Glycosaminoglycans from Litopenaeus vannamei Inhibit the Alzheimer's Disease β Secretase, BACE1

Only palliative therapeutic options exist for the treatment of Alzheimer's Disease; no new successful drug candidates have been developed in over 15 years. The widely used clinical anticoagulant heparin has been reported to exert beneficial effects through multiple pathophysiological pathways involved in the aetiology of Alzheimer's Disease, for example, amyloid peptide production and clearance, tau phosphorylation, inflammation and oxidative stress. Despite the therapeutic potential of heparin as a multi-target drug for Alzheimer's disease, the repurposing of pharmaceutical heparin is proscribed owing to the potent anticoagulant activity of this drug. Here, a heterogenous non-anticoagulant glycosaminoglycan extract, obtained from the shrimp Litopenaeus vannamei, was found to inhibit the key neuronal beta-secretase, BACE1, displaying a more favorable therapeutic ratio compared to pharmaceutical heparin when anticoagulant activity is considered.

Automated summary

Currently, there are only palliative therapeutic options for Alzheimer's Disease with no successful new drug candidates developed in over 15 years. Heparin has potential therapeutic effects on Alzheimer's Disease, but its repurposing is limited due to its strong anticoagulant activity. A non-anticoagulant glycosaminoglycan extract from shrimp was found to inhibit the key neuronal beta-secretase BACE1, showing a more favorable therapeutic ratio compared to pharmaceutical heparin.