Evidence map›Paper›PMID 34679362›Full record

ReviewBrain sciences2021

Glial PAMPering and DAMPening of Adult Hippocampal Neurogenesis.

Luke Parkitny, Mirjana Maletic-Savatic

Open access · goldAbstract readReview
In one paragraph

Review in Brain sciences, 2021. 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
0.5field-weighted citation impact, top 37% 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, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. E2F2 inhibits hippocampal neurogenesis in poststroke depression rats via the miR-1290/CBR1 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
  4. Review
  5. Article
  6. Review
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

2 authors at 1 institution in 1 country.

Luke ParkitnyBaylor College of Medicine and Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX 77030, USA.ORCID 0000-0002-4473-0211
Mirjana Maletic-SavaticBaylor College of Medicine and Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, TX 77030, USA.ORCID 0000-0002-6548-4662
Baylor College of Medicine · US

Funding

Imaging Mass Spectrometry for metabolome mappingR01GM120033 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI LIU, ZHANDONG, MALETIC-SAVATIC, MIRJANA · 2017 to 2021
$2.5M
Cynthia and Anthony Petrello Endowment n/aMark A. Wallace Endowment n/aNational Institute of General Medical Sciences 5R01GM120033
6 · The paper itself

Abstract

Adult neurogenesis represents a mature brain's capacity to integrate newly generated neurons into functional circuits. Impairment of neurogenesis contributes to the pathophysiology of various mood and cognitive disorders such as depression and Alzheimer's Disease. The hippocampal neurogenic niche hosts neural progenitors, glia, and vasculature, which all respond to intrinsic and environmental cues, helping determine their current state and ultimate fate. In this article we focus on the major immune communication pathways and mechanisms through which glial cells sense, interact with, and modulate the neurogenic niche. We pay particular attention to those related to the sensing of and response to innate immune danger signals. Receptors for danger signals were first discovered as a critical component of the innate immune system response to pathogens but are now also recognized to play a crucial role in modulating non-pathogenic sterile inflammation. In the neurogenic niche, viable, stressed, apoptotic, and dying cells can activate danger responses in neuroimmune cells, resulting in neuroprotection or neurotoxicity. Through these mechanisms glial cells can influence hippocampal stem cell fate, survival, neuronal maturation, and integration. Depending on the context, such responses may be appropriate and on-target, as in the case of learning-associated synaptic pruning, or excessive and off-target, as in neurodegenerative disorders.

Indexed as

gliamicroglianeural stem cellsneurogenesisneuroinflammation

Identifiers

PMID34679362
PMCPMC8533961
OpenAlexW3202378626

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.