scholarly journals Deep sleep predicts the cognitive evolution of mild‐moderate Alzheimer’s disease patients

2021 ◽  
Vol 17 (S6) ◽  
Author(s):  
Adriano Targa ◽  
Ivan David Benitez ◽  
Faride Dakterzada ◽  
Olga Minguez ◽  
Ferran Barbe ◽  
...  
2020 ◽  
Author(s):  
Lara J. Mentink ◽  
Jana Thomas ◽  
René J.F. Melis ◽  
Marcel G.M. Olde Rikkert ◽  
Sebastiaan Overeem ◽  
...  

AbstractStudy objectivesWhile poor sleep quality has been related to increased risk of Alzheimer’s disease, long-time shift workers (maritime pilots) did not manifest evidence of early Alzheimer’s disease in a recent study. We explored two hypotheses of possible compensatory mechanisms for sleep disruption: Increased efficiency in generating deep sleep during workweeks (model 1) and rebound sleep during rest weeks (model 2).MethodsWe used data from ten male maritime pilots (mean age: 51.6±2.4 years) with a history of approximately 18 years of irregular shift work. Subjective sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). A single lead EEG-device was used to investigate sleep in the home/work environment, quantifying total sleep time (TST), deep sleep time (DST), and deep sleep time percentage (DST%). Using multilevel models, we studied the sleep architecture of maritime pilots over time, at the transition of a workweek to a rest week.ResultsMaritime pilots reported worse sleep quality in workweeks compared to rest weeks (PSQI=8.2±2.2 vs. 3.9±2.0; p<0.001). Model 1 showed a trend towards an increase in DST% of 0.6% per day during the workweek (p=0.08). Model 2 did not display an increase in DST% in the rest week (p=0.87).ConclusionsOur findings indicated that increased efficiency in generating deep sleep during workweeks is a more likely compensatory mechanism for sleep disruption in the maritime pilot cohort than rebound sleep during rest weeks. Compensatory mechanisms for poor sleep quality might mitigate sleep disruption-related risk of developing Alzheimer’s disease. These results should be used as a starting point for future studies including larger, more diverse populations of shift workers.


2020 ◽  
Author(s):  
Carmen Jorge ◽  
Adriano Targa ◽  
Iván David Benítez ◽  
Faride Dakterzada ◽  
Gerard Torres ◽  
...  

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0237622
Author(s):  
Lara J. Mentink ◽  
Jana Thomas ◽  
René J. F. Melis ◽  
Marcel G. M. Olde Rikkert ◽  
Sebastiaan Overeem ◽  
...  

Study objectives While poor sleep quality has been related to increased risk of Alzheimer’s disease, long-time shift workers (maritime pilots) did not manifest evidence of early Alzheimer’s disease in a recent study. We explored two hypotheses of possible compensatory mechanisms for sleep disruption: Increased efficiency in generating deep sleep during workweeks (model 1) and rebound sleep during rest weeks (model 2). Methods We used data from ten male maritime pilots (mean age: 51.6±2.4 years) with a history of approximately 18 years of irregular shift work. Subjective sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). A single lead EEG-device was used to investigate sleep in the home/work environment, quantifying total sleep time (TST), deep sleep time (DST), and deep sleep time percentage (DST%). Using multilevel models, we studied the sleep architecture of maritime pilots over time, at the transition of a workweek to a rest week. Results Maritime pilots reported worse sleep quality in workweeks compared to rest weeks (PSQI = 8.2±2.2 vs. 3.9±2.0; p<0.001). Model 1 showed a trend towards an increase in DST% of 0.6% per day during the workweek (p = 0.08). Model 2 did not display an increase in DST% in the rest week (p = 0.87). Conclusions Our findings indicated that increased efficiency in generating deep sleep during workweeks is a more likely compensatory mechanism for sleep disruption in the maritime pilot cohort than rebound sleep during rest weeks. Compensatory mechanisms for poor sleep quality might mitigate sleep disruption-related risk of developing Alzheimer’s disease. These results should be used as a starting point for future studies including larger, more diverse populations of shift workers.


SLEEP ◽  
2020 ◽  
Author(s):  
A Targa ◽  
F Dakterzada ◽  
I Benítez ◽  
R López ◽  
M Pujol ◽  
...  

Abstract Study Objectives The majority of studies investigating the association between sleep and Alzheimer’s disease (AD) biomarkers have been performed in healthy subjects. Our objective was to investigate the association between sleep and several biomarkers that reflect distinct aspects of AD physiopathology. Methods The cohort included 104 individuals with mild-moderate AD. The subjects were submitted to one-night polysomnography, and cerebrospinal fluid was collected in the following morning to measure the selected biomarkers associated with amyloid deposition, tau pathology, neurodegeneration, axonal damage, synaptic integrity, neuroinflammation, and oxidative damage. Results There was a positive correlation between neurofilament light (NF-L) and the time spent in N1 sleep and a negative correlation between this marker and the time spent in N3 sleep. Accordingly, we observed that deep sleep was associated with lower levels of NF-L, whereas light sleep increased the probability of having higher levels of this marker. Furthermore, chitinase 3-like 1 (YKL-40) was negatively correlated with sleep efficiency, the time spent in N2 sleep and the time spent in N3 sleep. Conversely, there was a positive correlation between N3 sleep and the oxidative protein damage markers N-ε-(carboxyethyl)lysine and N-ε-(malondialdehyde)lysine. Conclusions There were significant correlations between sleep parameters and AD biomarkers related to axonal damage and neuroinflammation, such as NF-L and YKL-40. A lack of deep sleep was associated with higher levels of NF-L. This highlights a potential role for NF-L as a biomarker of sleep disruption in mild-moderate AD patients in addition to its role in predicting neurodegeneration and cognitive decline.


2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Faride Dakterzada ◽  
Gerard Piñol ◽  
Anna Carnes ◽  
Adriano Targa ◽  
Anna Moncusi ◽  
...  

2020 ◽  
Vol 16 (S5) ◽  
Author(s):  
Anna Carnes ◽  
Gerard Piñol ◽  
Faride Dakterzada ◽  
Adriano Targa ◽  
Ivan David Benitez ◽  
...  

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.


Author(s):  
J. Metuzals ◽  
D. F. Clapin ◽  
V. Montpetit

Information on the conformation of paired helical filaments (PHF) and the neurofilamentous (NF) network is essential for an understanding of the mechanisms involved in the formation of the primary lesions of Alzheimer's disease (AD): tangles and plaques. The structural and chemical relationships between the NF and the PHF have to be clarified in order to discover the etiological factors of this disease. We are investigating by stereo electron microscopic and biochemical techniques frontal lobe biopsies from patients with AD and squid giant axon preparations. The helical nature of the lesion in AD is related to pathological alterations of basic properties of the nervous system due to the helical symmetry that exists at all hierarchic structural levels in the normal brain. Because of this helical symmetry of NF protein assemblies and PHF, the employment of structure reconstruction techniques to determine the conformation, particularly the handedness of these structures, is most promising. Figs. 1-3 are frontal lobe biopsies.


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