Evidence map›Paper›PMID 26778781›Full record

ArticleBehavioural brain research2016

GRK5 deficiency leads to susceptibility to intermittent hypoxia-induced cognitive impairment.

Prabhakar Singh, Wei Peng, Qiang Zhang, XueFeng Ding, William Z Suo

Open access · greenAbstract read
In one paragraph

Article in Behavioural brain research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Targeting GRK5 for Treating Chronic Degenerative Diseases.International journal of molecular sciences · 2021
    Review
  3. Review
  4. Review
  5. Article
  6. 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

5 authors at 3 institutions in 2 countries.

Prabhakar SinghLaboratory for Alzheimer's Disease and Aging Research, Kansas City Veterans Affairs Medical Center, Kansas City, MO 64128, USA.
Wei PengLaboratory for Alzheimer's Disease and Aging Research, Kansas City Veterans Affairs Medical Center, Kansas City, MO 64128, USA.
Qiang ZhangLaboratory for Alzheimer's Disease and Aging Research, Kansas City Veterans Affairs Medical Center, Kansas City, MO 64128, USA.
XueFeng DingLaboratory for Alzheimer's Disease and Aging Research, Kansas City Veterans Affairs Medical Center, Kansas City, MO 64128, USA; Department of Cognitive Sciences, Beijing Institute of Basic Medical Sciences, Beijing 100850, PR China.
William Z SuoLaboratory for Alzheimer's Disease and Aging Research, Kansas City Veterans Affairs Medical Center, Kansas City, MO 64128, USA; Departments of Neurology, University of Kansas Medical College, Kansas City, KS 66170, USA; Departments of Physiology, University of Kansas Medical College, Kansas City, KS 66170, USA; The University of Kansas Alzheimer's Disease Center, Kansas City, KS 66160, USA. Electronic address: William.Suo@va.gov.
Veterans Health Administration · USBeijing Institute of Education · CNUniversity of Kansas · US

Funding

University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
New Strategy to Fight Selective Cholinergic Neuronal Loss in Alzheimer DiseaseI01BX001067 · VA · KANSAS CITY VA MEDICAL CENTER · PI SUO, WILLIAM Z. · 2012 to 2015
–
BLRD VA I01 BX001067NIA NIH HHS P30 AG035982
6 · The paper itself

Abstract

Obstructive sleep apnea (OSA) leads to cognitive impairment in about 25% patients, though it remains elusive what makes one more susceptible than the other to be cognitively impaired. G protein-coupled receptor kinase-5 (GRK5) deficiency is recently found to render subjects more susceptible to cognitive impairment triggered by over-expression of Swedish mutant ß-amyloid precursor protein. This study is to determine whether GRK5 deficiency also renders subjects more susceptible to the OSA-triggered cognitive impairment. Both wild type (WT) and GRK5 knockout (KO) mice were placed in conditions absence and presence of intermittent hypoxia (IH) with 8%/21% O2 90-s cycle for 8h a day for a month, and then followed by behavioral assessments with battery of tasks. We found that the selected IH condition only induced marginally abnormal behavior (slightly elevated anxiety with most others unchanged) in the WT mice but it caused significantly more behavioral deficits in the KO mice, ranging from elevated anxiety, impaired balancing coordination, and impaired short-term spatial memory. These results suggest that GRK5 deficiency indeed makes the mice more susceptible to wide range of behavioral impairments, including cognitive impairments.

Indexed as

AnimalsCholine O-AcetyltransferaseCognition DisordersDisease Models, AnimalDisease SusceptibilityExploratory BehaviorFemaleG-Protein-Coupled Receptor Kinase 5Green Fluorescent ProteinsGroomingHypoxiaMaleMaze LearningMiceMice, Inbred C57BLMice, TransgenicCholine O-Acetyltransferaseenhanced green fluorescent proteinG-Protein-Coupled Receptor Kinase 5Green Fluorescent ProteinsGrk5 protein, mouseCognitive impairmentGRK5 deficiencyIntermittent hypoxiaMemorySleep apneaSusceptibility

Identifiers

PMID26778781
PMCPMC5068244
OpenAlexW2232689128

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.