1 results match your criteria: "USA and Hugo W. Moser Research Institute at Kennedy Krieger[Affiliation]"
Dendrimer-tesaglitazar conjugate induces a phenotype shift of microglia and enhances β-amyloid phagocytosis.
Nanoscale
January 2021
Center for Nanomedicine, Department of Ophthalmology, Wilmer Eye Institute Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA. and Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21218, USA and Hugo W. Moser Research Institute at Kennedy Krieger, Inc., Baltimore, MD 21205, USA.
Switching microglia from a disease exacerbating, 'pro-inflammatory' state into a neuroprotective, 'anti-inflammatory' phenotype is a promising strategy for addressing multiple neurodegenerative diseases. Pro-inflammatory microglia contribute to disease progression by releasing neurotoxic substances and accelerating pathogenic protein accumulation. PPARα and PPARγ agonists have both been shown to shift microglia from a pro-inflammatory ('M1-like') to an alternatively activated ('M2-like') phenotype.
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