Imagine your bloodstream as a bustling highway, with red blood cells (RBCs) zooming around to deliver essential cargo. Well, it turns out that RBCs can also act as transporters for a protein called α-Synuclein, which has been linked to Parkinson’s disease. In a recent study, scientists injected artificial forms of α-Synuclein into mice and observed how it spread throughout the bloodstream. They found that while the levels of α-Synuclein in the plasma initially increased and then stabilized, the levels in RBCs continued to rise steadily. Not only did the RBCs accumulate α-Synuclein, but they also actively took it up and enriched themselves with this troublesome protein. The researchers discovered that this process relies on receptor-dependent endocytosis, which is like RBCs having special docking stations to pick up their cargo. To prove their point, they used inhibitors of this process and effectively halted the uptake of α-Synuclein by RBCs. This intriguing study provides valuable insights into how Parkinson’s-related proteins can be transported and detected within RBCs, opening new possibilities for diagnosing and understanding synucleinopathies. If you’re eager to dive deeper into this research, check out the full article!
Detection of oligomeric α-synuclein (o-α-Syn) in red blood cells (RBCs) has been shown to be promising in diagnosing Parkinson’s disease and other synucleinopathies. However, if RBC o-α-Syn derive from plasma and can reflect changes of plasma o-α-Syn remains unclear. In this study, synthetic o-α-Syn was intravenously injected into mice and dynamic changes in plasma and RBC o-α-Syn levels were investigated. Injection of o-α-Syn induced a temporary increase in plasma o-α-Syn levels, which then decreased to a relatively stable level. In contrast, levels of RBC o-α-Syn increased steadily and significantly. Besides, α-Syn-immunoreactive particles were observed in RBCs of the injected mice, suggesting that RBCs can actively take up and enrich o-α-Syn from plasma. Moreover, incubation of o-α-Syn with isolated RBCs at concentrations lower than those of endogenous o-α-Syn led to a time- and concentration-dependent o-α-Syn elevation in RBCs, which was impaired by lowering the temperature and treatment with proteinase K. The o-α-Syn accumulation in RBCs was also inhibited by specific inhibitors of receptor-dependent endocytosis, including dynamin- and clathrin-dependent endocytosis. The above results suggest that plasma o-α-Syn can be actively transported into RBCs via receptor-dependent endocytic pathways.
Dr. David Lowemann, M.Sc, Ph.D., is a co-founder of the Institute for the Future of Human Potential, where he leads the charge in pioneering Self-Enhancement Science for the Success of Society. With a keen interest in exploring the untapped potential of the human mind, Dr. Lowemann has dedicated his career to pushing the boundaries of human capabilities and understanding.
Armed with a Master of Science degree and a Ph.D. in his field, Dr. Lowemann has consistently been at the forefront of research and innovation, delving into ways to optimize human performance, cognition, and overall well-being. His work at the Institute revolves around a profound commitment to harnessing cutting-edge science and technology to help individuals lead more fulfilling and intelligent lives.
Dr. Lowemann’s influence extends to the educational platform BetterSmarter.me, where he shares his insights, findings, and personal development strategies with a broader audience. His ongoing mission is shaping the way we perceive and leverage the vast capacities of the human mind, offering invaluable contributions to society’s overall success and collective well-being.