• Title/Summary/Keyword: Amyloid protein

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The Effect of Exercise Training on Aβ-42, BDNF, GLUT-1 and HSP-70 Proteins in a NSE/ APPsw-transgenic Model for Alzheimer's Disease. (지구성 운동이 NSE/APPsw 알츠하이머 질환 생쥐의 인지능력, Aβ-42, BDNF, GLUT-1과 HSP-70 단백질 발현에 미치는 영향)

  • Eum, Hyun-Sub;Kang, Eun-Bum;Lim, Yea-Hyun;Lee, Jong-Rok;Cho, In-Ho;Kim, Young-Soo;Chae, Kab-Ryoung;Hwang, Dae-Yean;Kwak, Yi-Sub;Oh, Yoo-Sung;Cho, Joon-Yong
    • Journal of Life Science
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    • v.18 no.6
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    • pp.796-803
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    • 2008
  • Mutations in the APP gene lead to enhanced cleavage by ${\beta}-$ and ${\gamma}-secretase$, and increased $A{\beta}$ formation, which are closely associated with Alzheimer's disease (AD)-like neuropathological changes. Recent studies have shown that exercise training can ameliorate pathogenic phenotypes ($A{\beta}-42$, BDNF, GLUT-1 and HSP70) in experimental models of Alzheimer's disease. Here, we have used NSE/APPsw transgenic mice to investigate directly whether exercise training ameliorates pathogenic phenotypes within Alzheimer's brains. Sixteen weeks of exercise training resulted in a reduction of $A{\beta}-42$ peptides and also facilitated improvement of cognitive function. Furthermore, GLUT -1 and BDNF proteins produced by exercise training may protect brain neurons by inducing the concomitant expression of genes that encode proteins (HSP-70) which suppress stress induced neuron cell damages from APPsw transgenic mice. Thus, the improved cognitive function by exercise training may be mechanistically linked to a reduction of $A{\beta}-42$ peptides, possibly via activation of BDNF, GLUT-1, and HSP-70 proteins. On the basis of the evidences presented in this study, exercise training may represent a practical therapeutic management strategy for human subjects suffering from Alzheimer's disease.

Anti-oxidative and Neuroprotective Activities of Pig Skin Gelatin Hydrolysates (돈피젤라틴 효소분해물의 항산화 활성 및 신경세포보호효과)

  • Kim, Dong Wook;Park, Kimoon;Ha, Goeun;Jung, Ju Ri;Chang, Ounki;Ham, Jun-Sang;Jeong, Seok-Geun;Park, Beom-Young;Song, Jin;Jang, Aera
    • Food Science of Animal Resources
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    • v.33 no.2
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    • pp.258-267
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    • 2013
  • This study was conducted to determine the antioxidative and neuroprotective effect of pig skin extracts (PS) and pig skin gelatin hydrolysates (LPS) using a human neuroblastoma cell line (SH-SY5Y). The extraction yield of PS was 3 fold higher than that of LPS. The protein content of PS was about 10 fold higher than that of LPS (p<0.05). Also LPS increased antioxidative activity dose dependently, and the activity was significantly higher than PS at all concentration (p<0.05). DPPH radical scavenging activity of LPS at 50 mg/mL was 92.97%, which was similar to $1{\mu}M$ vitamin C as a positive control. ABTS radical scavenging activity of LPS (20 mg/mL) was 89.83% and oxygen radical absorbance capacity of LPS at 1 mg/mL was $141.39{\mu}M$ Trolox Equvalent/g. No significant change of human neuroblastoma cells was determined by MTT test. Cell death by oxidative stress induced by $H_2O_2$ and amyloid beta 1-42 ($A{\beta}_{1-42}$) was protected by LPS rather than PS. Acetylcholine esterase was significantly inhibited, by up to 33.62% by LPS at 10 mg/mL. Therefore, these results suggest that pig skin gelatin hydrolysates below 3 kDa have potential to be used as anti-oxidative and neuroprotective functional additives in the food industry, while further animal test should be determined in the future.

Double-processed ginseng berry extracts enhance learning and memory in an Aβ42-induced Alzheimer's mouse model (Aβ42로 유도된 알츠하이머 마우스 모델에서 이중 가공 인삼열매 추출물의 학습 및 기억 손실 개선 효과)

  • Jang, Su Kil;Ahn, Jeong Won;Jo, Boram;Kim, Hyun Soo;Kim, Seo Jin;Sung, Eun Ah;Lee, Do Ik;Park, Hee Yong;Jin, Duk Hee;Joo, Seong Soo
    • Korean Journal of Food Science and Technology
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    • v.51 no.2
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    • pp.160-168
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    • 2019
  • This study aimed to determine whether double-processed ginseng berry extract (PGBC) could improve learning and memory in an $A\hat{a}42$-induced Alzheimer's mouse model. Passive avoidance test (PAT) and Morris water-maze test (MWMT) were performed after mice were treated with PGBC, followed by acetylcholine (ACh) measurement and glial fibrillary acidic protein (GFAP) detection for brain damage. Furthermore, acetylcholinesterase (AChE) activity and choline acetyltransferase (ChAT) expression were analyzed using Ellman's and qPCR assays, respectively. Results demonstrated that PGBC contained a high amount of ginsenosides (Re, Rd, and Rg3), which are responsible for the clearance of $A{\hat{a}} 42$. They also helped to significantly improve PAT and MWMT performance in the $A{\hat{a}} 42-induced$ Alzheimer's mouse model when compared to the normal group. Interestingly, ACh and ChAT were remarkably upregulated and AChE activities were significantly inhibited, suggesting PGBC to be a palliative adjuvant for treating Alzheimer's disease. Altogether, PGBC was found to play a positive role in improving cognitive abilities. Thus, it could be a new alternative solution for alleviating Alzheimer's disease symptoms.

Bioactive compounds in food for age-associated cognitive decline: A systematic review (인지기능 개선을 위한 식품유래 생리활성소재에 대한 체계적 문헌고찰)

  • Kang, Eun Young;Cui, Fengjiao;Kim, Hyun Kyung;Go, Gwang-woong
    • Korean Journal of Food Science and Technology
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    • v.53 no.3
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    • pp.278-289
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    • 2021
  • The rapid aging of society has led to a surge in cognitive dysfunction in the elderly. As there is limited evidence for the development of dementia in medicine, a shift in focus on prevention strategies using bioactive compounds in food is required. This systematic review evaluated the effects of various bioactive compounds on age-associated cognitive decline. The literature was searched for terms related to bioactive compounds in cognitive decline and article selection was limited to clinical randomized controlled trials for a single bioactive compound. We identified 21 studies that evaluated the strength of the evidence. ω-3 fatty acids and vitamin B presented a strong evidence level, whereas vitamin D and E, anserine/carnosine, and chromium were defined as having moderate levels of evidence. ω-3 fatty acids relieved cognitive decline and reduced amyloid β-related protein accumulation. Vitamin B decreased homocysteine levels, which is accompanied by alleviation of cognitive function. In conclusion, ω-3 and vitamin B have the potential to improve age-associated cognitive decline.