Early intraneuronal amyloid triggers neuron-derived inflammatory signaling in APP transgenic rats and human brain.

ABSTRACT: Chronic inflammation during Alzheimer's disease (AD) is most often attributed to sustained microglial activation in response to amyloid-β (Aβ) plaque deposits and cell death. However, cytokine release and microgliosis are consistently observed in AD transgenic animal models devoid of such pathologies, bringing into question the underlying processes that may be at play during the earliest AD-related immune response. We propose that this plaque-independent inflammatory reaction originates from neurons burdened with increasing levels of soluble and oligomeric Aβ, which are known to be the most toxic amyloid species within the brain. Laser microdissected neurons extracted from preplaque amyloid precursor protein (APP) transgenic rats were found to produce a variety of potent immune factors, bo

SUBMITTER: Welikovitch LA 

PROVIDER: S-EPMC7104377 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature