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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2015.1
- 수록면
- 13 - 18 (6page)
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초록· 키워드
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Alzheimer's disease severely compromises cognitive function.
One of the mechanisms to explain the pathology of Alzheimer’sdisease has been the hypotheses of amyloid-pore/channel formationby complex Aβ-aggregates. Clinical studies suggestedthe moderate alcohol consumption can reduces probability developingneurodegenerative pathologies. A recent report exploredthe ability of ethanol to disrupt the generation of complexAβ in vitro and reduce the toxicity in two cell lines.
Molecular dynamics simulations were applied to understandhow ethanol blocks the aggregation of amyloid. On the otherhand, the in silico modeling showed ethanol effect over thedynamics assembling for complex Aβ-aggregates mediated bybreak the hydrosaline bridges between Asp 23 and Lys 28, wasare key element for amyloid dimerization. The amyloid pore/channel hypothesis has been explored only in neuronal models,however recently experiments suggested the frog oocytessuch an excellent model to explore the mechanism of the amyloidpore/channel hypothesis. So, the used of frog oocytes toexplored the mechanism of amyloid aggregates is new, mainlyfor amyloid/pore hypothesis. Therefore, this experimentalmodel is a powerful tool to explore the mechanism implicatesin the Alzheimer’s disease pathology and also suggests a modelto prevent the Alzheimer’s disease pathology.
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참고문헌 (24)
참고문헌 신청
Arispe N / 1994 / The ability of amyloid beta-protein [A beta P(1-40)] to form Ca2+ channels provides a mechanism for neuronal death in Alzheimer's disease / Ann N Y Acad Sc
Bell KF / 2006 / Altered synaptic function in Alzheimer's disease / Eur J Pharmacol 545 : 11 ~ 21
Bourin M / 2003 / Nicotinic receptors and Alzheimer's disease / Curr Med Res Opin 19 : 169 ~ 177
Clark EM / 1993 / Toxicity of beta-amyloid25-35 peptide in PC12 cells / Proc West Pharmacol Soc 36 : 273 ~ 276
Haass C / 2007 / Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide / Nat Rev Mol Cell Biol 8 : 101 ~ 112
Bell KF / 2006 / Altered synaptic function in Alzheimer's disease / Eur J Pharmacol 545 : 11 ~ 21
Bourin M / 2003 / Nicotinic receptors and Alzheimer's disease / Curr Med Res Opin 19 : 169 ~ 177
Clark EM / 1993 / Toxicity of beta-amyloid25-35 peptide in PC12 cells / Proc West Pharmacol Soc 36 : 273 ~ 276
Haass C / 2007 / Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide / Nat Rev Mol Cell Biol 8 : 101 ~ 112
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