Publications by authors named "JinHan Nam"
Article Synopsis
- Felodipine, an L-type calcium channel blocker, was previously shown to reduce neuroinflammation in microglial cells and mice, but its effects on tau pathology in Alzheimer's disease were unknown.
- In the study, felodipine was found to decrease tau pathology-induced microglial activation and tau hyperphosphorylation in a transgenic mouse model of Alzheimer's disease but did not affect astrogliosis.
- The findings suggest that felodipine may be a promising therapeutic option for reducing tau hyper-phosphorylation and neuroinflammatory responses in Alzheimer's disease.
Cerebral dopamine neurotrophic factor (CDNF) and its close structural relative, mesencephalic astrocyte-derived neurotrophic factor (MANF), are proteins with neurotrophic properties. CDNF protects and restores the function of dopamine (DA) neurons in rodent and non-human primate (NHP) toxin models of Parkinson's disease (PD) and therefore shows promise as a drug candidate for disease-modifying treatment of PD. Moreover, CDNF was found to be safe and to have some therapeutic effects on PD patients in phase 1/2 clinical trials.
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- Dopamine is crucial for cognitive functions and inflammation, linking it to neurodegenerative diseases like Alzheimer's disease (AD).
- L-DOPA treatment in 5xFAD mice (an AD model) reduced neuroinflammation and decreased Aβ plaques by increasing specific enzyme levels.
- However, L-DOPA did not affect tau hyperphosphorylation or tau kinase levels, indicating its limitations in influencing tau pathology in this context.
Amyotrophic lateral sclerosis is a progressive neurodegenerative disease that affects motor neurons in the spinal cord, brainstem and motor cortex, leading to paralysis and eventually to death within 3-5 years of symptom onset. To date, no cure or effective therapy is available. The role of chronic endoplasmic reticulum stress in the pathophysiology of amyotrophic lateral sclerosis, as well as a potential drug target, has received increasing attention.
View Article and Find Full Text PDFMesencephalic astrocyte-derived neurotrophic factor (MANF) is an endoplasmic reticulum (ER)-located protein with cytoprotective effects in neurons and pancreatic β cells in vitro and in models of neurodegeneration and diabetes in vivo. However, the exact mode of MANF action has remained elusive. Here, we show that MANF directly interacts with the ER transmembrane unfolded protein response (UPR) sensor IRE1α, and we identify the binding interface between MANF and IRE1α.
View Article and Find Full Text PDFMultiple sclerosis (MS) is a progressive autoimmune disease characterized by T-cell mediated demyelination in central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is a widely used disease model of MS. Glucocorticoids such as dexamethasone (dex) function as immunosuppressants and are commonly used to treat acute exacerbations of MS.
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