Evidence map›Paper›PMID 27245308›Full record

ReviewGenomics, proteomics & bioinformatics2016

Connecting Malfunctioning Glial Cells and Brain Degenerative Disorders.

Natalie Kaminsky, Ofer Bihari, Sivan Kanner, Ari Barzilai

Open access · goldAbstract readReview
In one paragraph

Review in Genomics, proteomics & bioinformatics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Emerging Role of Neuron-Glia in Neurological Disorders: At a Glance.Oxidative medicine and cellular longevity · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. International journal of molecular sciences · 2020
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Natalie KaminskyDepartment of Neurobiology, George S. Wise, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 6997801, Israel.
Ofer BihariDepartment of Neurobiology, George S. Wise, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 6997801, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 6997801, Israel.
Sivan KannerDepartment of Neurobiology, George S. Wise, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 6997801, Israel. Electronic address: sivankan@gmail.com.
Ari BarzilaiDepartment of Neurobiology, George S. Wise, Faculty of Life Sciences, Tel Aviv University, Tel Aviv 6997801, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv 6997801, Israel. Electronic address: arib@tauex.tau.ac.il.
Tel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DNA damage response (DDR) is a complex biological system activated by different types of DNA damage. Mutations in certain components of the DDR machinery can lead to genomic instability disorders that culminate in tissue degeneration, premature aging, and various types of cancers. Intriguingly, malfunctioning DDR plays a role in the etiology of late onset brain degenerative disorders such as Parkinson's, Alzheimer's, and Huntington's diseases. For many years, brain degenerative disorders were thought to result from aberrant neural death. Here we discuss the evidence that supports our novel hypothesis that brain degenerative diseases involve dysfunction of glial cells (astrocytes, microglia, and oligodendrocytes). Impairment in the functionality of glial cells results in pathological neuro-glial interactions that, in turn, generate a "hostile" environment that impairs the functionality of neuronal cells. These events can lead to systematic neural demise on a scale that appears to be proportional to the severity of the neurological deficit.

Indexed as

DNA RepairAnimalsAstrocytesAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsGenomic InstabilityHumansNeurodegenerative DiseasesNeurogliaAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsAstrocytesBrain degenerative diseasesDNA damage responseGenomic instabilityGlial cellsMicroglia

Identifiers

PMID27245308
PMCPMC4936608
OpenAlexW2412822495

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.