Evidence map›Paper›PMID 32961023›Full record

ArticleCNS neuroscience & therapeutics2021

Neuron-specific deletion of presenilin enhancer2 causes progressive astrogliosis and age-related neurodegeneration in the cortex independent of the Notch signaling.

Hui-Ru Bi, Cui-Hua Zhou, Yi-Zhi Zhang, Xu-Dong Cai, Mu-Huo Ji, Jian-Jun Yang, Gui-Quan Chen, Yi-Min Hu

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Pen-2 Negatively Regulates the Differentiation of Oligodendrocyte Precursor Cells into Astrocytes in the Central Nervous System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  8. 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

8 authors.

Hui-Ru BiModel Animal Research Center, MOE Key Laboratory of Model Animal for Disease Study, Medical School, Nanjing University, Nanjing, China.ORCID 0000-0003-2609-2364
Cui-Hua ZhouDepartment of Anesthesiology, The Second Affiliated Changzhou People's Hospital of Nanjing Medical University, Changzhou, China.
Yi-Zhi ZhangModel Animal Research Center, MOE Key Laboratory of Model Animal for Disease Study, Medical School, Nanjing University, Nanjing, China.
Xu-Dong CaiModel Animal Research Center, MOE Key Laboratory of Model Animal for Disease Study, Medical School, Nanjing University, Nanjing, China.
Mu-Huo JiDepartment of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jian-Jun YangDepartment of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Gui-Quan ChenModel Animal Research Center, MOE Key Laboratory of Model Animal for Disease Study, Medical School, Nanjing University, Nanjing, China.ORCID 0000-0002-4674-5548
Yi-Min HuDepartment of Anesthesiology, The Second Affiliated Changzhou People's Hospital of Nanjing Medical University, Changzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPresenilin enhancer2 (Pen-2) is an essential subunit of γ-secretase, which is a key protease responsible for the cleavage of amyloid precursor protein (APP) and Notch. Mutations on Pen-2 cause familial Alzheimer disease (AD). However, it remains unknown whether Pen-2 regulates neuronal survival and neuroinflammation in the adult brain.

methodsForebrain neuron-specific Pen-2 conditional knockout (Pen-2 cKO) mice were generated for this study. Pen-2 cKO mice expressing Notch1 intracellular domain (NICD) conditionally in cortical neurons were also generated.

resultsLoss of Pen-2 causes astrogliosis followed by age-dependent cortical atrophy and neuronal loss. Loss of Pen-2 results in microgliosis and enhanced inflammatory responses in the cortex. Expression of NICD in Pen-2 cKO cortices ameliorates neither neurodegeneration nor neuroinflammation.

conclusionsPen-2 is required for neuronal survival in the adult cerebral cortex. The Notch signaling may not be involved in neurodegeneration caused by loss of Pen-2.

Indexed as

AgingAmyloid Precursor Protein SecretasesAnimalsAtrophyCerebral CortexDisease ProgressionFemaleGene DeletionGliosisMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNeuronsReceptors, NotchAmyloid Precursor Protein Secretasespresenilin enhancer 2, mouseReceptors, NotchAlzheimer diseaseastrogliosismicrogliosisneurodegenerationpresenilin enhancer2

Identifiers

PMID32961023
PMCPMC7816208

What Socratic holds

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LicenceCC BY
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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 Socratic graph.