative Diseases, The University of Texas Medical Branch, Galveston, Texas; and.
Fernanda LaezzaDepartment of Pharmacology and Toxicology, The University of Texas Medical Branch, Galveston, Texas; Center for Addiction Research, The University of Texas Medical Branch, Galveston, Texas; Mitchell Center for Neurodegenerative Diseases, The University of Texas Medical Branch, Galveston, Texas; and Center for Biomedical Engineering, The University of Texas Medical Branch, Galveston, Texas felaezza@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

UTMB Clinical and Translational Science AwardUL1TR000071 · NCATS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI BRASIER, ALLAN R. · 2012 to 2014
$14.4M
Mechanisms of PPAR-gamma Enhancement of Cognitive Function in Alzheimer's DiseaseR01AG031859 · NIA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI DENNER, LARRY, DINELEY, KELLY T · 2009 to 2013
$1.6M
NCATS NIH HHS UL1TR000071NIA NIH HHS AG031859-01A1
6 · The paper itself

Abstract

Early cognitive impairment in Alzheimer's disease (AD) correlates with medial temporal lobe dysfunction, including two areas essential for memory formation: the entorhinal cortex and dentate gyrus (DG). In the Tg2576 animal model for AD amyloidosis, activation of the peroxisome proliferator-activated receptor-gamma (PPARγ) with rosiglitazone (RSG) ameliorates hippocampus-dependent cognitive impairment and restores aberrant synaptic activity at the entorhinal cortex to DG granule neuron inputs. It is unknown, however, whether intrinsic firing properties of DG granule neurons in these animals are affected by amyloid-β pathology and if they are sensitive to RSG treatment. Here, we report that granule neurons from 9-mo-old wild-type and Tg2576 animals can be segregated into two cell types with distinct firing properties and input resistance that correlate with less mature type I and more mature type II neurons. The DG type I cell population was greater than type II in wild-type littermates. In the Tg2576 animals, the type I and type II cell populations were nearly equal but could be restored to wild-type levels through cognitive enhancement with RSG. Furthermore, Tg2576 cell firing frequency and spike after depolarization were decreased in type I and increased in type II cells, both of which could also be restored to wild-type levels upon RSG treatment. That these parameters were restored by PPARγ activation emphasizes the therapeutic value of RSG against early AD cognitive impairment.

Indexed as

Action PotentialsAlzheimer DiseaseAnimalsCognitionEntorhinal CortexMaleMiceMice, Inbred C57BLNeuronsPPAR gammaRosiglitazoneThiazolidinedionesPPAR gammaRosiglitazoneThiazolidinedionesAlzheimer's diseasedentate gyrusexcitabilitypatch clampperoxisome proliferator-activated receptor-γ

Identifiers

PMID25540218
PMCPMC4359997
OpenAlexW2158164249

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.