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PMID |
Sentence |
1 |
10362543
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Presenilin 2 was identified in primitive islet and duct cells of human foetal pancreas and in proliferating exocrine duct cells in human pancreatitis but not found in islet amyloid deposits in Type 2 diabetic subjects.
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2 |
10362543
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Oral glucose tolerance tests on subjects with the presenilin 2 Met239Val mutation unaffected by early onset familial Alzheimer's disease (mean age 35 years) and on their first-degree relatives without the mutation demonstrated no evidence of glucose intolerance or increased proinsulin secretion.
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3 |
10362543
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Presenilin 2 was identified in primitive islet and duct cells of human foetal pancreas and in proliferating exocrine duct cells in human pancreatitis but not found in islet amyloid deposits in Type 2 diabetic subjects.
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4 |
10362543
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Oral glucose tolerance tests on subjects with the presenilin 2 Met239Val mutation unaffected by early onset familial Alzheimer's disease (mean age 35 years) and on their first-degree relatives without the mutation demonstrated no evidence of glucose intolerance or increased proinsulin secretion.
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5 |
12522107
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Trefoil peptides as proangiogenic factors in vivo and in vitro: implication of cyclooxygenase-2 and EGF receptor signaling.
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6 |
12522107
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Angiogenic activity of TFFs is comparable to that induced by vascular endothelial growth factor, leptin, and transforming growth factor-alpha.
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7 |
12522107
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Stimulation of angiogenesis by pS2 in the CAM assay is blocked by pharmacological inhibitors of cyclooxygenase COX-2 (NS-398) and epidermal growth factor receptor (EGF-R) tyrosine kinase (ZD1839), but is independent of KDR/Flk-1 and thromboxane A2 receptors.
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8 |
12522107
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In contrast, the morphogenic switch induced by pS2 in HUVEC cells could be inhibited by the specific KDR heptapeptide antagonist ATWLPPR and by inhibitors of COX-2 and EGF-R signaling.
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9 |
14503010
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In addition, the genomic profiles of patients with dementia integrating AD-related genes (APOE, PS1, PS2, cFOS) in a mini-tetragenic haplotype significantly differ from controls with an absolute genetic variation of about 50%-60%.
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10 |
18332245
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The genetics of Alzheimer disease (AD) to date support an age-dependent dichotomous model whereby earlier age of disease onset (< 60 years) is explained by 3 fully penetrant genes (APP [NCBI Entrez gene 351], PSEN1 [NCBI Entrez gene 5663], and PSEN2 [NCBI Entrez gene 5664]), whereas later age of disease onset (> or = 65 years) representing most cases of AD has yet to be explained by a purely genetic model.
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11 |
23091515
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Effects of Red Liriope platyphylla on NGF secretion ability, NGF receptor signaling pathway and γ-secretase components in NSE/hAPPsw transgenic mice expressing Alzheimer's Disease.
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12 |
23091515
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However, downstream effectors of the NGF receptor signaling pathway, including TrkA and p75(NTR) proteins, were suppressed in RLP-treated NSE/hAPPsw Tg mice.
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13 |
23091515
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Especially, Tg mice showed decreased levels of TrkA, p75(NTR), and RhoA expression.
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14 |
23091515
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Of the four components, the expression of APH-1 and Nicastrin (NCT) decreased in RLP-treated NSE/hAPPsw Tg mice, whereas expression of PS-2 and Pen-2 was maintained or increased within the same group.
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15 |
23919770
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The mutations in APP, PSEN1 and PSEN2 are inherited in a Mendelian fashion and directly lead to the EOAD, while recent genome-wide association studies have identified numbers of risky genes, which influences the susceptibility to LOAD.
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