Synthetic amyloid beta does not induce a robust transcriptional response in innate immune cell culture systems.

ABSTRACT:

Background

Alzheimer's disease (AD) is a progressive neurodegenerative disease that impacts nearly 400 million people worldwide. The accumulation of amyloid beta (Aβ) in the brain has historically been associated with AD, and recent evidence suggests that neuroinflammation plays a central role in its origin and progression. These observations have given rise to the theory that Aβ is the primary trigger of AD, and induces proinflammatory activation of immune brain cells (i.e., microglia), which culminates in neuronal damage and cognitive decline. To test this hypothesis, many in vitro systems have been established to study Aβ-mediated activation of innate immune cells. Nevertheless, the transcriptional resemblance of these models to the microglia in the AD brain has never been compr

SUBMITTER: Quiroga IY 

PROVIDER: S-EPMC9034485 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature