Evidence map›Paper›PMID 27251043›Full record

ArticleJournal of neuropathology and experimental neurology2016

Protective Effects of Forskolin on Behavioral Deficits and Neuropathological Changes in a Mouse Model of Cerebral Amyloidosis.

Brice Ayissi Owona, Caroline Zug, Hermann J Schluesener, Zhi-Yuan Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Adenylyl Cyclases as Therapeutic Targets in Neuroregeneration.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Research progress on intranasal treatment for Parkinson's disease.Neuroprotection (Chichester, England) · 2024
    Review
  6. Biotechnological interventions for the production of forskolin, an active compound from the medicinal plant,Physiology and molecular biology of plants : an international journal of functional plant biology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. 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

4 authors at 1 institution in 1 country.

Brice Ayissi OwonaFrom the Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tubingen, Tubingen, Germany (BAO, CZ, HJS, ZYZ). briceayissi03@yahoo.fr.
Caroline ZugFrom the Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tubingen, Tubingen, Germany (BAO, CZ, HJS, ZYZ).
Hermann J SchluesenerFrom the Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tubingen, Tubingen, Germany (BAO, CZ, HJS, ZYZ).
Zhi-Yuan ZhangFrom the Division of Immunopathology of the Nervous System, Institute of Pathology and Neuropathology, University of Tubingen, Tubingen, Germany (BAO, CZ, HJS, ZYZ).
University of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The production of amyloid-β peptides in the brains of patients with Alzheimer disease (AD) may contribute to memory loss and impairments in social behavior. Here, an efficient adenylate cyclase activator, forskolin, was orally administered by gavage (100 mg/kg body weight) to 5-month-old transgenic APP/PS1 mice, which serve as an animal model of cerebral amyloidosis. Analyses of nest construction, sociability, and immunohistochemical features were used to determine the effects of forskolin treatment. After a relatively short term of treatment (10 days), forskolin-treated transgenic mice showed restored nest construction ability (p < 0.05) and their sociability (p < 0.01). There was a reduction of Aβ plaque deposition in the cortex and in the hippocampus. Furthermore, expression of transforming growth factor β, glial fibrillary acidic protein, and Iba-1 in the cortex was reduced in the forskolin-treated group, suggesting regulation of the inflammatory response mediated by activated microglia and astrocytes in the brains of the APP/PS1 mice (p < 0.01). Taken together, these findings suggest that forskolin shows neuroprotective effects in APP/PS1 Tg mice and may be a promising drug in the treatment of patients with AD.

Indexed as

Disease Models, AnimalInterpersonal RelationsAmyloid beta-Protein PrecursorAmyloidosisAnimalsColforsinMaleMiceMice, Inbred C57BLMice, TransgenicNeuroprotective AgentsPresenilin-1Treatment OutcomeAmyloid beta-Protein PrecursorColforsinNeuroprotective AgentsPresenilin-1Alzheimer diseaseAPP/PS1 transgenic miceCerebral amyloidosisForskolin.β-amyloid

Identifiers

PMID27251043
PMCPMC4913438
OpenAlexW2414779396

What OpenQuestion holds

Textmetadata
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.