Title |
Protective properties of lysozyme on β-amyloid pathology: implications for Alzheimer disease
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Published in |
Neurobiology of Disease, September 2015
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DOI | 10.1016/j.nbd.2015.08.024 |
Pubmed ID | |
Authors |
Linda Helmfors, Andrea Boman, Livia Civitelli, Sangeeta Nath, Linnea Sandin, Camilla Janefjord, Heather McCann, Henrik Zetterberg, Kaj Blennow, Glenda Halliday, Ann-Christin Brorsson, Katarina Kågedal |
Abstract |
The hallmarks of Alzheimer disease are amyloid-β plaques and neurofibrillary tangles accompanied by signs of neuroinflammation. Lysozyme is a major player in the innate immune system and has recently been shown to prevent the aggregation of amyloid-β1-40in vitro. In this study we found that patients with Alzheimer disease have increased lysozyme levels in the cerebrospinal fluid and lysozyme co-localized with amyloid-β in plaques. In Drosophila neuronal co-expression of lysozyme and amyloid-β1-42 reduced the formation of soluble and insoluble amyloid-β species, prolonged survival and improved the activity of amyloid-β1-42 transgenic flies. This suggests that lysozyme levels rise in Alzheimer disease as a compensatory response to amyloid-β increases and aggregation. In support of this, in vitro aggregation assays revealed that lysozyme associates with amyloid-β1-42 and alters its aggregation pathway to counteract the formation of toxic amyloid-β species. Overall, these studies establish a protective role for lysozyme against amyloid-β associated toxicities and identify increased lysozyme in patients with Alzheimer disease. Therefore, lysozyme has potential as a new biomarker as well as a therapeutic target for Alzheimer disease. |
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