Publications by authors named "Youngji Kwon"

Parkinson's disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic neurons. In particular, neuroinflammation associated with phosphorylation of c-Jun N-terminal kinase (JNK) is likely to cause the death of dopaminergic neurons. Therefore, protecting dopaminergic neurons through anti-neuroinflammation is a promising therapeutic strategy for PD.

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Corticotropin-releasing hormone (CRH) is a key mediator in stress-induced hair growth inhibition. Here, we investigated the impact of stress-induced senescence and evaluated the potential of (GL) extract in mitigating CRH-induced senescence in human hair follicle cells (hHFCs). We show that CRH treatment increased the senescence-associated beta-galactosidase (SA-β-GAL) activity and reactive oxygen species (ROS) formation in hHFCs and suppressed alkaline phosphatase (ALP) activity and anagen-inducing genes.

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Loss of dopamine (DA) is one of the primary features of Parkinson's disease (PD); however, imbalances of non-dopaminergic neurotransmitters significantly contribute to the disabilities noted in advanced PD patients. DA-9805 is the ethanolic extraction of the root bark of × Andrews (), the root of (Hoffm.) Benth.

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With the elderly population rapidly growing, the prevalence of Parkinson's disease (PD) is quickly increasing because neurodegenerative disorders are usually late-onset. Herbal medicines and formula are adjuvant therapies of conventional PD agents, which result in serious side effects with long-term use. This study evaluated the neuroprotective effects of DA-9805, a standardized herbal formula that consists of an ethanolic extract of Moutan Cortex Radix, Angelica Dahuricae Radix, and Bupleuri Radix against 6-hydroxydopamine (6-OHDA)-induced cytotoxicity in vitro and in vivo.

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Article Synopsis
  • Kinase irregularity is linked to neurodegenerative tauopathies, prompting research into selective inhibitors for potential anti-tauopathy therapies.
  • Novel dual inhibitors targeting CSF1R and DAPK1 were developed, showing effectiveness in reducing tau aggregate formation and neuroinflammation, with compound 3l emerging as the most potent.
  • The compound 3l exhibits strong inhibitory effects on both DAPK1 and CSF1R, lacks off-target toxicity, and shows potential for crossing the blood-brain barrier, suggesting it could be a promising therapeutic option for tauopathies.
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