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Titlebook: Alzheimer Disease; Therapeutic Strategi Ezio Giacobini (Chairman of Pharmacology),Robert E Conference proceedings 1994 Springer Science+Bus

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發(fā)表于 2025-3-21 19:34:34 | 只看該作者 |倒序?yàn)g覽 |閱讀模式
期刊全稱Alzheimer Disease
期刊簡(jiǎn)稱Therapeutic Strategi
影響因子2023Ezio Giacobini (Chairman of Pharmacology),Robert E
視頻videohttp://file.papertrans.cn/155/154252/154252.mp4
學(xué)科分類Advances in Alzheimer Disease Therapy
圖書封面Titlebook: Alzheimer Disease; Therapeutic Strategi Ezio Giacobini (Chairman of Pharmacology),Robert E Conference proceedings 1994 Springer Science+Bus
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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書目名稱Alzheimer Disease影響因子(影響力)




書目名稱Alzheimer Disease影響因子(影響力)學(xué)科排名




書目名稱Alzheimer Disease網(wǎng)絡(luò)公開(kāi)度




書目名稱Alzheimer Disease網(wǎng)絡(luò)公開(kāi)度學(xué)科排名




書目名稱Alzheimer Disease被引頻次




書目名稱Alzheimer Disease被引頻次學(xué)科排名




書目名稱Alzheimer Disease年度引用




書目名稱Alzheimer Disease年度引用學(xué)科排名




書目名稱Alzheimer Disease讀者反饋




書目名稱Alzheimer Disease讀者反饋學(xué)科排名




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Modulating Cholinergic Neurotransmission Through Transgenic Overexpression of Human Cholinesterasescholinergic synapses of . tadpoles and mice. Cholinesterase over-expression should create a local deficit of acetylcholine at the “engineered” synapses and initiate feedback responses from which one may learn about the role of cholinergic neurotransmission in regulating synaptic structure and function.
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Die Bankkalkulation in der Praxischolinergic synapses of . tadpoles and mice. Cholinesterase over-expression should create a local deficit of acetylcholine at the “engineered” synapses and initiate feedback responses from which one may learn about the role of cholinergic neurotransmission in regulating synaptic structure and function.
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https://doi.org/10.1007/978-3-322-98662-7 of ACh (Quinn, 1987). A second, ‘peripheral’ anionic site is so named since it is distant from the active site (Taylor and Lappi, 1975). Bisquaternary AChE inhibitors derive their enhanced potency, relative to homologous monoquatemary ligands (Main, 1976), from their ability to span these two `anionic’ sites, which are .. 14 à apart.
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Conference proceedings 1994 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 unde
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ay 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 critic
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