Evidence map›Paper›PMID 29926829›Full record

ArticleNeural regeneration research2018

Synaptic aging disrupts synaptic morphology and function in cerebellar Purkinje cells.

Wen-Juan Fan, Ming-Chao Yan, Lai Wang, Yi-Zheng Sun, Jin-Bo Deng, Jie-Xin Deng

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Aging, Neurodegenerative Disorders, and Cerebellum.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Early Adversity and Accelerated Brain Aging: A Mini-Review.Frontiers in molecular neuroscience · 2022
    Review
  12. 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

6 authors at 1 institution in 1 country.

Wen-Juan FanInstitute of Neurobiology, School of Life Science, Henan University, Kaifeng, Henan Province, China.
Ming-Chao YanInstitute of Neurobiology, School of Life Science, Henan University, Kaifeng, Henan Province, China.
Lai WangInstitute of Neurobiology, School of Life Science, Henan University, Kaifeng, Henan Province, China.
Yi-Zheng SunInstitute of Neurobiology, School of Life Science, Henan University, Kaifeng, Henan Province, China.
Jin-Bo DengInstitute of Neurobiology, School of Life Science, Henan University, Kaifeng, Henan Province, China.
Jie-Xin DengInstitute of Neurobiology, School of Life Science, Henan University, Kaifeng, Henan Province, China.
Henan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synapses are key structures in neural networks, and are involved in learning and memory in the central nervous system. Investigating synaptogenesis and synaptic aging is important in understanding neural development and neural degeneration in diseases such as Alzheimer disease and Parkinson's disease. Our previous study found that synaptogenesis and synaptic maturation were harmonized with brain development and maturation. However, synaptic damage and loss in the aging cerebellum are not well understood. This study was designed to investigate the occurrence of synaptic aging in the cerebellum by observing the ultrastructural changes of dendritic spines and synapses in cerebellar Purkinje cells of aging mice. Immunocytochemistry, DiI diolistic assays, and transmission electron microscopy were used to visualize the morphological characteristics of synaptic buttons, dendritic spines and synapses of Purkinje cells in mice at various ages. With synaptic aging in the cerebellum, dendritic spines and synaptic buttons were lost, and the synaptic ultrastructure was altered, including a reduction in the number of synaptic vesicles and mitochondria in presynaptic termini and smaller thin specialized zones in pre- and post-synaptic membranes. These findings confirm that synaptic morphology and function is disrupted in aging synapses, which may be an important pathological cause of neurodegenerative diseases.

Indexed as

agingcerebellumdegenerative diseasedendritic spinemicenerve regenerationneural regenerationneurodegenerative diseasesPurkinje cellssynapsesynaptic ultrastructuresynaptogenesis

Identifiers

PMID29926829
PMCPMC6022458
OpenAlexW2808902787

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.