Evidence map›Paper›PMID 27242425›Full record

ReviewFrontiers in molecular neuroscience2016

Activin Signaling in the Pathogenesis and Therapy of Neuropsychiatric Diseases.

Andrea S Link, Fang Zheng, Christian Alzheimer

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Gendering the Menstrual Cycle in Behavioral Neuroendocrinology.American journal of human biology : the official journal of the Human Biology Council · 2026
    Review
  3. Article
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  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer's Disease?International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Seasonal changes in NRF2 antioxidant pathway regulates winter depression-like behavior.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Post-injury Nose-to-Brain Delivery of Activin A and SerpinB2 Reduces Brain Damage in a Mouse Stroke Model.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  19. Nasal Spray to the Rescue of Neurons in Stroke.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    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

3 authors at 1 institution in 1 country.

Andrea S LinkInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen, Germany.
Fang ZhengInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen, Germany.
Christian AlzheimerInstitute of Physiology and Pathophysiology, Friedrich-Alexander-Universität Erlangen-Nürnberg Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activins are members of the transforming growth factor β (TGFβ) family and serve as multifunctional regulatory proteins in many tissues and organs. In the brain, activin A, which is formed by two disulfide-linked βA subunits, is recognized as the predominant player in activin signaling. Over the last years, considerable progress has been made in elucidating novel and unexpected functions of activin in the normal and diseased brain and in deciphering the underlying molecular mechanisms. Initially identified as a neurotrophic and protective factor during development and in several forms of acute injury, the scope of effects of activin A in the adult central nervous system (CNS) has been considerably broadened by now. Here, we will highlight recent findings that bear significance for a better understanding of the pathogenesis of various neuropsychiatric diseases and might hold promise for novel therapeutic strategies. While the basal level of activin A in the adult brain is low, significant short-term up-regulation occurs in response to increased neuronal activity. In fact, brief exposure to an enriched environment (EE) is already sufficient to considerably strengthen activin signaling. Enhancement of this pathway tunes the performance of glutamatergic and GABAergic synapses in a fashion that impacts on cognitive functions and affective behavior, counteracts death-inducing signals through extrasynaptic NMDA receptors (NMDARs), and stimulates adult neurogenesis in the hippocampus. We will discuss how impaired activin signaling is involved in anxiety disorders, depression, drug dependence, and neurodegenerative diseases such as Alzheimer's and Parkinson's, and how reinforcement of activin signaling might be exploited for therapeutic interventions.

Indexed as

activinanxiety disordersdepressiondrug cravingneurodegenerative disease

Identifiers

PMID27242425
PMCPMC4861723
OpenAlexW2353648028

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.