Researchers Discover New Insights Into Neuroinflammation in Alzheimer’s Disease

Researchers Discover New Insights Into Neuroinflammation in Alzheimer’s Disease
In a recent study published in the Journal of Neuroinflammation, researchers from China were able to identify a new target to address the Neuroinflammation found in patients with Alzheimer’s disease. Neuroinflammation, characterized by excessive glial activation and overproduction of proinflammatory cytokine and chemokines, plays a critical role in the pathogenesis of neurodegeneration in Alzheimer’s disease (AD). Inhibition of glial activation is shown to improve synaptic dysfunction and behavioral deficits in AD animal models. Amyloid-β (Aβ) peptides are key molecules in AD pathology as they aggregate to form amyloid plaques, the primary neuropathological hallmarks of AD. Aggregated Aβ peptides, in the forms of fibrils and oligomers, are prominent triggers for microglial activation. Accumulating evidence demonstrates that the redox-active Cu(II) ions can be coordinated with other molecules leading to formation of the Cu(II)-Aβ complex. The concentration of extracellular Cu(II), especially within the amyloid plaques, is markedly elevated in the brains of patients with AD. The transcription factor nuclear factor (NF)-κB has been identified as a key regulator of cellular immune responses, including microglial activation. NF-κB activation can be directly driven by reactive oxygen species (ROS). ROS, derived from NADPH oxidase (NOX) or mitochondria, play important roles in regulating microglial responses to various stimuli. With the aim of determining if whether Cu(II) coordination is able to enhance the effect of Aβ
Subscribe or to access all post and page content.

Leave a Comment

Your email address will not be published. Required fields are marked *