ArticleFrontiers in neuroscience2018
Analysis of α-Synuclein Pathology in PINK1 Knockout Rat Brains.
Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Rethinking 'rare'Journal of Parkinson's disease · 2025Pooled it
- Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.Behavioral and brain functions : BBF · 2025Review
- The Ubiquitin Proteasome System as a Therapeutic Area in Parkinson's Disease.Neuromolecular medicine · 2023Review
- Alpha-synuclein-associated changes in PINK1-PRKN-mediated mitophagy are disease context dependent.Brain pathology (Zurich, Switzerland) · 2023Article
- Parkinson's disease relevant pathological features are manifested in male Pink1/Parkin deficient rats.Brain, behavior, & immunity - health · 2023Article
- Outlook of PINK1/Parkin signaling in molecular etiology of Parkinson's disease, with insights intoZoological research · 2023Review
- Mitochondrial Bioenergy in Neurodegenerative Disease: Huntington and Parkinson.International journal of molecular sciences · 2023Review
- Intranasal Administration of Forskolin and Noopept Reverses Parkinsonian Pathology in PINK1 Knockout Rats.International journal of molecular sciences · 2022Article
- The role of amyloid β in the pathological mechanism of GNE myopathy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- PTEN-Induced Putative Kinase 1 Dysfunction Accelerates Synucleinopathy.Journal of Parkinson's disease · 2022Article
- Spontaneous Object Exploration in a Recessive Gene Knockout Model of Parkinson's Disease: Development and Progression of Object Recognition Memory Deficits in MaleFrontiers in behavioral neuroscience · 2022Article
- Lipids, lysosomes and mitochondria: insights into Lewy body formation from rare monogenic disorders.Acta neuropathologica · 2021Review
- Review
- Increased glutamate transmission onto dorsal striatum spiny projection neurons in Pink1 knockout rats.Neurobiology of disease · 2021Article
- Basal Synaptic Transmission and Long-Term Plasticity at CA3-CA1 Synapses Are Unaffected in Young Adult PINK1-Deficient Rats.Frontiers in neuroscience · 2021Article
- Review
- Article
- Intramitochondrial proteostasis is directly coupled to α-synuclein and amyloid β1-42 pathologies.The Journal of biological chemistry · 2020Article
- Enhanced Susceptibility of PINK1 Knockout Rats to α-Synuclein Fibrils.Neuroscience · 2020Article
- Autophagy in the mammalian nervous system: a primer for neuroscientists.Neuronal signaling · 2019Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in PTEN induced kinase 1 (PINK1) cause autosomal recessive Parkinson's disease (PD). The main pathological hallmarks of PD are loss of dopaminergic neurons in the substantia nigra pars compacta and the formation of protein aggregates containing α-synuclein. Previous studies of PINK1 knockout (PINK1-/-) rats have reported mitochondrial dysfunction, locomotor behavioral deficits, loss of neurons in the substantia nigra and α-synuclein aggregates in various brain regions. We sought to characterize PINK1-/- rats in more detail specifically with respect to α-synuclein pathology because abnormal α-synuclein has been implicated genetically, biophysically and neuropathologically as a mechanism of PD pathogenesis. Moreover, the spontaneous formation of α-synuclein aggregates without α-synuclein overexpression, injection or toxin administration is a rare and important characteristic for an animal model of PD or other synucleinopathies, such as dementia with Lewy bodies and multiple system atrophy. We observed α-synuclein-immunoreactive aggregates in various brain regions of PINK1-/- rats including cortex, thalamus, striatum and ventral midbrain, but nowhere in wild-type (WT) rats. Co-immunofluorescence showed that the α-synuclein-immunoreactive aggregates are both thioflavin S and ubiquitin positive. Many cells in the brains of PINK1-/- rats but not WT rats contained protease-resistant α-synuclein. Total synuclein protein levels were unchanged; however, biochemical fractionation showed a significant shift of α-synuclein from the cytosolic fraction to the synaptic vesicle-enriched fraction of PINK1-/- brain homogenates compared to WT. This data indicates that PINK1 deficiency results in abnormal α-synuclein localization, protease resistance and aggregation
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