Amyloid Beta Peptide Is Released during Thrombosis in the Skin

While it is known that amyloid beta (A) deposits are found in different tissues of both Alzheimer's disease (AD) patients and healthy individuals, there remain questions about the physiological role of these deposits, the origin of the A peptide, and the mechanisms of its localization to the tissues. Using immunostaining with specific antibodies, as well as enzyme-linked immunosorbent assay, this study demonstrated A40 peptide accumulation in the skin during local experimental photothrombosis in mice. Specifically, A peptide accumulation was concentrated near the dermal blood vessels in thrombotic skin. It was also studied whether the released peptide affects microorganisms. Application of A40 (4 mu M) to the external membrane of yeast cells significantly increased membrane conductance with no visible effect on mouse host cells. The results suggest that A release in the skin is related to skin injury and thrombosis, and occurs along with clotting whenever skin is damaged. These results support the proposition that A release during thrombosis serves as part of a natural defense against infection.