Sleep dysregulation, memory impairment, and CSF biomarkers during different levels of neurocognitive functioning in Alzheimer’s disease course

• Published in: Alzheimer's research & therapy Vol. 12; no. 1; pp. 5 - 13
• Main Authors: Liguori, Claudio, Placidi, Fabio, Izzi, Francesca, Spanetta, Matteo, Mercuri, Nicola Biagio, Di Pucchio, Alessandra
• Format: Journal Article
• Language: English
• Published: London BioMed Central 04.01.2020; BioMed Central Ltd; Springer Nature B.V; BMC
• Subjects: 10 Years of Alzheimer's Research & Therapy; Adult; Advertising executives; Aged; Aged, 80 and over; Alzheimer Disease - cerebrospinal fluid; Alzheimer Disease - complications; Alzheimer's disease; Amyloid beta-Peptides - cerebrospinal fluid; Biological markers; Biomarkers; Biomarkers - cerebrospinal fluid; Biomedical and Life Sciences; Biomedicine; Causes of; Cognition & reasoning; Cognitive ability; Cognitive Dysfunction - cerebrospinal fluid; Cognitive Dysfunction - etiology; Complications and side effects; CSF biomarkers; Dementia; Development and progression; Disease Progression; Diseases; Female; Geriatric Psychiatry; Geriatrics/Gerontology; Health aspects; Humans; Laboratories; Lumbar puncture; Male; Memory; Memory disorders; Memory Disorders - cerebrospinal fluid; Memory Disorders - etiology; Middle Aged; Neurodegeneration; Neurology; Neurosciences; NREM sleep; Physiological aspects; Principal components analysis; Proteins; REM sleep; Sleep; Sleep disorders; Sleep Wake Disorders - cerebrospinal fluid; Sleep Wake Disorders - etiology; tau Proteins - cerebrospinal fluid; Italy; Alzheimer’s disease; CSF biomarkers; Sleep
• ISSN: 1758-9193; 1758-9193
• DOI: 10.1186/s13195-019-0571-3

Background Alzheimer's disease (AD) is frequently accompanied by sleep impairment, which can induce AD-related neurodegeneration. We herein investigated the sleep architecture, cognition, and cerebrospinal fluid (CSF) biomarkers (tau proteins and β-amyloid 42 ) during AD progression from subjective cognitive impairment (SCI) to mild cognitive impairment (MCI) and eventually to AD dementia, and compared the results with cognitively normal (CN) subjects. Methods We included patients affected by SCI, MCI, mild AD, and moderate-to-severe AD in our study along with CN subjects as controls. All the subjects underwent nocturnal polysomnography to investigate sleep, neuropsychological testing to evaluate cognition, and lumbar puncture for CSF AD biomarkers assessment. Results Sleep (both rapid eye movement (REM) and non-REM sleep) and memory function are both progressively impaired during the course of AD from SCI to mild and subsequently to moderate AD. Further, sleep dysregulation appears earlier than cognitive deterioration, with a reduction of CSF β-amyloid 42 level. Conclusion Sleep, memory, and CSF AD biomarkers are closely interrelated in AD progression from the earliest asymptomatic and preclinical stages of the disease related in AD since the earliest and preclinical stages of the disease.