Session 1G: Amyloid beta oligomers (AβO) drive morphological shift in microglia in the 5XFAD Mouse Model for Alzheimer’s disease and in AβO-injected Simian Models
Session Number
Session 1G: 2nd Presentation
Advisor(s)
Drs. Maira Bicca, Kirsten Viola, and William Klein, Northwestern University
Location
Room A115
Start Date
26-4-2018 9:40 AM
End Date
26-4-2018 10:25 AM
Abstract
Neurodegeneration and cognitive impairment in Alzheimer’s disease (AD) are believed to be driven by the accumulation of the Aβ peptide and phosphorylated tau protein. Recent research suggests that in addition to Aβ peptide and phosphorylated tau deposition, neuroinflammation plays a pivotal role in Alzheimer’s disease dementia. Microglia are the resident macrophages of the brain’s immune system that are responsible for antigen presentation and inflammatory signaling. In the presence of soluble, neurotoxic forms of Aβ, known as Aβ oligomers, microglia have been hypothesized to be activated and differentiated into a more proinflammatory phenotype that drives deleterious AD neuroinflammation. Here, we confirm that microglia are functionally activated using Iba1 antibody immunofluorescent staining of activated microglia in the 5XFAD mouse model and in AβO injected monkey models. However, our results show that the relationship between microglia and Aβ oligomers is more complex than the literature shows, as Aβ oligomers induce morphological changes in microglia. Our analysis of various brain regions exhibits that these morphological changes are regionally specific, but all stimulate an increase in morphologies associated with deadly proinflammatory behavior at later ages in AD brain.
Session 1G: Amyloid beta oligomers (AβO) drive morphological shift in microglia in the 5XFAD Mouse Model for Alzheimer’s disease and in AβO-injected Simian Models
Room A115
Neurodegeneration and cognitive impairment in Alzheimer’s disease (AD) are believed to be driven by the accumulation of the Aβ peptide and phosphorylated tau protein. Recent research suggests that in addition to Aβ peptide and phosphorylated tau deposition, neuroinflammation plays a pivotal role in Alzheimer’s disease dementia. Microglia are the resident macrophages of the brain’s immune system that are responsible for antigen presentation and inflammatory signaling. In the presence of soluble, neurotoxic forms of Aβ, known as Aβ oligomers, microglia have been hypothesized to be activated and differentiated into a more proinflammatory phenotype that drives deleterious AD neuroinflammation. Here, we confirm that microglia are functionally activated using Iba1 antibody immunofluorescent staining of activated microglia in the 5XFAD mouse model and in AβO injected monkey models. However, our results show that the relationship between microglia and Aβ oligomers is more complex than the literature shows, as Aβ oligomers induce morphological changes in microglia. Our analysis of various brain regions exhibits that these morphological changes are regionally specific, but all stimulate an increase in morphologies associated with deadly proinflammatory behavior at later ages in AD brain.