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Neurotoxicity, α-Synuclein Pathology, and Mitochondrial Dysfunction: A Comparative Study of Three Parkinson’s Disease Mouse Models

ABSTRACT: The pathogenesis of Parkinson’s disease (PD) is complex, and it is difficult for a single animal model to fully mimic its pathological features. In this study, a comprehensive analysis of behaviors, PD-like pathologies, and gene and protein expression profiles was carried out in PD mouse models (MPTP-induced, α-Syn A53T transgenic, and MitoPark models). The three PD models showed motor impairments, with MitoPark mice displaying particularly pronounced age-related worsening. Pathologically, they all exhibited nigrostriatal pathway damage but showed differential patterns of glial cell activation. All three PD model mice showed no α-Syn aggregates. However, a few pS129-α-Syn-positive signals were detected in the substantia nigra of α-Syn A53T transgenic mice. Molecularly, RNA sequencing and proteomics revealed significant changes in gene and protein expression, with both unique and common features. Five common differentially expressed genes (Ifi27l2a, Ifitm3, Oasl2, Rtp4, and Ankk1) and two common differentially expressed proteins (Timm8a1 and Sephs1) were identified. Functional enrichment analysis indicated that immune responses, cytokines, and neurotransmitter transport were crucial in PD pathogenesis. Pathway analysis revealed the involvement of ferroptosis in all models, with additional IL-17 pathway activation specifically in MitoPark mice. These findings provide a comprehensive molecular and phenotypic characterization of PD models, offering valuable insights into disease mechanisms and potential therapeutic targets.

ORGANISM(S): Mus musculus

PROVIDER: GSE300519 | GEO | 2026/06/10

REPOSITORIES: GEO

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Project description:Kuznetsov2016(II) - α-syn aggregation kinetics in Parkinson's This theoretical model uses 2-step Finke-Watzky (FW) kinetics todescribe the production, misfolding, aggregation, transport and degradation of α-syn that may lead to Parkinson's Disease (PD). Deregulated α-syn degradation is predicted to be crucialfor PD pathogenesis. This model is described in the article: What can trigger the onset of Parkinson's disease - A modeling study based on a compartmental model of α-synuclein transport and aggregation in neurons. Kuznetsov IA, Kuznetsov AV. Math Biosci 2016 Aug; 278: 22-29 Abstract: The aim of this paper is to develop a minimal model describing events leading to the onset of Parkinson's disease (PD). The model accounts for α-synuclein (α-syn) production in the soma, transport toward the synapse, misfolding, and aggregation. The production and aggregation of polymeric α-syn is simulated using a minimalistic 2-step Finke-Watzky model. We utilized the developed model to analyze what changes in a healthy neuron are likely to lead to the onset of α-syn aggregation. We checked the effects of interruption of α-syn transport toward the synapse, entry of misfolded (infectious) α-syn into the somatic and synaptic compartments, increasing the rate of α-syn synthesis in the soma, and failure of α-syn degradation machinery. Our model suggests that failure of α-syn degradation machinery is probably the most likely cause for the onset of α-syn aggregation leading to PD. This model is hosted on BioModels Database and identified by: BIOMD0000000615. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Neurotoxicity, α-Synuclein Pathology, and Mitochondrial Dysfunction: A Comparative Study of Three Parkinson’s Disease Mouse Models

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