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Altered apolipoprotein E glycosylation is associated with Abeta(42) accumulation in an animal model of Niemann-Pick Type C disease.
J Neurochem 2010; 112(6):1619-26JN

Abstract

Neurodegeneration is the final cause of death in Niemann-Pick Type C (NPC) disease, a cholesterol-storage disorder. Accumulating evidence indicates that NPC may share common pathological mechanisms with Alzheimer's disease, including the link between aberrant cholesterol metabolism and amyloid-beta (Abeta) deposition. Apolipoprotein E (apoE) is highly expressed in the brain and plays a pivotal role in cholesterol metabolism. ApoE can also modulate Abeta production and clearance, and it is a major genetic risk factor for Alzheimer's disease. Although apoE is glycosylated, the functional significance of this chemical alteration on Abeta catabolism is unclear. In this study using an NPC animal model, we detect specific changes in apoE glycosylation that correlate with increased Abeta(42) accumulation prior to the appearance of neurological abnormalities. This suggests that increased apoE expression could be a compensatory response to the increased Abeta(42) deposition in NPC(nih) mice. We also observe what appears to be a simplification of the glycosylation process on apoE during neurodegeneration.

Authors+Show Affiliations

Department of Physiology and National University Medical Institutes, Yong Loo Lin School of Medicine, and Neurobiology Programme, Life Science Institute, National University of Singapore, Singapore.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20070866

Citation

Chua, Ching-Ching, et al. "Altered Apolipoprotein E Glycosylation Is Associated With Abeta(42) Accumulation in an Animal Model of Niemann-Pick Type C Disease." Journal of Neurochemistry, vol. 112, no. 6, 2010, pp. 1619-26.
Chua CC, Lim ML, Wong BS. Altered apolipoprotein E glycosylation is associated with Abeta(42) accumulation in an animal model of Niemann-Pick Type C disease. J Neurochem. 2010;112(6):1619-26.
Chua, C. C., Lim, M. L., & Wong, B. S. (2010). Altered apolipoprotein E glycosylation is associated with Abeta(42) accumulation in an animal model of Niemann-Pick Type C disease. Journal of Neurochemistry, 112(6), pp. 1619-26. doi:10.1111/j.1471-4159.2010.06586.x.
Chua CC, Lim ML, Wong BS. Altered Apolipoprotein E Glycosylation Is Associated With Abeta(42) Accumulation in an Animal Model of Niemann-Pick Type C Disease. J Neurochem. 2010;112(6):1619-26. PubMed PMID: 20070866.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Altered apolipoprotein E glycosylation is associated with Abeta(42) accumulation in an animal model of Niemann-Pick Type C disease. AU - Chua,Ching-Ching, AU - Lim,Mei-Li, AU - Wong,Boon-Seng, Y1 - 2010/01/13/ PY - 2010/1/15/entrez PY - 2010/1/15/pubmed PY - 2010/5/1/medline SP - 1619 EP - 26 JF - Journal of neurochemistry JO - J. Neurochem. VL - 112 IS - 6 N2 - Neurodegeneration is the final cause of death in Niemann-Pick Type C (NPC) disease, a cholesterol-storage disorder. Accumulating evidence indicates that NPC may share common pathological mechanisms with Alzheimer's disease, including the link between aberrant cholesterol metabolism and amyloid-beta (Abeta) deposition. Apolipoprotein E (apoE) is highly expressed in the brain and plays a pivotal role in cholesterol metabolism. ApoE can also modulate Abeta production and clearance, and it is a major genetic risk factor for Alzheimer's disease. Although apoE is glycosylated, the functional significance of this chemical alteration on Abeta catabolism is unclear. In this study using an NPC animal model, we detect specific changes in apoE glycosylation that correlate with increased Abeta(42) accumulation prior to the appearance of neurological abnormalities. This suggests that increased apoE expression could be a compensatory response to the increased Abeta(42) deposition in NPC(nih) mice. We also observe what appears to be a simplification of the glycosylation process on apoE during neurodegeneration. SN - 1471-4159 UR - https://www.unboundmedicine.com/medline/citation/20070866/Altered_apolipoprotein_E_glycosylation_is_associated_with_Abeta_42__accumulation_in_an_animal_model_of_Niemann_Pick_Type_C_disease_ L2 - https://doi.org/10.1111/j.1471-4159.2010.06586.x DB - PRIME DP - Unbound Medicine ER -