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Tet2 loss and enhanced ciliogenesis suppress α-synuclein pathology
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Tet2 loss and enhanced ciliogenesis suppress α-synuclein pathology
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Journal Article
Tet2 loss and enhanced ciliogenesis suppress α-synuclein pathology
2025
Overview
There are no approved treatments that slow Parkinson’s disease (PD) progression and therefore it is important to identify novel pathogenic mechanisms that can be targeted. Loss of the epigenetic marker,
Tet2
appears to have some beneficial effects in PD models, but the underlying mechanism of action is not well understood. We performed an unbiased transcriptomic analysis of cortical neurons isolated from patients with PD to identify dysregulated pathways and determine their potential contributions to the disease process. We discovered that genes associated with primary cilia, non-synaptic sensory and signaling organelles, are upregulated in both early and late stage PD patients. Enhancing ciliogenesis in primary cortical neurons via sonic hedgehog signaling suppressed the accumulation of α-synuclein pathology in vitro. Interestingly, deletion of
Tet2
in mice also enhanced the expression of primary cilia and sonic hedgehog signaling genes and reduced the accumulation of α-synuclein pathology and dopamine neuron degeneration in vivo. Our findings demonstrate the crucial role of TET2 loss in regulating ciliogenesis and potentially affecting the progression of PD pathology.
Publisher
BioMed Central,BMC
Subject
/ alpha-Synuclein - metabolism
/ Animals
/ Biomedical and Life Sciences
/ Cerebral Cortex - metabolism
/ DNA-Binding Proteins - deficiency
/ DNA-Binding Proteins - genetics
/ DNA-Binding Proteins - metabolism
/ Female
/ Hedgehog Proteins - metabolism
/ Humans
/ Male
/ Mice
/ Parkinson Disease - genetics
/ Parkinson Disease - metabolism
/ Parkinson Disease - pathology
/ Proto-Oncogene Proteins - deficiency
/ Proto-Oncogene Proteins - genetics
/ Proto-Oncogene Proteins - metabolism
/ Tet2
