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Your search keyword '"Du, Yan"' showing total 4 results
Start Over Author "Du, Yan" Topic alcohol dehydrogenase Topic alzheimer's disease
4 results on '"Du, Yan"'

1. Ovariectomy increases neuronal amyloid-β binding alcohol dehydrogenase level in the mouse hippocampus

Author

Kiyofumi Yamada, Shi Du Yan, Kazuhiro Takuma, Masaki Inoue, Y. Himeno, Emiko Fukuzaki, Daisuke Ibi, Bin Gu, Hiroyuki Mizoguchi, Yoko Funatsu, Koji Koike, and Yuko Kitahara

Subjects
medicine.medical_specialty, medicine.drug_class, Ovariectomy, Blotting, Western, Receptor for Advanced Glycation End Products, Central nervous system, Nerve Tissue Proteins, Biology, Hippocampal formation, Hippocampus, Article, Mice, Cellular and Molecular Neuroscience, Internal medicine, Glial Fibrillary Acidic Protein, medicine, Animals, Receptors, Immunologic, Receptor, Neurons, Mice, Inbred ICR, Amyloid beta-Peptides, Estradiol, Alcohol Dehydrogenase, Nuclear Proteins, Cell Biology, medicine.disease, DNA-Binding Proteins, Menopause, medicine.anatomical_structure, Endocrinology, Estrogen, Astrocytes, Ovariectomized rat, Female, Alzheimer's disease, Hormone
Abstract

Ovarian hormone decline after menopause may influence cognitive performance and increase the risk for Alzheimer's disease (AD) in women. Amyloid-beta peptide (Abeta) has been proposed to be the primary cause of AD. In this study, we examined whether ovariectomy (OVX) could affect the levels of cofactors Abeta-binding alcohol dehydrogenase (ABAD) and receptor for advanced glycation endproducts (RAGE), which have been reported to potentiate Abeta-mediated neuronal perturbation, in mouse hippocampus, correlating with estrogen and Abeta levels. Female ICR mice were randomly divided into ovariectomized or sham-operated groups, and biochemical analyses were carried out at 5 weeks after the operation. OVX for 5 weeks significantly decreased hippocampal 17beta-estradiol level, while it tended to reduce the hormone level in serum, compared with the sham-operated control. In contrast, OVX did not affect hippocampal Abeta(1-40) level, although it significantly increased serum Abeta(1-40) level. Furthermore, we demonstrated that OVX increased hippocampal ABAD level in neurons, but not astrocytes, while it did not affect RAGE level. These findings suggest that the expression of neuronal ABAD depends on estrogen level in the hippocampus and the increase in serum Abeta and hippocampal ABAD induced by ovarian hormone decline may be associated with pre-stage of memory deficit in postmenopausal women and Abeta-mediated AD pathology.

Published
2008

2. Endophilin I Expression Is Increased in the Brains of Alzheimer Disease Patients

Author

Shi Du Yan, Jim Aiton, John Xi Chen, Fleur Davey, Margaret Taylor, Jun Yao, Fang Fang, Frank J. Gunn-Moore, Peter J. Coote, Doris Chen, Hongwei Xu, and Yimin Ren

Subjects
Genetically modified mouse, medicine.medical_specialty, Amyloid, Transgene, Mice, Transgenic, Biology, Biochemistry, Mice, Alzheimer Disease, Memory, Internal medicine, medicine, Animals, Humans, Binding site, Molecular Biology, Alcohol dehydrogenase, Neurons, Amyloid beta-Peptides, Cell Death, Kinase, Alcohol Dehydrogenase, JNK Mitogen-Activated Protein Kinases, Brain, Cell Biology, medicine.disease, Endocrinology, biology.protein, Alzheimer's disease, Acyltransferases, Biomarkers, Intracellular, Protein Binding
Abstract

Alzheimer patients have increased levels of both the 42 amyloid-beta-peptide (Abeta) and the amyloid binding alcohol dehydrogenase (ABAD), which is an intracellular binding site for Abeta. The overexpression of Abeta and ABAD in transgenic mice has shown that the binding of Abeta to ABAD results in amplified neuronal stress and impairment of learning and memory. From a proteomic analysis of the brains from these animals, we have identified for the first time that the protein endophilin I increases in Alzheimer diseased brain. The increase in endophilin I levels in neurons is linked to an increase in the activation of the stress kinase c-Jun N-terminal kinase with the subsequent death of the neurons. We also demonstrate in living animals that the expression level of endophilin I is an indicator for the interaction of ABAD and Abeta as its expression levels return to normal if this interaction is perturbed. Therefore this identifies endophilin I as a new indicator of the progression of Alzheimer disease.

Published
2008

3. Collapsin response mediator protein-2 hyperphosphorylation is an early event in Alzheimer’s disease progression.

Author

Cole, Adam R., Noble, Wendy, Aalten, Lidy van, Plattner, Florian, Meimaridou, Rena, Hogan, Dale, Taylor, Margaret, LaFrancois, John, Gunn-Moore, Frank, Verkhratsky, Alex, Oddo, Salvatore, LaFerla, Frank, Giese, K. Peter, Dineley, Kelly T., Duff, Karen, Richardson, Jill C., Shi Du Yan, Hanger, Diane P., Allan, Stuart M., and Sutherland, Calum

Subjects
ALCOHOL dehydrogenase, HIPPOCAMPUS (Brain), ALZHEIMER'S disease, PHOSPHORYLATION, NEURONS, SEA horses
Abstract

Collapsin response mediator protein 2 (CRMP2) is an abundant brain-enriched protein that can regulate microtubule assembly in neurons. This function of CRMP2 is regulated by phosphorylation by glycogen synthase kinase 3 (GSK3) and cyclin-dependent kinase 5 (Cdk5). Here, using novel phosphospecific antibodies, we demonstrate that phosphorylation of CRMP2 at Ser522 (Cdk5-mediated) is increased in Alzheimer’s disease (AD) brain, while CRMP2 expression and phosphorylation of the closely related isoform CRMP4 are not altered. In addition, CRMP2 phosphorylation at the Cdk5 and GSK3 sites is increased in cortex and hippocampus of the triple transgenic mouse [presenilin-1 (PS1)M146VKI; Thy1.2-amyloid precursor protein (APP)swe; Thy1.2tauP301L] that develops AD-like plaques and tangles, as well as the double (PS1M146VKI; Thy1.2-APPswe) transgenic mouse. The hyperphosphorylation is similar in magnitude to that in human AD and is evident by 2 months of age, ahead of plaque or tangle formation. Meanwhile, there is no change in CRMP2 phosphorylation in two other transgenic mouse lines that display elevated amyloid β peptide levels (Tg2576 and APP/amyloid β-binding alcohol dehydrogenase). Similarly, CRMP2 phosphorylation is normal in hippocampus and cortex of Tau(P301L) mice that develop tangles but not plaques. These observations implicate hyperphosphorylation of CRMP2 as an early event in the development of AD and suggest that it can be induced by a severe APP over-expression and/or processing defect. [ABSTRACT FROM AUTHOR]

Published
2007
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4. Endophilin I Expression Is Increased in the Brains of Alzheimer Disease Patients.

Author

Yimin Ren, Hong Wei Xu, Fleur Davey, Taylor, Margaret, Aiton, Jim, Coote, Peter, Fang Fang, Jun Yao, Chen, Doris, John Xi Chen, Shi Du Yan, and Gunn-Moore, Frank J.

Subjects
*ALZHEIMER'S disease, *PROTEINS, *AMYLOID, *ALCOHOL dehydrogenase, *BINDING sites, *PROTEOMICS
Abstract

Alzheimer patients have increased levels of both the 42 amyloid-β-peptide (Aβ) and the amyloid binding alcohol dehydrogenase (ABAD), which is an intracellular binding site for Aβ. The overexpression of A and ABAD in transgenic mice has shown that the binding of Aβ to ABAD results in amplified neuronal stress and impairment of learning and memory. From a proteomic analysis of the brains from these animals, we have identified for the first time that the protein endophilin I increases in Alzheimer diseased brain. The increase in endophilin I levels in neurons is linked to an increase in the activation of the stress kinase c-Jun N-terminal kinase with the subsequent death of the neurons. We also demonstrate in living animals that the expression level of endophilin I is an indicator for the interaction of ABAD and Aβ as its expression levels return to normal if this interaction is perturbed. Therefore this identifies endophilin I as a new indicator of the progression of Alzheimer disease. [ABSTRACT FROM AUTHOR]

Published
2008
Full Text
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