Imagine your brain is a vast computer with different components working together. One important system is sleep, and when it malfunctions, like in obstructive sleep apnea (OSA), other parts of the computer can be affected. Researchers have found that OSA, a common sleep disorder, may be connected to Alzheimer’s disease (AD). In a recent study, scientists investigated the levels of certain biomarkers in the cerebrospinal fluid (CSF) and through positron emission tomography (PET) scans in OSA patients. These biomarkers, such as amyloid-β 42, total tau, and phosphorylated tau, can provide clues about AD before symptoms appear. The analysis revealed significant differences in CSF Aβ42 levels and Aβ burden tested by PET scans between OSA patients and controls. Notably, patients with moderate/severe OSA showed differences in CSF Aβ42 levels compared to healthy individuals, suggesting a potential link between OSA severity and AD neuropathology. Age and BMI were also found to influence these results. This exciting study adds to the growing evidence that sleep disorders like OSA might contribute to the development of AD. To learn more about this research, check out the full article!
Increasing evidence links Alzheimer’s disease (AD) to various sleep disorders, including obstructive sleep apnea (OSA). The core AD cerebrospinal fluid (CSF) biomarkers, including amyloid-β 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau), can reflect key elements of AD pathophysiology before the emergence of symptoms. Besides, the amyloid-β (Aβ) and tau burden can also be tested by positron emission tomography (PET) scans. Electronic databases (PubMed, Embase, Web of Science, and The Cochrane Library) were searched until August 2022 to assess the AD-related biomarkers measured by PET scans and CSF in OSA patients. The overall analysis showed significant differences in Aβ42 levels (SMD = −0.93, 95% CI:−1.57 to −0.29, P < 0.001) and total tau (t-tau) levels (SMD = 0.24, 95% CI: 0.01–0.48, P = 0.308) of CSF, and Aβ burden (SMD = 0.37, 95% CI = 0.13–0.61, P = 0.69) tested by PET scans between the OSA and controls. Furthermore, CSF Aβ42 levels showed significant differences in patients with moderate/severe OSA compared with healthy control, and levels of CSF Aβ42 showed differences in OSA patients with normal cognition as well. Besides, age and BMI have influences on heterogeneity. Our meta-analysis indicated abnormal AD-related biomarkers (CSF and PET scans) in patients with OSA, supporting the current hypothesis that OSA, especially moderate/severe OSA, may start the AD neuropathological process.Systematic review registration[https://www.crd.york.ac.uk/PROSPERO/], identifier [CRD42021289559].
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.