Cathepsin B plays a critical role in inducing Alzheimer’s Disease-like phenotypes following chronic systemic exposure to lipopolysaccharide from Porphyromonas gingivalis in mice

Highlights • Systemic exposure to LPS from Porphyromonas gingivalis induces AD-like phenotypes. • Cathepsin B is critical for inducing microglia-mediated neuroinflammation. • Cathepsin B is critical for inducing microglia-dependent Aβ accumulation in neurons.

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 2017-10, Vol.65, p.350-361
Main Authors: Wu, Zhou, Ni, Junjun, Liu, Yicong, Teeling, Jessica L, Takayama, Fumiko, Collcutt, Alex, Ibbett, Paul, Nakanishi, Hiroshi
Format: Article
Language:English
Subjects:
Allergy and Immunology
Alzheimer Disease - chemically induced
Alzheimer’s disease
Amyloid beta-Peptides - metabolism
Amyloid beta-Protein Precursor - genetics
Animals
Cathepsin B
Cathepsin B - metabolism
Cathepsin B - pharmacology
Disease Models, Animal
Hippocampus - metabolism
Intracellular amyloid beta accumulation
Lipopolysaccharide from Porphyromonas gingivalis
Lipopolysaccharides - adverse effects
Memory - drug effects
Memory Disorders - metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Microglia
Microglia - drug effects
Middle age
Neuroimmunomodulation - drug effects
Neuroinflammation
Neurons - metabolism
Phenotype
Plaque, Amyloid - metabolism
Porphyromonas gingivalis - pathogenicity
Psychiatry
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Description
Summary:Highlights • Systemic exposure to LPS from Porphyromonas gingivalis induces AD-like phenotypes. • Cathepsin B is critical for inducing microglia-mediated neuroinflammation. • Cathepsin B is critical for inducing microglia-dependent Aβ accumulation in neurons.
ISSN:0889-1591
1090-2139
DOI:10.1016/j.bbi.2017.06.002