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α-Synuclein propagation leads to synaptic abnormalities in the cortex through microglial synapse phagocytosis
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Pérez-Acuña, Dayana | - |
dc.contributor.author | Shin, Soo Jean | - |
dc.contributor.author | Rhee, Ka Hyun | - |
dc.contributor.author | Kim, Sang Jeong | - |
dc.contributor.author | Lee, Seung-Jae | - |
dc.date.accessioned | 2023-10-30T00:47:57Z | - |
dc.date.available | 2023-10-30T09:48:47Z | - |
dc.date.issued | 2023-10-17 | - |
dc.identifier.citation | Molecular Brain, Vol.16(1):72 | ko_KR |
dc.identifier.issn | 1756-6606 | - |
dc.identifier.uri | https://hdl.handle.net/10371/195795 | - |
dc.description.abstract | The major neuropathologic feature of Parkinsons disease is the presence of widespread intracellular inclusions of α-synuclein known as Lewy bodies. Evidence suggests that these misfolded protein inclusions spread through the brain with disease progression. Changes in synaptic function precede neurodegeneration, and this extracellular α-synuclein can affect synaptic transmission. However, whether and how the spreading of α-synuclein aggregates modulates synaptic function before neuronal loss remains unknown. In the present study, we investigated the effect of intrastriatal injection of α-synuclein preformed fibrils (PFFs) on synaptic activity in the somatosensory cortex using a combination of whole-cell patch-clamp electrophysiology, histology, and Golgi-Cox staining. Intrastriatal PFF injection was followed by formation of phosphorylated α-synuclein inclusions in layer 5 of the somatosensory cortex, leading to a decrease in synapse density, dendritic spines, and spontaneous excitatory post-synaptic currents, without apparent neuronal loss. Additionally, three-dimensional reconstruction of microglia using confocal imaging showed an increase in the engulfment of synapses. Collectively, our data indicate that propagation of α-synuclein through neural networks causes abnormalities in synaptic structure and dynamics prior to neuronal loss. | ko_KR |
dc.description.sponsorship | This work was supported by a National Research Foundation (NRF) grant funded by the Korean Government (MSIT) (NRF-2018R1A5A2025964 to S.-J.L.). Dayana Pérez-Acuña was supported by the Agencia Nacional de Investigacion y Desarrollo (ANID) through the Becas Chile scholarship program PFCHA/DOCTORADO BECAS CHILE/ 2018-72190194 | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BMC | ko_KR |
dc.subject | Parkinson’s disease | - |
dc.subject | α-synuclein | - |
dc.subject | Protein aggregation | - |
dc.subject | Microglia | - |
dc.subject | Synapse degeneration | - |
dc.title | α-Synuclein propagation leads to synaptic abnormalities in the cortex through microglial synapse phagocytosis | ko_KR |
dc.type | Article | ko_KR |
dc.identifier.doi | 10.1186/s13041-023-01059-1 | ko_KR |
dc.citation.journaltitle | Molecular Brain | ko_KR |
dc.language.rfc3066 | en | - |
dc.rights.holder | Min Zhuo, Bong-Kiun Kaang and BioMed central Ltd. | - |
dc.date.updated | 2023-10-22T03:14:59Z | - |
dc.citation.endpage | 12 | ko_KR |
dc.citation.number | 1 | ko_KR |
dc.citation.startpage | 1 | ko_KR |
dc.citation.volume | 16 | ko_KR |
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