Evidence map›Paper›PMID 32785075›Full record

ArticleInternational journal of molecular sciences2020

Alzheimer's Disease Mouse as a Model of Testis Degeneration.

Vince Szegeczki, Gabriella Horváth, Helga Perényi, Andrea Tamás, Zsolt Radák, Dóra Ábrahám, Róza Zákány, Dora Reglodi, Tamás Juhász

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Vince SzegeczkiDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98, H-4032 Debrecen, Hungary.
Gabriella HorváthDepartment of Anatomy, PTE-MTA PACAP Research Team, University of Pécs Medical School, Szigeti út 12, H-7624 Pécs, Hungary.
Helga PerényiDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98, H-4032 Debrecen, Hungary.
Andrea TamásDepartment of Anatomy, PTE-MTA PACAP Research Team, University of Pécs Medical School, Szigeti út 12, H-7624 Pécs, Hungary.
Zsolt RadákResearch Institute of Sport Science, University of Physical Education, Budapest, Alkotas út 44, H-1123 Budapest, Hungary.ORCID 0000-0003-1297-6804
Dóra ÁbrahámResearch Institute of Sport Science, University of Physical Education, Budapest, Alkotas út 44, H-1123 Budapest, Hungary.
Róza ZákányDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98, H-4032 Debrecen, Hungary.
Dora ReglodiDepartment of Anatomy, PTE-MTA PACAP Research Team, University of Pécs Medical School, Szigeti út 12, H-7624 Pécs, Hungary.
Tamás JuhászDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Nagyerdei krt. 98, H-4032 Debrecen, Hungary.ORCID 0000-0003-0489-5676
University of Debrecen · HUUniversity of Pecs · HUHungarian University of Sports Science · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pituitary adenylate cyclase activating polypeptide (PACAP) is a neuropeptide with protective functions in the central nervous system and various peripheral organs. PACAP has the highest expression level in the testes, among the peripheral organs, and has a positive regulative role in spermatogenesis and in sperm motility. In the present study, we explored testicular degenerative alterations in a mouse model of Alzheimer's disease (AD) (B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J) and demonstrated changes in PACAP-regulated signaling pathways. In addition, the effects of increased physical activity of AD (trained AD (TAD)) mice on testis were also followed. Reduced cell number and decreased thickness of basement membrane were detected in AD samples. These changes were compensated by physical activity. Expression of PACAP receptors and canonical signaling elements such as PKA, P-PKA, PP2A significantly decreased in AD mice, and altered Sox transcription factor expression was also detected. Via this signaling mechanism, physical activity compensated the negative effects of AD on the expression of type IV collagen. Our findings suggest that the testes of AD mice can be a good model of testis degeneration. Moreover, it can be an appropriate organ to follow the effects of various interventions such as physical activity on tissue regeneration and signaling alterations.

Indexed as

Alzheimer DiseaseAnimalsCell CountCollagen Type IVDisease Models, AnimalHumansMaleMiceMice, TransgenicPhysical Conditioning, AnimalPituitary Adenylate Cyclase-Activating PolypeptideReceptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type ISignal TransductionSOX9 Transcription FactorSpermatocytesSpermatogenesisAdcyap1 protein, mouseCollagen Type IVPituitary Adenylate Cyclase-Activating PolypeptideReceptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type ISox9 protein, mouseSOX9 Transcription FactorAlzheimer’s diseasecollagen type IVphysical activitySox9testis degeneration

Identifiers

PMID32785075
PMCPMC7460847
OpenAlexW3047657795

What OpenQuestion holds

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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 OpenQuestion graph.