ArticleScientific reports2016
Parkinson-like phenotype in insulin-resistant PED/PEA-15 transgenic mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Narrative Review "Dual Frontiers in Neurodegeneration: Pharmacological Synergies and Divergences in Parkinson's Disease and Type 2 Diabetes Mellitus".Cellular and molecular neurobiology · 2026Review
- Characterization of NLRP3 Inflammasome-Associated Hub Genes in the Progression of Diabetic Nephropathy.Immunity, inflammation and disease · 2026Article
- Multiscale Imaging of Human Adipose Tissue: A Neglected Partner in Proteinuria Linked to Obesity.Biomedicines · 2025Review
- Unraveling the Ties: Type 2 Diabetes and Parkinson's Disease - A Nano-Based Targeted Drug Delivery Approach.Current diabetes reviews · 2025Review
- Epigenetics, Microbiome and Personalized Medicine: Focus on Kidney Disease.International journal of molecular sciences · 2024Review
- The Contribution of Type 2 Diabetes to Parkinson's Disease Aetiology.International journal of molecular sciences · 2024Review
- Potential molecular mechanism of exercise reversing insulin resistance and improving neurodegenerative diseases.Frontiers in physiology · 2024Review
- Mechanisms of Diabetic Nephropathy Not Mediated by Hyperglycemia.Journal of clinical medicine · 2023Review
- The Molecular Mechanisms of the Relationship between Insulin Resistance and Parkinson's Disease Pathogenesis.Nutrients · 2023Review
- Actions and Consequences of Insulin in the Striatum.Biomolecules · 2023Review
- Sphingolipid metabolism in brain insulin resistance and neurological diseases.Frontiers in endocrinology · 2023Review
- Long-term hyperglycemia aggravates α-synuclein aggregation and dopaminergic neuronal loss in a Parkinson's disease mouse model.Translational neurodegeneration · 2022Article
- Complexin I knockout rats exhibit a complex neurobehavioral phenotype including profound ataxia and marked deficits in lifespan.Pflugers Archiv : European journal of physiology · 2020Article
- Transcriptional correlates of the pathological phenotype in a Huntington's disease mouse model.Scientific reports · 2019Article
- Analysis of the Relationship between Type II Diabetes Mellitus and Parkinson's Disease: A Systematic Review.Parkinson's disease · 2019Review
- The Relevance of Insulin Action in the Dopaminergic System.Frontiers in neuroscience · 2019Review
- Post-treatment with PT302, a long-acting Exendin-4 sustained release formulation, reduces dopaminergic neurodegeneration in a 6-Hydroxydopamine rat model of Parkinson's disease.Scientific reports · 2018Article
- Transcriptomic Analysis of Zebrafish TDP-43 Transgenic Lines.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurological abnormalities, such as Parkinson-like disorders (PlD), are often co-morbidities of Type 2 Diabetic (T2D) patients, although the epidemiological link between these two disorders remains controversial. The PED/PEA-15 protein represents a possible candidate linking T2D and PD, because it is increased in subjects with T2D and is highly expressed in the brain. To test this hypothesis, we have analyzed the neurological and neurochemical phenotype of transgenic mice overexpressing PED/PEA-15 (tgPED). These mice develop impaired glucose tolerance and insulin resistance, accompanied by neurological features resembling PlD: feet clasping, slow and delayed locomotor movements in different behavioral tests in absence of clear cognitive deficits, ataxia or anxiety. Morphological analysis of the brains showed selective modifications of metabolic activity in the striatal region. In the same region, we have observed 26% decrease of dopamine fibers, confirmed by immunohistochemistry and Western Blot for tyrosine hydroxylase. Moreover, they also showed 48% reduction of dopamine levels in the striatum. Thus the tgPED mice may represent a genetic animal model of neurological disease linked to T2D.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.