Abstract
While it is known that amyloid beta (Aβ) 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 Aβ 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 Aβ40 peptide accumulation in the skin during local experimental photothrombosis in mice. Specifically, Aβ peptide accumulation was concentrated near the dermal blood vessels in thrombotic skin. It was also studied whether the released peptide affects microorganisms. Application of Aβ40 (4 µM) to the external membrane of yeast cells significantly increased membrane conductance with no visible effect on mouse host cells. The results suggest that Aβ 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 Aβ release during thrombosis serves as part of a natural defense against infection.
Highlights
In 1906, Dr Alois Alzheimer showed that amyloid beta (Aβ) peptide is the major constituent of amyloid plaques in the brain, implicating these peptides in Alzheimer’s disease (AD) [1]
To study the distribution of Aβ peptide in skin after thrombosis, we applied a standard model of photo-induced coagulation to obtain thrombotic clots in skin blood vessels
Mice were injected intraperitoneally with the photoactivated dye Rose Bengal, and the bruised spot became visible after application of intense green laser light to the shaved skin
Summary
In 1906, Dr Alois Alzheimer showed that amyloid beta (Aβ) peptide is the major constituent of amyloid plaques in the brain, implicating these peptides in Alzheimer’s disease (AD) [1]. Aβ protein deposits in the skin were described many years ago, in and around the endothelium of dermal blood vessels in aged AD patients, and were proposed as a marker for this disease [8]. Skin accumulation of Aβ around blood vessels was found to be unrelated to the severity of symptoms in AD patients, occurring in some healthy subjects [9]. We showed that activated blood platelets aggregated in blood clots contribute to the accumulation of Aβ peptide in the brain: Aβ peptide was found in and around brain blood vessels in mice after thrombosis, as revealed by immunostaining, while in thrombocytopenic animals, this release was severely reduced [11]
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