biostudies-literatureUnknown13Chung LYNational Taiwan University HospitalMinistry of Science and Technology, TaiwanNational Health Research Institutes<b>Background:</b> Parkinson's disease (PD) is characterized by intraneuronal α-synuclein aggregation called Lewy bodies and progressive dopaminergic neurodegeneration. Toll-like receptor (TLR) signaling is a major pathway mediating inflammation. The molecular link on how neuroinflammation upregulates neuronal TLRs and induces accumulation of α-synuclein aggregates to drive synucleinopathy remains to be determined. <b>Objective:</b> Despite conditioned medium from microglia and TLR agonists were utilized to study their effects on neuronal cells, a Transwell coculture system, comprising lipopolysaccharide-activated microglia on top and retinoic acid-differentiated SH-SY5Y cells at the bottom more mimicking <i>in vivo</i> neuroinflammation, was employed to elucidate the mechanism of activateFrontiers in pharmacology845930https://www.ebi.ac.uk/biostudies/studies/S-EPMC8987529biostudies-literatureNeuroinflammation Upregulated Neuronal Toll-Like Receptors 2 and 4 to Drive Synucleinopathy in Neurodegeneration.PMC8987529Lin YTTai YCChen CCLin HYLiu CLin CHChung LYfalseNeuroinflammation Upregulated Neuronal Toll-Like Receptors 2 and 4 to Drive Synucleinopathy in Neurodegeneration.<b>Background:</b> Parkinson's disease (PD) is characterized by intraneuronal α-synuclein aggregation called Lewy bodies and progressive dopaminergic neurodegeneration. Toll-like receptor (TLR) signaling is a major pathway mediating inflammation. The molecular link on how neuroinflammation upregulates neuronal TLRs and induces accumulation of α-synuclein aggregates to drive synucleinopathy remains to be determined. <b>Objective:</b> Despite conditioned medium from microglia and TLR agonists were utilized to study their effects on neuronal cells, a Transwell coculture system, comprising lipopolysaccharide-activated microglia on top and retinoic acid-differentiated SH-SY5Y cells at the bottom more mimicking <i>in vivo</i> neuroinflammation, was employed to elucidate the mechanism of activate2022-01-01T00:00:00Z20222026-05-31T13:00:17.715Z2025-04-06T21:52:10.617ZS-EPMC89875293540119810.3389/fphar.2022.845930