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Metabolism-Centric Overview of the Pathogenesis of Alzheimer’s Disease
강소망,이종은,이용호 연세대학교의과대학 2017 Yonsei medical journal Vol.58 No.3
Alzheimer’s disease (AD) is a degenerative brain disease and the most common cause of dementia. AD is characterized by the extracellularamyloid beta (Aβ) plaques and intraneuronal deposits of neurofibrillary tangles (NFTs). Recently, as aging has become a familiarphenomenon around the world, patients with AD are increasing in number. Thus, many researchers are working toward finding effective therapeutics for AD focused on Aβ hypothesis, although there has been no success yet. In this review paper, we suggest that AD is a metabolic disease and that we should focus on metabolites that are affected by metabolic alterations to find effective therapeuticsfor AD. Aging is associated with not only AD but also obesity and type 2 diabetes (T2DM). AD, obesity, and T2DM share demographicprofiles, risk factors, and clinical and biochemical features in common. Considering AD as a kind of metabolic disease, we suggest insulin, adiponectin, and antioxidants as mechanistic links among these diseases and targets for AD therapeutics. Patients with AD show reduced insulin signal transductions in the brain, and intranasal injection of insulin has been found to have an effect on AD treatment. In addition, adiponectin is decreased in the patients with obesity and T2DM. This reduction induces metabolic dysfunctionboth in the body and the brain, leading to AD pathogenesis. Oxidative stress is known to be induced by Aβ and NFTs, and we suggest that oxidative stress caused by metabolic alterations in the body induce brain metabolic alterations, resulting in AD.
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정제된 특징과 보조 신뢰 모듈을 이용한 다중 모달 감정 인식
강소망(So-Mang Kang),김성호(Seong-Ho Kim),송병철(Byung Cheol Song) 대한전자공학회 2023 대한전자공학회 학술대회 Vol.2023 No.6
With the recent development of deep learning, multi-modal emotion recognition is being actively studied. However, previous studies have focused only on fusion of heterogeneous modalities without considering the influence of each modality on the model. This can decrease emotion recognition performance. Therefore, this paper introduces a feature extraction method by which fine-grained features can be encoded for more meaningful modality fusion. In addition, we improve the performance of multi-modal emotion recognition by increasing the prediction reliability for each modality through a model regularization using an auxiliary confidence module. The proposed method can be attached to the front and rear ends of any multi-modal emotion recognition model, that is, can be flexibly applied to various baselines. We experimentally show that the proposed method ultimately improves the performance of multi-modal emotion recognition.
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송주현,이별이,강소망,오유미,김어수,김철훈,송호택,이종은 한국뇌신경과학회 2016 Experimental Neurobiology Vol.25 No.1
Neuronal senescence caused by diabetic neuropathy is considered a common complication of diabetes mellitus. Neuronal senescence leads to the secretion of pro-inflammatory cytokines, the production of reactive oxygen species, and the alteration of cellular homeostasis. Agmatine, which is biosynthesized by arginine decarboxylation, has been reported in previous in vitro to exert a protective effect against various stresses. In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions. Moreover, the senescence associated-β-galatosidase’s activity in high glucose exposed neuronal cells was reduced by agmatine. Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine. Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21. Here, we propose that agmatine may ameliorate neuronal cell senescence in hyperglycemia.
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송주현,이원택,박경아,강소망,Bokara Kiran Kumar,이종은 한국뇌신경과학회 2013 Experimental Neurobiology Vol.22 No.4
Differentiation of neural progenitor cells (NPCs) is important for protecting neural cells and brain tissue during inflammation. Interleukin-1 beta (IL-1β) is the most common pro- inflammatory cytokine in brain inflammation, and increased IL-1β levels candecrease the proliferation of NPCs. We aimed to investigate whether agmatine (Agm), a primary polyamine that protects neural cells,could trigger differentiation of NPCs by activating IL-1β in vitro. The cortex of ICR mouse embryos (E14) was dissociated to cultureNPCs. NPCs were stimulated by lipopolysaccharide (LPS). After 6 days, protein expression of stem cell markers and differentiationsignal factors was confirmed by using western blot analysis. Also, immunocytochemistry was used to confirm the cell fate. Agmtreatment activated NPC differentiation significantly more than in the control group, which was evident by the increased expressionof a neuronal marker, MAP2, in the LPS-induced, Agm-treated group. Differentiation of LPS-induced, Agm-treated NPCs wasregulated by the MAPK pathway and is thought to be related to IL-1β activation and decreased expression of TLX, a transcriptionfactor that regulates NPC differentiation. Our results reveal that Agm can promote NPC differentiation to neural stem cells bymodulating IL-1β expression under inflammatory condition, and they suggest that Agm may be a novel therapeutic strategy forneuroinflammatory diseases.
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