Ageing Research Reviews, Год журнала: 2021, Номер 72, С. 101462 - 101462
Опубликована: Сен. 15, 2021
Язык: Английский
Science, Год журнала: 2019, Номер 363(6429), С. 880 - 884
Опубликована: Янв. 25, 2019
Sleep may protect the brain from AD Two main proteins accumulate in Alzheimer's disease (AD), β-amyloid (Aβ) and tau. Aβ appears to instigate AD, but tau drive damage cognitive decline. deprivation is known increase acutely chronically. Now, Holth et al. show that chronic sleep strongly increases over hours also drives pathology spreading brains of mice humans (see Perspective by Noble Spires-Jones). Thus, have a direct protective effect on key protein pathology. Science , this issue p. 880 ; see 813
Язык: Английский
Процитировано
606
Cellular and Molecular Life Sciences, Год журнала: 2019, Номер 77(9), С. 1721 - 1744
Опубликована: Окт. 30, 2019
Abstract Accumulation of misfolded and aggregated forms tau protein in the brain is a neuropathological hallmark tauopathies, such as Alzheimer’s disease frontotemporal lobar degeneration. Tau aggregates have ability to transfer from one cell another induce templated misfolding aggregation healthy molecules previously cells, thereby propagating pathology across different areas prion-like manner. The molecular mechanisms involved cell-to-cell are diverse, not mutually exclusive only partially understood. Intracellular accumulation induces several that aim reduce cellular burden proteins also promote secretion aggregates. However, may be released cells physiologically unrelated aggregation. involves multiple vesicular non-vesicle-mediated pathways, including directly through plasma membrane. Consequently, extracellular can found various forms, both free vesicles, exosomes ectosomes. Once space, internalized by neighboring neurons glial via endocytic, pinocytic phagocytic mechanisms. Importantly, accumulating evidence suggests propagation could provide general mechanism for progression tauopathies other related neurodegenerative diseases. Here, we review recent literature on tau, with particular focus secretion.
Язык: Английский
Процитировано
252
Journal of Neuroscience, Год журнала: 2019, Номер 39(32), С. 6315 - 6324
Опубликована: Июнь 17, 2019
Recent proposals suggest that sleep may be a factor associated with accumulation of two core pathological features Alzheimer9s disease (AD): tau and β-amyloid (Aβ). Here we combined PET measures Aβ tau, electroencephalogram recordings, retrospective evaluations to investigate the potential utility in predicting in vivo AD pathology male female older adults. Regression analyses revealed severity impaired slow oscillation-sleep spindle coupling predicted greater medial temporal lobe burden. burden was not impairment but instead diminished amplitude <1 Hz slow-wave-activity, results were statistically dissociable from each other. Additionally, comparisons retrospective, self-reported changes duration demonstrated across lifespan can predict late-life Thus, quantitative qualitative human represent noninvasive, cost-effective, scalable biomarkers (current future forecasting) pathology, carry both therapeutic public health implications. SIGNIFICANCE STATEMENT Several studies have linked disruption progression (AD). Tau (Aβ), primary AD, are objective subjective sleep. However, it remains unknown whether late life distinct impairments physiology or lifespan. Using polysomnography, questionnaires, tau- Aβ-specific PET, present study reveals signatures dissociably levels brain These night polysomnography aid evaluating burden, treating deficiencies within decade-specific time windows serve delaying progression.
Язык: Английский
Процитировано
200
Sleep Medicine Reviews, Год журнала: 2022, Номер 62, С. 101592 - 101592
Опубликована: Янв. 21, 2022
Five decades ago, seminal studies positioned the brainstem locus coeruleus (LC) norepinephrine (NE) system as a key substrate for regulation of wakefulness and sleep, this picture has recently been elaborated thanks to methodological advances in precise investigation experimental modulation LC structure functions. This review presents discusses findings that support major role LC-NE at different levels sleep-wake organization, ranging from its involvement overall architecture cycle associations with sleep microstructure, while accounting intricate neuroanatomy surrounding LC. Given particular position held by being intersection dysregulation initial pathophysiological processes Alzheimer's disease (AD), we conclude examining emerging opportunities investigate mediated relationships between alteration AD human aging. We further propose several research perspectives could promising target identification at-risk individuals preclinical stages AD, development novel preventive interventions.
Язык: Английский
Процитировано
77
Neurobiology of Disease, Год журнала: 2020, Номер 139, С. 104832 - 104832
Опубликована: Март 13, 2020
A substantial body of research now implicates the circadian clock in regulation an array diverse biological processes including glial function, metabolism, peripheral immune responses, and redox homeostasis. Sleep abnormalities other forms disruption are common symptoms aging neurodegeneration. Circadian may also influence pathogenesis neurodegenerative diseases. The specific mechanisms governing interaction between systems, aging, system still being uncovered. Here, we review evidence supporting a bidirectional relationship system. Further, explore hypothesis that age-related deterioration exacerbate multiple pathogenic processes, priming brain for
Язык: Английский
Процитировано
106
Trends in Neurosciences, Год журнала: 2022, Номер 45(9), С. 678 - 691
Опубликована: Июнь 9, 2022
Recent evidence in humans reveals that chronic sleep disruption can lead to protracted recovery of neurobehavioral performance, particularly sustained vigilance and episodic memory.Studies animal models demonstrate even incomplete recovery, including neuron loss brain areas critical for memory, specifically, the locus coeruleus hippocampus.The severity neural injury incurred by varies with duration type disruption, age at which exposure occurs, neuronal populations being assessed, genetic predisposition neurodegenerative processes.Early oxidative stress inflammation contribute a metabolic resetting, behavioral impairment, pathologic findings associated disruption. studies both call into question completeness after Studies have identified cognitive domains vulnerable delayed or memory. These findings, turn, provide focus model critically test lasting impact on brain. Here, we summarize human response then discuss recent examining responses circuits pertinent We propose pathways common various forms consider implications this aging disorders. Chronic humans: evolving thoughts recoveryChronic curtailment is modern society related part increased work demands, lifestyle choices, development use medications substances suppress disrupt sleep, addition artificial light-emitting devices delay sleep. A generally held presumption has been while results impairments, performance deficits are reversed limited-period (e.g., over weekend). collection loss, however, challenges belief suggests impairments persist, additionally, individuals may be poor judges their time. From 1 2 weeks restriction <7 h sleep/night adults shown repeatedly result cumulative increases propensity, along decrements mood [1.Dinges D.F. et al.Cumulative sleepiness, disturbance, psychomotor during week restricted 4-5 hours per night.Sleep. 1997; 20: 267-277PubMed Google Scholar, 2.Van Dongen H.P. al.The cost additional wakefulness: dose-response effects functions physiology from total deprivation.Sleep. 2003; 26: 117-126Crossref PubMed Scopus (2126) 3.Belenky G. al.Patterns degradation restoration subsequent recovery: study.J. Sleep Res. 12: 1-12Crossref (979) Scholar]. Objective subjective discrepancies, were evident, as study participants unaware progressive deterioration across Scholar,2.Van While (sleepiness mood) typically normalized 1–2 nights objective measures showed persistent deficits, relative baseline 2–3 [3.Belenky 4.Banks S. al.Neurobehavioral dynamics following restriction: one night recovery.Sleep. 2010; 33: 1013-1026Crossref 5.Pejovic al.Effects mild interleukin-6 cortisol secretion daytime sleepiness performance.Am. J. Physiol. Endocrinol. Metab. 2013; 305: E890-E896Crossref (105) similarly was evident adolescents [6.Lo J.C. successive cycles without naps adolescents.Sleep. 2017; 40zsw042Crossref (51) In young adults, impaired 5 days 4 h/night restriction, frequency lapses not despite 3 [7.Axelsson al.Sleepiness repeated semi-laboratory conditions.Chronobiol. Int. 2008; 25: 297-308Crossref (93) More recently, field conducted time reduced third 10 consecutive [8.Ochab J.K. al.Observing changes functioning induced deficiency periods.PLoS One. 2021; 16e0255771Crossref (0) Neither accuracy interference assay (Stroop) nor eyes-open alpha power spectra had 7-day period When deprived all 40 hours, resolved tasks requiring higher function reading comprehension, serial addition, go-no-go tasks) did normalize [9.Ikegami K. al.Recovery fatigue deprivation.J. Occup. Health. 2009; 51: 412-422Crossref (28) As deprivation overestimate own [10.Boardman J.M. ability self-monitor 60 sleep.J. 2018; 27e12633Crossref (12) vigilance, impairs memory hippocampal connectivity prefrontal cortex default mode network [11.Chai Y. al.Two restores but deprivation.Sci. Rep. 2020; 10: 8774Crossref (14) connectivity, persists. Collectively, these lines strongly support notion manifest imperceptions impairments. The latter finding contributed false sense security upon weekend sleep.Neurobehavioral largely attributed homeostatic wake-induced extracellular adenosine; levels readily reverse short-term [12.Porkka-Heiskanen T. al.Adenosine: mediator sleep-inducing prolonged wakefulness.Science. 276: 1265-1268Crossref (895) 13.Kalinchuk A.V. course adenosine, nitric oxide (NO) inducible NO synthase role non-rapid eye movement cascade.J. Neurochem. 2011; 116: 260-272Crossref 14.McKenna J.T. al.Sleep fragmentation elevates behavioral, electrographic neurochemical sleepiness.Neuroscience. 2007; 146: 1462-1473Crossref (90) 15.Porkka-Heiskanen al.Brain site-specificity adenosine concentration spontaneous sleep: an vivo microdialysis study.Neuroscience. 2000; 99: 507-517Crossref (376) 16.Portas C.M. al.Role state modulation: freely moving cat.Neuroscience. 79: 225-235Crossref With longer durations do necessarily parallel undergoing deprivation, increase any regions measurements made, hippocampus [17.Zeitzer al.Extracellular deprivation: study.Sleep. 2006; 29: 455-461Crossref (33) study, histories epilepsy, values compared samples allowed determine expected drift rats exposed measured slices reduced, rather than elevated, 2-week opportunity, slice remained below [18.Clasadonte al.Chronic disrupts homeostasis sensitivity alcohol reducing accumulation adenosine.J. Neurosci. 2014; 34: 1879-1891Crossref By contrast, Thus, caused acute loss. However, presence recoveries partial absence elevations raises possibility sleep-loss-induced injury.Neural difficult assess predefined indices indicative glial modification, and/or dysfunction. This challenge illustrated series experiments performed three decades ago, aimed potential cell damage using methodologies available Adult extreme form weeks. resulted profound systemic (severe weight malnutrition, bacterial sepsis, hormonal dysregulation, ultimately death), yet examination brains immediately general histology, apoptosis, necrosis, yielded no significant abnormalities [19.Cirelli C. al.No degeneration long-term rats.Brain 1999; 840: 184-193Crossref Does mean does injure brain? would argue when defined impairment circuit dysfunction, analyses needed exclude injury.With improved definitions, assays strategies paradigm shift emerging, transition considering reversible response, greater appreciation Review, begin highlighting models, emphasizing more how reversibility influenced, only chronicity also exposure, interval used assessment, subtypes regions, propensity protein aggregation. review what learned regarding mechanisms suggest future directions identify therapies lessen commonly encountered scenarios disruption.Neural modelsConsideration paradigmsVarious modalities developed rapid (REM) fragmentation. There some inherent overlap modes For example, definition, includes REM methods impart non-REM (NREM) [20.Arthaud al.Paradoxical mice small-platforms-over-water method: polysomnographic melanin-concentrating hormone hypocretin/orexin activation before, 2015; 24: 309-319Crossref Scholar,21.Silva R.H. mice.Neuropharmacology. 2004; 46: 895-903Crossref (250) simple technique platform-over-water prevent depending size platforms animals studied. platform should adjusted so initiate disrupted, state-dependent reductions postural muscle tone falling water abruptly waking up. Larger control environment; show [22.Machado R.B. modified multiple technique: quantification recovery.Brain 1004: 45-51Crossref (285) Platform approaches elevated plasma corticosterone Scholar,23.Tobler I. effect rat.Neurosci. Lett. 1983; 35: 297-300Crossref Scholar,24.Suchecki D. al.Increased ACTH different paradoxical 1998; 7: 276-281Crossref Additionally, each continuum NREM patterns 24-h cycle.Most date, those discussed here, implemented physical means although it now possible elicit chemogenetic wake [25.Holth sleep-wake cycle regulates interstitial fluid tau CSF humans.Science. 2019; 363: 880-884Crossref (252) Scholar] or, potentially, inactivation circuits. Commonly paradigms types targeted Figure 1, advantages, disadvantages, confounding factors. there differences level arousal amount learning experienced where exploratory wakefulness induce robust immediate early gene wake-activated neurons, gentle handling same [26.Deurveilher al.Social environmental contexts modulate deprivation-induced c-Fos rats.Behav. Brain 256: 238-249Crossref (8) Exploratory locomotor activity, providing continuously enriched changing environment, involve other constant (or expected) environments. Techniques require continuous experimenter like handling, allow breakthrough automated systems rotating platform) intervene soon electroencephalographic detected computer algorithm [27.Leenaars C.H. al.A new method rat minimal activity.J. Methods. 196: 107-117Crossref Scholar,28.Deboer al.Long term mammalian circadian pacemaker.Sleep. 30: 257-262Crossref elicited either bar sweeping floor cage set intervals way rotor table briskly moves cages fraction every minute two. Methods fragment shorten amounts [29.Sinton al.Validation novel interrupt mouse.J. 184: 71-78Crossref approach effective long periods (weeks) seems influence body [30.Li wake-active neurons hypercapnic response.Sleep. 37: 51-64Crossref Scholar,31.Wallace E. al.Differential spatial synaptic plasticity pubertal mice.Brain 1615: 116-128Crossref (15) allows group housing, ad libitum eating drinking, access undisturbed nests. sweeper nests cannot maintained, group-housed. its strengths limitations, techniques provided similar results.Locus coeruleus: hitDelayed supports concept could affect within circuit, anterior cingulate cortical [32.Gompf H.S. al.Locus ceruleus sustain environment.J. 14543-14551Crossref (109) Locus (LCn) noradrenergic pontine firing rates highest unexpected uncertainties Scholar,33.Bliss-Moreau al.Anterior ablation affective vigor vigilance.J. 41: 8075-8087Crossref (4) change wakefulness, influences LCn. Upon brief (3 h) LCn adult upregulate mitochondrial deacetylase sirtuin (SirT3), initiates antioxidant maintain redox [34.Zhang al.Extended compromised metabolics neurons.J. 4418-4431Crossref (Figure 2) . 8 wakefulness/day environment paradigm, SirT3 activating enzymes upregulated develop stress, acetylation, acetylation electron transport chain proteins, counts Whether observed represent adaptation dysfunction injury, requires point further termination outlined above adaptive temporarily downregulate activity tyrosine hydroxylase; marker forementioned study. Of note, noradrenaline metabolites, 3,4-dihydroxyphenylglycoaldehyde, modifies tau, increasing aggregate propagate [35.Kang S.S. al.Norepinephrine metabolite DOPEGAL activates AEP pathological Tau aggregation coeruleus.J. Clin. Invest. 130: 422-437Crossref (26) hydroxylase faced restriction. According scenario, once reinstated, resume. continued 12 weeks, year counts, [36.Owen J.E. al.Late-in-life neurodegeneration mice.Sleep. 44zsab057Crossref (7) Scholar], indicating irreversible Similarly, whole-cell patch clamp recordings step currents after-hyperpolarization amplitudes supporting functional [37.Li hypercapneic remaining LCn, [38.Zhu al.Degeneration modeling apnea.Front. Neurol. 6: 109Crossref Not studies, One rats, instance, drum alternated enforced ambulation rest, days/week nonrotating drums [39.Deurveilher orexin/hypocretin, restriction.Eur. 54: 6027-6043Crossref count variability high controls, conceivable brevity prevented engaged protective wakefulness. output Rats task, [40.Lu H.J. Lv β-Adrenergic receptor dentate gyrus participates sleep-deprived rats.Exp. Neurobiol. 144-154Crossref Because unclear whether reduction represents dysfunction.Figure 2Duration-dependent (LCn).Show full captionShort-term [awake habitual (lights-on) period] upregulates (SirT3) nuclear translocation FoxO3a transcriptional antioxidants PGC-1α enhance biogenesis. extended (for day lights-on days) reduces NAD+-synthesizing enzymes, thereby (and inactivating) FoxO3a. Mechanisms switch maladaptive known.View Large Image ViewerDownload Hi-res image Download (PPT)Why disruption? status dictate vulnerability Mice deficient lower baseline, decline suggesting susceptible waking. second because exposures [41.Vankov A. al.Response novelty habituation exploring rat.Eur. 1995; 1180-1187Crossref (201) most active autoreceptor lowest, [42.Aston-Jones Bloom F.E. Activity norepinephrine-containing behaving anticipates fluctuations sleep-waking cycle.J. 1981; 1: 876-886Crossref Opening l-type calcium channels arousal, mitochondria activate calcium-dependent synthesis, impairing superoxide production [43.Sanchez-Padilla al.Mitochondrial oxidant regulated synthase.Nat. 17: 832-840Crossref (92) identification underlying (see Outstanding questions), determined implemented, resolve perturbance.Hippocampal disruptionIn humans, hippocampal-dependent persist Th
Язык: Английский
Процитировано
62
Journal of Neurochemistry, Год журнала: 2023, Номер 166(1), С. 24 - 46
Опубликована: Фев. 18, 2023
Abstract In countries around the world, sleep deprivation represents a widespread problem affecting school‐age children, teenagers, and adults. Acute more chronic restriction adversely affect individual health, impairing memory cognitive performance as well increasing risk progression of numerous diseases. mammals, hippocampus hippocampus‐dependent are vulnerable to effects acute deprivation. Sleep induces changes in molecular signaling, gene expression may cause dendritic structure neurons. Genome wide studies have shown that alters transcription, although pool genes affected varies between brain regions. More recently, advances research drawn attention differences regulation level transcriptome compared with mRNA associated ribosomes for protein translation following Thus, addition transcriptional changes, also affects downstream processes alter translation. this review, we focus on multiple levels through which impacts regulation, highlighting potential post‐transcriptional translational be by Understanding impacted is essential future development therapeutics mitigate loss. image
Язык: Английский
Процитировано
29
Annals of Neurology, Год журнала: 2024, Номер 95(4), С. 653 - 664
Опубликована: Фев. 26, 2024
While studies suggested that locus coeruleus (LC) neurodegeneration contributes to sleep-wake dysregulation in Alzheimer's disease (AD), the association between LC integrity and circadian rest-activity patterns remains unknown. Here, we investigated relationships 24-hour rhythms, cognitive trajectories, autopsy-derived older adults with without cortical AD neuropathology.
Язык: Английский
Процитировано
9
Frontiers in Neuroscience, Год журнала: 2020, Номер 14
Опубликована: Сен. 23, 2020
Even prior to the onset of prodromal stages Alzheimer's disease (AD), a constellation sleep disturbances are apparent. A series epidemiological studies indicate that multiple forms these associated with increased risk for developing mild cognitive impairment (MCI) and AD, even triggering at an earlier age. Through combination causal manipulation in humans rodents, as well targeted examination disturbance respect AD biomarkers, mechanisms linking beginning emerge. In this review, we explore recent evidence local deficits brain oscillatory function during pathological burden circuit-level dysfunction degeneration. short, three expression oscillations have been identified relation pathophysiology: 1) frequency-specific frontal slow wave non-rapid eye movement (NREM) sleep, 2) parietal spindle expression, 3) quality electroencephalographic (EEG) desynchrony characteristic REM sleep. These noteworthy since they differ from seen normal aging, indicating potential presence abnormal aging process. How each β-amyloid (Aβ) tau pathology, neurodegeneration circuits sensitive pathophysiology, examined present focus on role within fronto-hippocampal subcortical sleep-wake circuits. It is hypothesized arise distinct network-specific dysfunctions driven by regionally-specific accumulation pathologies, their neurodegeneration. Overall, evolution offer unique windows into circuit-specific progression pathophysiological processes onset, impact function. This includes erosion sleep-dependent memory mechanisms, which may contribute decline AD. review closes discussion remaining critical knowledge gaps implications work future mechanistic implementing sleep-based treatment interventions.
Язык: Английский
Процитировано
69
International Journal of Molecular Sciences, Год журнала: 2020, Номер 21(3), С. 1168 - 1168
Опубликована: Фев. 10, 2020
In recent years, the idea that sleep is critical for cognitive processing has gained strength. Alzheimer’s disease (AD) most common form of dementia worldwide and presents a high prevalence disturbances. However, it difficult to establish causal relations, since vicious circle emerges between different aspects disease. Nowadays, we know crucial consolidate memory remove excess beta-amyloid hyperphosphorilated tau accumulated in AD patients’ brains. this review, discuss how disturbances often precede years some pathological traits, as well decline, AD. We describe relevance consolidation, focusing on changes patterns contrast normal aging. also analyze whether alterations could be useful biomarkers predict risk developing compile sleep-related proposed biomarkers. The analysis microstructure highlighted detect specific oscillatory
Язык: Английский
Процитировано
57