期刊全稱 | Alzheimer Disease | 期刊簡(jiǎn)稱 | Therapeutic Strategi | 影響因子2023 | Ezio Giacobini (Chairman of Pharmacology),Robert E | 視頻video | http://file.papertrans.cn/155/154252/154252.mp4 | 學(xué)科分類 | Advances in Alzheimer Disease Therapy | 圖書封面 |  | 影響因子 | Since the apoE4 allele is a risk factor or susceptibility gene in late-onset familial and sporadic AD, the mechanism of disease expression may involve metabolic effects that are isoform specific. Isoform-specific interactions of apoE therefore become critical in the mechanism of AD pathogenesis. Detailed characterization of the binding of the apoE isoforms with proteins and peptides relevant to the pathology of the disease may be critical in understanding disease pathogenesis. These critical isoform-specific interactions of apoE may involve interactions with proteins and pep tides in the defining neuropathologic lesions of the disease, the neurofibrillary tangle and senile plaque. Other possible critical isoform-specific interactions include the mechanism of internalization, intracellular trafficking, and subsequent metabolism. In addition, differential post-translational modifications of apoE isoforms may determine differences in metabolism contributing to the pathogenesis of the disease. Oxidation of apoE may confer several isoform-specific, biochemically distinct properties. Since {3A peptide binds apoE in the lipoprotein binding domain of the protein and not in the receptor-bin | Pindex | Conference proceedings 1994 |
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