Imagine the brain as a bustling city and the platelets as delivery trucks. In people with Parkinson’s disease, these platelets release Aβ1-42-containing extracellular vesicles (EVs) that can make their way to the brain. This study found that patients with Parkinson’s disease dementia had higher concentrations of these platelet-derived vesicles containing Aβ1-42 compared to healthy individuals. The ratio of Aβ1-42-containing vesicles to total vesicles was significantly higher in dementia patients than in non-dementia Parkinson’s patients and healthy controls, suggesting a potential role in cognitive decline. Furthermore, the change in this ratio over 14 months correlated with cognitive decline, indicating it may be a useful biomarker for tracking disease progression. By uncovering the role of these platelet-derived vesicles in cognitive decline, researchers are one step closer to understanding the mechanisms behind Parkinson’s disease dementia. Now, if you want to dive deeper into this exciting research, don’t forget to check out the full article!
BackgroundCortical amyloid deposition is a common observation in Parkinson’s disease dementia (PDD) patients. Aβ1-42 is linked to a more rapid progression of dementia. Platelets, which degranulate upon activation, are a primary source of Aβ. It has been repeatedly reported that peripheral extracellular vesicles (EVs) can partially reach the central nervous system. Thus, we speculate that activated platelet-derived Aβ1-42-containing EVs (PEV-Aβ1-42) play a crucial role in the cognitive decline of PD patients.MethodsThe study included 189 participants: 66 with non-dementia PD, 73 with PDD, and 50 healthy controls. All participants underwent blood collection and clinical assessments. Twenty PD patients underwent re-examination and repeated blood collection 14 months later. A nano-scale flow cytometry assay was used to detect PEVs and PEV-Aβ1-42 using fluorescence-labeled CD62P and Aβ1-42 antibodies.ResultsParkinson’s disease dementia patients had higher PEV-Aβ1-42 concentrations than healthy controls (p = 0.028). The ratio of PEV-Aβ1-42 to PEV was significantly higher in PDD patients compared to those in non-dementia PD and healthy controls (pPD-ND < 0.001, pHC = 0.041). The PEV-Aβ1-42/PEV ratio appears to influence the odds of developing dementia (OR = 1.76, p < 0.001). The change in the PEV-Aβ1-42/PEV ratio was also correlated with cognitive decline over 14 months (r = −0.447, p < 0.05).ConclusionThe plasma PEV-Aβ1-42/PEV ratio may serve as a diagnostic and prognostic biomarker for PDD patients.
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.