Yonsei University · Medicine
Professor Do Young Kim's research lab focuses on the neuroprotective mechanisms of metabolic therapies, particularly the ketogenic diet and ketone bodies, in neurological disorders. The lab investigates how metabolic substrates modulate neuronal excitability, mitochondrial function, and protein homeostasis to protect against neurodegeneration and neuroinflammation. Key research directions include the role of ketones in preventing oxidative stress, regulating mitochondrial permeability transition pores, and enhancing synaptic plasticity in models of multiple sclerosis, Parkinson’s, and Alzheimer’s disease. The lab integrates electrophysiology, mass spectrometry, and in vivo imaging to uncover metabolic pathways underlying neurological resilience.
Figures are computed from collected data and may differ slightly.
A prominent clinical symptom in multiple sclerosis (MS), a progressive disorder of the central nervous system (CNS) due to heightened neuro-inflammation, is learning and memory dysfunction. Here, we investigated the effects of a ketogenic diet (KD) on memory impairment and CNS-inflammation in a murine model of experimental autoimmune encephalomyelitis (EAE), using electrophysiological, behavioral, biochemical and in vivo imaging approaches. Behavioral spatial learning deficits were associated wi
The posttranslational addition of ubiquitin (Ub) profoundly controls the half-life, interactions, and/or trafficking of numerous intracellular proteins. Using stringent two-step affinity methods to purify Ub-protein conjugates followed by high-sensitivity mass spectrometry, we identified almost 950 ubiquitylation substrates in whole Arabidopsis thaliana seedlings. The list includes key factors regulating a wide range of biological processes, including metabolism, cellular transport, signal trans
Ketone bodies (KB) have been shown to prevent neurodegeneration in models of Parkinson's and Alzheimer's diseases, but the mechanisms underlying these effects remain unclear. One possibility is that KB may exert antioxidant activity. In the current study, we explored the effects of KB on rat neocortical neurons exposed to hydrogen peroxide (H(2)O(2)) or diamide - a thiol oxidant and activator of mitochondrial permeability transition (mPT). We found that: (i) KB completely blocked large inward cu
The present data reveal the first direct link between mPT and seizure control, and provide a potential mechanistic explanation for the KD. Given that mPT is increasingly being implicated in diverse neurological disorders, our results suggest that metabolism-based treatments and/or metabolic substrates might represent a worthy paradigm for therapeutic development.
While the mechanisms underlying the broad clinical efficacy of the ketogenic diet remain unclear, there is growing evidence that the ketogenic diet alters the fundamental biochemistry of neurons in a manner that not only inhibits neuronal hyperexcitability but also induces a protective effect. Thus, the ketogenic diet may ultimately be useful in the treatment of a variety of neurological disorders.
Dietary and metabolic therapies are increasingly being considered for a variety of neurological disorders, based in part on growing evidence for the neuroprotective properties of the ketogenic diet (KD) and ketones. Earlier, we demonstrated that ketones afford hippocampal synaptic protection against exogenous oxidative stress, but the mechanisms underlying these actions remain unclear. Recent studies have shown that ketones may modulate neuronal firing through interactions with ATP-sensitive pot
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