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Purpose Of The Review: The purpose of this review is to provide an overview of potential mechanisms mediating the bi-directional relationship between sleep and neurodegenerative diseases such as Alzheimer's disease. We provide updates on previously proposed mechanisms and identify new mechanisms particularly concerning how sleep disturbances affect memory-related neural circuits.
Recent Findings: In this review, we focus on the multiple mechanisms that potentially mediate the relationship between sleep and Alzheimer's disease. We present updates for previously hypothesized mechanisms such as sleep-related changes in production/release and clearance of amyloid-β and tau proteins as well as more recently proposed mechanisms relating to tau phosphorylation, the orexin system, astrocytes, and microglia. We also highlight how disruptions in sleep EEG oscillations that underlie memory-related neural circuits, such as slow wave activity, theta bursts, sleep spindles, and gamma ripples, change in Alzheimer's disease.
Summary: Disturbed sleep increases Alzheimer's disease risk via multiple potential mechanisms that suggest multiple targets to test approved and effective treatments of sleep disorders to prevent or delay Alzheimer's disease.
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http://dx.doi.org/10.1007/s40675-024-00316-6 | DOI Listing |
JAMA Neurol
September 2025
Translational Neuropathology Research Laboratory, Department of Pathology and Laboratory Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia.
Importance: Exposure to fine particulate matter air pollution (PM2.5) may increase risk for dementia. It is unknown whether this association is mediated by dementia-related neuropathologic change found at autopsy.
View Article and Find Full Text PDFArch Pharm Res
September 2025
College of Pharmacy, Hanyang University, Ansan, 15588, Republic of Korea.
c-Jun N-terminal kinases (JNKs), a subfamily of mitogen-activated protein kinases (MAPKs), are key mediators of cellular responses to environmental stress, inflammation, and apoptotic signals. The three isoforms-JNK1, JNK2, and JNK3 exhibit both overlapping and isoform-specific functions. While JNK1 and JNK2 are broadly expressed across tissues and regulate immune signaling, cell proliferation, and apoptosis, JNK3 expression is largely restricted to the brain, heart, and testis, where it plays a crucial role in neuronal function and survival.
View Article and Find Full Text PDFNeurochem Res
September 2025
International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
The concept of the central nervous system (CNS) reserve emerged from the mismatch often observed between the extent of brain pathology and its clinical manifestations. The cognitive reserve reflects an "active" capacity, driven by the plasticity of CNS cellular components and shaped by experience, learning, and memory processes that increase resilience. We propose that neuroglial cells are central to defining this resilience and cognitive reserve.
View Article and Find Full Text PDFJ Neurol
September 2025
Neuroimaging Research Unit, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Background: The "Systematic Screening of Handwriting Difficulties in Parkinson's Disease" (SOS) test is the only tool specifically designed to evaluate handwriting in people with Parkinson's Disease (pwPD). It is language specific.
Objective: To assess the construct validity, intrarater and interrater reliability of the Italian version of the SOS test.
Fish Physiol Biochem
September 2025
Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM's Narsee Monjee Institute of Management Studies, Mumbai, 56, India.
Zebrafish models have been used to research Alzheimer's disease and other neurodegenerative disorders because of their similarities to the human genetic composition and behavior. Researchers have detected iron accumulation in the post-mortem brain sections of neurodegenerative disorder patients. Therefore, the development an animal model to simulate these clinical pathological findings is important.
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