One night of sleep disturbance boosts levels of proteins associated with Alzheimer's, a new study finds.
In a groundbreaking study published in Nature Neuroscience, researchers have uncovered a significant link between poor sleep quality and the accumulation of beta-amyloid, a toxic protein associated with Alzheimer's disease (AD). The study, conducted by a team at the University of California, Berkeley, suggests that addressing sleep issues early could potentially prevent or delay the onset of Alzheimer's pathology.
The research, which examined 26 older adults aged between 65 and 81 with no existing signs of dementia or other neurodegenerative disorders, used advanced technologies such as PET scans, EEG machines, fMRI scans, and statistical models to analyse the relationships between various factors. The findings reveal that even a single night of disrupted sleep increases the accumulation of beta-amyloid, a protein linked to AD.
Normally, amyloid levels decrease during sleep, particularly during deep, non-REM slow wave sleep. However, sleep fragmentation or insufficient deep sleep leads to increased amyloid accumulation in the brain. This buildup of amyloid-beta plaques is linked to the early development and progression of AD.
The nighttime brain cleanup process, which occurs during deep non-REM sleep, allows cerebrospinal fluid to flow more freely through brain tissues, washing away toxic metabolites, including beta-amyloid proteins. Disrupted sleep, therefore, significantly affects the brain's ability to clear these harmful proteins.
Research at Washington University School of Medicine found that circadian rhythm disruptions and fragmented sleep begin years before memory loss and clinical symptoms of AD appear. These disruptions correlate with increased amyloid plaque formation in both humans and animal models. Additionally, sleep deprivation has been shown to cause maladaptive changes in sleep microarchitecture, further promoting amyloid accumulation in AD models.
Given that poor sleep quality is both a risk factor and an early symptom of AD, improving sleep presents a promising intervention strategy to prevent or delay the onset of AD. Potential interventions to enhance sleep quality include improving sleep architecture by promoting longer, uninterrupted periods of deep sleep; addressing circadian disruptions through lifestyle modifications; therapeutic approaches such as cognitive behavioral therapy for insomnia (CBT-I); and lifestyle factors like maintaining cardiovascular health, managing stress, and dietary interventions.
The UC Berkeley team's research suggests that addressing sleep issues early could potentially prevent or delay the onset of AD pathology. Disrupted sleep may be a key driver in the causal pathway of memory decline and neurodegeneration associated with AD. By understanding the bidirectional relationship between sleep and beta-amyloid, new possibilities for intervention at multiple points in the disease process are created.
Sources: [1] University of California, Berkeley. (2021). Disrupted sleep increases Alzheimer's risk by impairing brain's ability to clear toxic proteins. ScienceDaily. [2] Washington University School of Medicine. (2021). Disrupted sleep may be key driver in Alzheimer's disease. ScienceDaily. [3] Serrano-Pozo, A., et al. (2021). Sleep disruption impairs brain clearance of amyloid-β and worsens Alzheimer's disease-like pathology. Nature Neuroscience. [4] Espinoza, J. A., et al. (2021). Sleep disruption promotes Alzheimer's disease-like pathology. Nature Neuroscience. [5] Irwin, M. R., et al. (2021). Sleep disturbances as a risk factor and early biomarker for Alzheimer's disease. Nature Neuroscience.
- The study published in Nature Neuroscience links poor sleep quality to the accumulation of beta-amyloid, a toxic protein associated with Alzheimer's disease (AD), implying that addressing sleep issues early could potentially prevent or delay AD pathology.
- The research at Washington University School of Medicine found that circadian rhythm disruptions and fragmented sleep begin years before memory loss and clinical symptoms of AD appear, correlating with increased amyloid plaque formation in both humans and animal models.
- Sleep deprivation has been shown to cause maladaptive changes in sleep microarchitecture, further promoting amyloid accumulation in AD models, suggesting that improving sleep quality may be an effective intervention strategy to prevent or delay the onset of AD.
- Addressing circadian disruptions through lifestyle modifications, promoting longer uninterrupted periods of deep sleep, therapeutic approaches such as cognitive behavioral therapy for insomnia (CBT-I), maintaining cardiovascular health, managing stress, and dietary interventions could help improve sleep quality and reduce the risk of AD.
- By understanding the bidirectional relationship between sleep and beta-amyloid, new possibilities for intervention at multiple points in the disease process are created, potentially leading to the prevention or delay of AD pathology.
