Evidence map›Paper›PMID 26473169›Full record

ArticleeNeuro2015

Cognitive Deficits, Changes in Synaptic Function, and Brain Pathology in a Mouse Model of Normal Aging(1,2,3).

Martin Weber, Tiffany Wu, Jesse E Hanson, Nazia M Alam, Hilda Solanoy, Hai Ngu, Benjamin E Lauffer, Han H Lin, Sara L Dominguez, Jens Reeder and 5 more

Open access · goldAbstract read
In one paragraph

Article in eNeuro, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 73 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

15 authors at 6 institutions in 3 countries.

Martin WeberDepartment of Neuroscience, Genentech , South San Francisco, California 94080 ; Department of Psychiatry, University of California, San Diego , La Jolla, California 92093.
Tiffany WuDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Jesse E HansonDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Nazia M AlamBurke Medical Research Institute , White Plains, New York, 10605.
Hilda SolanoyDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Hai NguDepartment of Pathology, Genentech , South San Francisco, California 94080.
Benjamin E LaufferDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Han H LinDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Sara L DominguezDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Jens ReederDepartment of Bioinformatics, Genentech , South San Francisco, California 94080.
Jennifer TomDepartment of Bioinformatics, Genentech , South San Francisco, California 94080.
Pascal SteinerDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Oded ForemanDepartment of Pathology, Genentech , South San Francisco, California 94080.
Glen T PruskyDepartment of Physiology and Biophysics, Weill Cornell Medical College, Burke Medical Research Institute , White Plains, New York 10605.
Kimberly Scearce-LevieDepartment of Neuroscience, Genentech , South San Francisco, California 94080.
Neuroscience Institute · ITBioinformatics Institute · SGKaiser Permanente South San Francisco Medical Center · USBurke Medical Research Institute · USCornell University · USUniversity of California San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age is the main risk factor for sporadic Alzheimer's disease. Yet, cognitive decline in aged rodents has been less well studied, possibly due to concomitant changes in sensory or locomotor function that can complicate cognitive tests. We tested mice that were 3, 11, and 23 months old in cognitive, sensory, and motor measures, and postmortem measures of gliosis and neural activity (c-Fos). Hippocampal synaptic function was also examined. While age-related impairments were detectable in tests of spatial memory, greater age-dependent effects were observed in tests of associative learning [active avoidance (AA)]. Gross visual function was largely normal, but startle responses to acoustic stimuli decreased with increased age, possibly due to hearing impairments. Therefore, a novel AA variant in which light alone served as the conditioning stimuli was used. Age-related deficits were again observed. Mild changes in vision, as measured by optokinetic responses, were detected in 19- versus 4-month-old mice, but these were not correlated to AA performance. Thus, deficits in hearing or vision are unlikely to account for the observed deficits in cognitive measures. Increased gliosis was observed in the hippocampal formation at older ages. Age-related changes in neural function and plasticity were observed with decreased c-Fos in the dentate gyrus, and decreased synaptic strength and paired-pulse facilitation in CA1 slices. This work, which carefully outlines age-dependent impairments in cognitive and synaptic function, c-Fos activity, and gliosis during normal aging in the mouse, suggests robust translational measures that will facilitate further study of the biology of aging.

Indexed as

agec-Foscognitiongliosismicesynaptic function

Identifiers

PMID26473169
PMCPMC4606159
OpenAlexW2276374746

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.