National Academy of Sciences, Proceedings of the National Academy of Sciences, 41(115), 2018
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Significance We demonstrate that depletion of blood plasminogen is sufficient to protect against both innate immune cell activation in the brain and Alzheimer’s disease (AD) pathology in a mouse model of AD. This work provides a molecular mechanism for initiation of AD-related brain inflammation and for regulation of β-amyloid deposition, and could lead to therapeutic strategies in human AD patients, including the targeting of systemic molecules.