In vitro S100A9 forms neurotoxic linear and annular amyloids resembling Aβ protofilaments. S100A9 was observed in some hippocampal and cortical neurons in TBI, AD and non-demented aging. They may serve as precursor-plaques for AD, implicating TBI as an AD risk factor. In traumatic brain injury (TBI) S100A9 itself rapidly forms amyloid plaques, which were reactive with oligomer-specific antibodies, but not with Aβ and amyloid fibrillar antibodies. Due to its inherent amyloidogenicity S100A9 contributes to amyloid plaque formation together with Aβ. ![]() Here, we provide insights into S100A9 specific mechanisms of action in Alzheimer’s disease (AD). Pro-inflammatory S100A9 protein is increasingly recognized as an important contributor to inflammation-related neurodegeneration.
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