The role of HS (heparan sulphate) in the pathology of AD (Alzheimer's disease) is multifaceted. HS and other glycosaminoglycans have been widely reported to be associated with neuritic plaques. HS has also been shown to promote the aggregation of Aβ (amyloid β-peptide), the proteinaceous component of neuritic plaques. Recently, we described a novel and contrasting role for HS in the pathology of AD: HS can inhibit the formation of Aβ, by directly interacting with the protease BACE1 (β-site amyloid precursor protein cleaving enzyme 1; β-secretase 1), that cleaves the amyloid precursor protein and is the rate limiting step in the generation of Aβ. Here, we review the current roles of HS and the potential for HS-derivatives in the treatment of AD.
Novel heparan sulphate analogues: inhibition of β-secretase cleavage of amyloid precursor protein
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S.J. Patey, E.A. Yates, J.E. Turnbull; Novel heparan sulphate analogues: inhibition of β-secretase cleavage of amyloid precursor protein. Biochem Soc Trans 26 October 2005; 33 (5): 1116–1118. doi: https://doi.org/10.1042/BST0331116
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