The Sleep Side of Aging and Alzheimer’s Disease

Romanella, Sara M.; Roe, Dan; Tatti, Elisa; Cappon, Davide; Paciorek, Rachel; Testani, Elisa; Rossi, Alessandro; Rossi, Símone; Santarnecchi, Emiliano

doi:10.1016/j.sleep.2020.05.029

Cited by 42 publications

(28 citation statements)

References 229 publications

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“…AD is characterized by fragmented sleep, decreased slow‐wave activity and substantial reduction in REM sleep duration. 20 Therefore, it is essential that drugs aimed to reduce sleep‐related epileptiform activity do not further impair sleep quality. Of the effective drugs on epileptiform spiking, the smaller dose of LEV increased total sleep time ( P = .003, n = 7), while IST ( P < .05, n = 7) and MEM ( P < .01, n = 6) both reduced total sleep time dose‐dependently (Figure 4A ).…”

Section: Resultsmentioning

confidence: 99%

Preclinical evaluation of drug treatment options for sleep‐related epileptiform spiking in Alzheimer's disease

Jin

Gureviciene

Atalay

et al. 2022

A&D Transl Res & Clin Interv

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Introduction There are no published data on prospective clinical studies on drug treatment options for sleep‐related epileptiform spiking in Alzheimer's disease (AD). Methods Using video‐EEG with hippocampal electrodes in 17 APP/PS1 transgenic male mice we assessed the effects of donepezil and memantine, anti‐seizure drugs levetiracetam and lamotrigine, gamma‐secretase inhibitor semagacestat, anti‐inflammatory minocycline and adenosine receptor antagonist istradephylline on density of cortical and hippocampal spikes during sleep. Results Levetiracetam decreased the density of hippocampal giant spikes and cortical spikes. Lamotrigine reduced cortical single spikes and spike‐wave discharges but dramatically increased hippocampal giant spikes. Memantine increased cortical single spikes and spike‐wave discharges dose‐dependently. Memantine and istradephylline decreased total sleep time while levetiracetam increased it. Lamotrigine decreased REM sleep duration. Other drugs had no significant effects. Discussion Levetiracetam appears promising for treating sleep‐related epileptiform spiking in AD while lamotrigine should be used with caution. Donepezil at low doses appeared neutral but the memantine effects warrant further studies.

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Section: Resultsmentioning

confidence: 99%

Preclinical evaluation of drug treatment options for sleep‐related epileptiform spiking in Alzheimer's disease

Jin

Gureviciene

Atalay

et al. 2022

A&D Transl Res & Clin Interv

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“…Our stratified analyses suggested that women and the elderly aged 60 years and above with shorter sleep duration (≤ 4, 5, 6 h) had a higher risk of visual, hearing, and dual sensory impairments. Gender differences in sleep duration among the aged population cannot be ignored as insomnia is generally higher in women (Romanella et al, 2021). Our findings were in concordance with the United States National Institute on Aging's multicentered study entitled "Established Populations for Epidemiologic Studies of the Elderly" (EPESE) (Foley et al, 1995) and the Spanish National Health Survey 2017 (Pardhan et al, 2021), which found that women were more likely to sleep less or have trouble in sleeping, and had a higher risk of visual, hearing and dual sensory impairments than men.…”

Section: Discussionmentioning

confidence: 99%

Associations Between Sleep Duration and Sensory Impairments Among Older Adults in China

Rong

Wang²,

Lai³

et al. 2022

Front. Aging Neurosci.

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ObjectiveStudies of sleep duration in relation to the risk of sensory impairments other than dementia are scarce. Little is known about the associations between sleep duration and sensory impairments in China. This study aims to explore the associations between sleep duration and single or dual sensory impairments (visual and/or hearing).MethodsThis cross-sectional study used the data from 17,668 respondents were drawn from the 2018 survey of the China Health and Retirement Longitudinal Study (CHARLS), an ongoing national longitudinal study of Chinese adults aged 45 years and above. The duration of sleep per night was obtained from face-to-face interviews. The presence of sensory impairments was measured by self-reported visual and hearing functions. Multivariable generalized linear models (GLM) with binomial family and log link to assess the associations between sleep duration and sensory impairments.ResultsOf the 17,668 respondents, 8,396 (47.5%) were men. The mean (SD) age was 62.5 (10.0) years old. Respondents with short (≤ 4, 5 h per night) sleep duration had a significantly higher risk of visual, hearing and dual sensory impairments than those who slept for 7 h per night after adjusting for covariates (P < 0.05). Meanwhile, respondents who slept for 6 h per night had a higher risk of hearing impairment (P = 0.005). Further analysis suggested a U-shaped association between sleep duration and sensory impairments. When sleep duration fell below 8 h, increased sleep duration was associated with a significantly lower risk of visual (OR, 0.93; 95%CI, 0.88–0.98; P = 0.006), hearing (OR, 0.89; 95% CI, 0.86–0.93; P < 0.001), and dual (OR, 0.90; 95% CI, 0.87–0.94; P < 0.001) impairments. When sleep duration exceeded 8 h, the risk of visual (OR, 1.09; 95% CI, 1.00–1.19; P = 0.048), hearing (OR, 1.04; 95% CI, 0.97–1.11; P = 0.269), and dual (OR, 1.07; 95% CI, 1.00–1.14; P = 0.044) impairments would increase facing prolonged sleep duration. Women and the elderly aged over 60 years old were more sensitive to short sleep duration and experienced a higher risk of sensory impairments.ConclusionIn this study, short sleep duration was associated with a higher risk of visual and hearing impairments. Future studies are needed to examine the mechanisms of the associations between sleep duration and sensory impairments.

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“…PGO waves are originated from mesopontine cholinergic areas [17,19,258] and the neurodegeneration of mesopontine cholinergic neurons has been associated with AD [259,260], as well as Lewy body dementia [261]. Additionally, abnormalities in sleep spindles and sharp wave-ripples during NREM sleep have also been associated with AD [16,49,252,262]. Therefore, these sleep-related neural oscillations may be alternative targets for non-pharmacological interventions.…”

Section: Discussionmentioning

confidence: 99%

“…Secondly, it is worth exploring other brain states, not just gamma and slow oscillations, because a wide range of neural oscillations or events have been studied in general neuroscience [ 1 , 13 , 33 , 251 ]. With respect to sleep, the reduction in REM sleep duration is an early biomarker during AD pathogenesis [ 221 , 227 , 228 , 252 ]. During REM sleep, hippocampal theta rhythms and ponto-geniculo-occipital (PGO) waves are prominent electrophysiological markers [ 14 , 21 , 253 , 254 ].…”

Section: Discussionmentioning

confidence: 99%

Mutual Interactions between Brain States and Alzheimer’s Disease Pathology: A Focus on Gamma and Slow Oscillations

Byron

Семенова

Sakata

2021

Biology

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Brain state varies from moment to moment. While brain state can be defined by ongoing neuronal population activity, such as neuronal oscillations, this is tightly coupled with certain behavioural or vigilant states. In recent decades, abnormalities in brain state have been recognised as biomarkers of various brain diseases and disorders. Intriguingly, accumulating evidence also demonstrates mutual interactions between brain states and disease pathologies: while abnormalities in brain state arise during disease progression, manipulations of brain state can modify disease pathology, suggesting a therapeutic potential. In this review, by focusing on Alzheimer’s disease (AD), the most common form of dementia, we provide an overview of how brain states change in AD patients and mouse models, and how controlling brain states can modify AD pathology. Specifically, we summarise the relationship between AD and changes in gamma and slow oscillations. As pathological changes in these oscillations correlate with AD pathology, manipulations of either gamma or slow oscillations can modify AD pathology in mouse models. We argue that neuromodulation approaches to target brain states are a promising non-pharmacological intervention for neurodegenerative diseases.

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The Sleep Side of Aging and Alzheimer’s Disease

Cited by 42 publications

References 229 publications

Preclinical evaluation of drug treatment options for sleep‐related epileptiform spiking in Alzheimer's disease

Preclinical evaluation of drug treatment options for sleep‐related epileptiform spiking in Alzheimer's disease

Associations Between Sleep Duration and Sensory Impairments Among Older Adults in China

Mutual Interactions between Brain States and Alzheimer’s Disease Pathology: A Focus on Gamma and Slow Oscillations

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