Pohang University of Science and Technology · Neuroscience
Professor Joung-Hun Kim's research lab focuses on the cellular and molecular mechanisms underlying neurodegenerative diseases, particularly Alzheimer’s disease, with a strong emphasis on amyloid precursor protein (APP) processing, amyloid-beta toxicity, synaptic plasticity, and calcium homeostasis. The lab investigates the roles of key signaling molecules such as dopamine, neuritin (CPG15), eIF2α, and LIMK1 in neuronal function and synaptic regulation, using advanced techniques including atomic force microscopy, electrophysiology, and in vivo behavioral models. A central theme is understanding early pathogenic events in Alzheimer’s disease, including oxidative stress, disrupted protein synthesis, and impaired synaptic transmission. The lab also explores potential therapeutic targets, such as neuritin overexpression and antioxidant interventions, to rescue cognitive deficits in Alzheimer’s models.
Figures are computed from collected data and may differ slightly.
Despite the pivotal functions of the NMDA receptor (NMDAR) for neural circuit development and synaptic plasticity, the molecular mechanisms underlying the dynamics of NMDAR trafficking are poorly understood. The cell adhesion molecule neuroligin-1 (NL1) modifies NMDAR-dependent synaptic transmission and synaptic plasticity, but it is unclear whether NL1 controls synaptic accumulation or function of the receptors. Here, we provide evidence that NL1 regulates the abundance of NMDARs at postsynapti
These data suggest that exosomes can counteract the inhibitory action of Aβ, which contributes to perpetual capability for synaptic plasticity.
The Alzheimer's disease-related beta-amyloid precursor protein (beta-APP) is metabolized to a number of potentially amyloidogenic peptides that are believed to be pathogenic. Application of relatively low concentrations of the soluble forms of these peptides has previously been shown to block high-frequency stimulation-induced long-term potentiation (LTP) of glutamatergic transmission in the hippocampus. The present experiments examined how these peptides affect low-frequency stimulation-induced
In addition to modulating a number of cognitive functions including reward, punishment, motivation, and salience, dopamine (DA) plays a pivotal role in regulating threat-related emotional memory. Changes in neural circuits of the amygdala nuclei are also critically involved in the acquisition and expression of emotional memory. In this review, we summarize the regulation of amygdala circuits by DA. Specifically, we describe DA signaling in the amygdala, and DA regulation of synaptic transmission
Swedish double mutation (KM670/671NL) of amyloid precursor protein (Swe-APP), a prevailing cause of familial Alzheimer's disease (FAD), is known to increase in Abeta production both in vitro and in vivo, but its underlying molecular basis leading to Alzheimer's disease (AD) pathogenesis remains to be elucidated, especially for the early phase of disease. We have confirmed initially that the expression of Swe-APP mutant transgene reduced cell viability via ROS production but this effect was elimi
Neuritin, also known as CPG15, is a neurotrophic factor that was initially discovered in a screen to identify genes involved in activity-dependent synaptic plasticity. Neuritin plays multiple roles in the process of neural development and synaptic plasticity, although its binding receptor(s) and downstream signaling effectors remain unclear. In this study, we found that the cortical and hippocampal expression of neuritin is reduced in the brains of Alzheimer's disease (AD) patients and demonstra
The effects of Alzheimer's disease-related amyloidogenic peptides on inositol 1,4,5-trisphosphate receptor-mediated Ca(2+) mobilization were examined in Xenopus laevis oocytes. Intracellular Ca(2+) was monitored by electrophysiological measurement of the endogenous Ca(2+)-activated Cl(-) current. Application of a hyperpolarizing pulse released intracellular Ca(2+) in oocytes primed by pre-injection of a non-metabolizable inositol 1,4,5-trisphosphate analogue. The carboxyl terminus of the amyloid
Amygdala circuitry encodes associations between conditioned stimuli and aversive unconditioned stimuli and also controls fear expression. However, whether and how non-threatening information for unpaired conditioned stimuli (CS<sup>-</sup>) is discretely processed remains unknown. The fear expression toward CS<sup>-</sup> is robust immediately after fear conditioning but then becomes negligible after memory consolidation. The synaptic plasticity of the neural pathway from the lateral to the ante
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