Korea Advanced Institute of Science and Technology · Neuroscience
Professor Daesoo Kim's research lab focuses on bioelectronic and neuro-metabolic mechanisms underlying aging, pain modulation, and energy homeostasis. The lab pioneers self-powered neuromodulation technologies, such as flexible piezoelectric energy harvesters for deep brain stimulation, and investigates ion channel regulation—particularly T-type calcium channels—in thalamic processing of visceral pain. Additionally, the lab explores metabolic interventions, like NQO1 activation via β-lapachone, to mitigate age-related decline in motor and cognitive functions by enhancing mitochondrial health and energy metabolism. These interdisciplinary efforts bridge neuroscience, bioengineering, and aging biology to develop innovative therapeutic strategies.
Figures are computed from collected data and may differ slightly.
A self-powered deep brain stimulation has been demonstrated by a flexible piezoelectric PIMNT energy harvester to induce behavioural changes in a mouse.
Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking alpha1G T-type Ca2+ channels show hyperalgesia to visceral pain. Thalamic infusion of a T-type blocker induced similar hyperalgesia in wild-type mice. In response to visceral pain, the ventroposterolateral thalamic neurons evokeda surge of single spikes, which then slowly decayed as T type-dependent burst spikes gradually increased. In alpha1G-deficient neurons, the single-spike response persiste
NADH-quinone oxidoreductase 1 (NQO1) modulates cellular NAD(+)/NADH ratio which has been associated with the aging and anti-aging mechanisms of calorie restriction (CR). Here, we demonstrate that the facilitation of NQO1 activity by feeding β-lapachone (βL), an exogenous NQO1 co-substrate, prevented age-dependent decline of motor and cognitive function in aged mice. βL-fed mice did not alter their food-intake or locomotor activity but did increase their energy expenditure as measured by oxygen c
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