On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications
Mikhail Inyushin, Astrid Zayas-Santiago, Legier Rojas and Lilia Kucheryavykh
As do many other immunity-related blood cells, platelets release antimicrobial peptides that kill bacteria, fungi, and even certain viruses. Here we review the literature suggesting that there is a similarity between the antimicrobials released by other blood cells and the amyloid-related Aβ peptide released by platelets. Analyzing the literature, we also propose that platelet-generated Aβ amyloidosis may be more common than currently recognized. This systemic Aβ from a platelet source may participate in various forms of amyloidosis in pathologies ranging from brain cancer, glaucoma, skin Aβ accumulation, and preeclampsia to Alzheimer’s disease and late-stage Parkinson’s disease. We also discuss the advantages and disadvantages of specific animal models for studying platelet-related Aβ. This field is undergoing rapid change, as it evaluates competing ideas in the light of new experimental observations. We summarized both in order to clarify the role of platelet-generated Aβ peptides in amyloidosis-related health disorders, which may be helpful to researchers interested in this growing area of investigation.
On the Role of Platelet-Generated Amyloid Beta Peptides in Certain Amyloidosis Health Complications
Platelet-generated amyloid beta peptides in Alzheimer’s disease and glaucoma
Inyushin M, Zayas-Santiago A, Rojas L, Kucheryavykh Y, Kucheryavykh L.
Abstract
Amyloid beta (Aβ) peptides have been implicated in both Alzheimer’s disease (AD) and glaucoma and have been shown to be the key etiological factor in these dangerous health complications. On the other hand, it is well known that Aβ peptide can be generated from its precursor protein and massively released from the blood to nearby tissue upon the activation of platelets due to their involvement in innate immunity and inflammation processes. Here we review evidence about the development of AD and glaucoma neuronal damage showing their dependence on platelet count and activation. The correlation between the effect on platelet count and the effectiveness of anti-AD and anti-glaucoma therapies suggest that platelets may be an important player in these diseases.
Aβ Peptide Originated from Platelets Promises New Strategy in Anti-Alzheimer’s Drug Development.
Inyushin MY, Sanabria P, Rojas L, Kucheryavykh Y, Kucheryavykh L
Abstract
The amyloid beta (Aβ) peptide and its deposits in the brain are known to be implicated in the neurodegeneration that occurs during Alzheimer’s disease (AD). Recently, alternative theories views concerning both the source of this peptide and its functions have been developed. It has been shown that, as in all other known types of amyloidosis, the production of Aβ originates in blood cells or cells related to blood plasma, from which it can then spread from the blood to inside the brain, with the greatest concentration around brain blood vessels. In this review, we summarize research progress in this new area and outline some future perspectives. While it is still unclear whether the main source of Aβ deposits in AD is the blood, the possibility of blocking the chain of reactions that lead to constant Aβ release from the blood to the brain may be exploited in an attempt to reduce the amyloid burden in AD. Solving the problem of Aβ accumulation in this way may provide an alternative strategy for developing anti-AD drugs.