Evidence map›Paper›PMID 25972808›Full record

ReviewFrontiers in aging neuroscience2015

Impact of age-related neuroglial cell responses on hippocampal deterioration.

Joseph O Ojo, Payam Rezaie, Paul L Gabbott, Michael G Stewart

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 82 citations in OpenAlex.

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  16. Cellular Senescence in Brain Aging.Frontiers in aging neuroscience · 2021
    Review
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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

4 authors at 2 institutions in 2 countries.

Joseph O OjoDepartment of Life Sciences, The Open University Walton Hall, UK ; Department of Neuropathology, Roskamp Institute Sarasota, FL, USA.
Payam RezaieDepartment of Life Sciences, The Open University Walton Hall, UK.
Paul L GabbottDepartment of Life Sciences, The Open University Walton Hall, UK.
Michael G StewartDepartment of Life Sciences, The Open University Walton Hall, UK.
The Open University · GBRoskamp Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is one of the greatest risk factors for the development of sporadic age-related neurodegenerative diseases and neuroinflammation is a common feature of this disease phenotype. In the immunoprivileged brain, neuroglial cells, which mediate neuroinflammatory responses, are influenced by the physiological factors in the microenvironment of the central nervous system (CNS). These physiological factors include but are not limited to cell-to-cell communication involving cell adhesion molecules, neuronal electrical activity and neurotransmitter and neuromodulator action. However, despite this dynamic control of neuroglial activity, in the healthy aged brain there is an alteration in the underlying neuroinflammatory response notably seen in the hippocampus, typified by astrocyte/microglia activation and increased pro-inflammatory cytokine production and signaling. These changes may occur without any overt concurrent pathology, however, they typically correlate with deteriorations in hippocamapal or cognitive function. In this review we examine two important phenomenons, firstly the relationship between age-related brain deterioration (focusing on hippocampal function) and underlying neuroglial response(s), and secondly how the latter affects molecular and cellular processes within the hippocampus that makes it vulnerable to age-related cognitive decline.

Indexed as

agingastrocytescognitionhippocampusmicroglianeuroinflammation

Identifiers

PMID25972808
PMCPMC4413780
OpenAlexW2049083004

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.