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Enregistrement W4414554709 · doi:10.1186/s13024-025-00877-2

Autophagic impairment in sleep–wake circuitry is linked to sleep loss at the early stages of Alzheimer’s disease

2025· article· en· W4414554709 sur OpenAlexaff
Christopher D. Morrone, Arielle A. Tsang, Wai Haung Yu

Notice bibliographique

RevueMolecular Neurodegeneration · 2025
Typearticle
Langueen
DomaineNeuroscience
ThématiqueSleep and Wakefulness Research
Établissements canadiensThe Scarborough HospitalUniversity of TorontoCentre for Addiction and Mental Health
Organismes subventionnairesNational Institutes of HealthBrightFocus Foundation
Mots-clésDiseaseAutophagyNeurologyHuman physiologyVulnerability (computing)Sleep lossSleep (system call)

Résumé

récupéré en direct d'OpenAlex

Abstract Background Proteostasis, in particular the impairment of autophagic activity, is linked to sleep dysregulation and is an early sign of dementias including Alzheimer’s disease (AD). This coupling of events may be a critical alteration driving proteinopathy and AD progression. In the present study, we investigated sleep–wake and memory regulating neurons for vulnerability to autophagic impediment, and related these findings to progression of the sleep and cognitive phenotype. Methods Using the double knock-in AD mouse model, App NL−G−F x MAPT , we examined phenotypic and pathological alterations at several timepoints and compared to age-matched single knock-in MAPT mice. Spatial learning, memory and executive Function were investigated in the Barnes maze. Sleep was investigated by 24-h locomotor activity and EEG. Immunostaining for autophagic, neuronal and pathological markers was conducted in brain regions related to memory (hippocampus, prefrontal cortex, entorhinal cortex) and the sleep–wake cycle (hypothalamus, locus coeruleus). Hippocampal electrophysiological recordings were conducted to probe neuronal Function during object investigation. A 3-day sleep disruption was conducted in MAPT mice to investigate autophagic changes following sleep loss. Autophagy was activated in MAPT mice with trehalose to probe effects on sleep recovery. Results We identified that disrupted sleep occurred from early-stages in App NL−G−F x MAPT mice, that sleep declined over age, and sleep deficits preceded cognitive impairments in late-stages. Cytoplasmic autophagic impediment in hypothalamic and locus coeruleus sleep–wake neurons occurred in early-stage App NL−G−F x MAPT mice, prior to significant β-amyloid deposition in these regions, with a failure of lysosomal flux over disease progression. Autophagic changes in the hippocampus and cortex at early-stage were predominantly in processes and less frequently associated with the lysosome. Plaque-associated autophagic and lysosomal accumulations were frequent from the early-stage. Sex differences in the AD phenotype were prominent, including greater cognitive decline in males than females, linked to increased proteostasis burden in EC layer II neurons and hippocampal tau in the late-stage. Conversely, sleep impairments were more rapid in females including less REM sleep recovery than males, along with greater autophagic burden in hippocampal processes of female App NL−G−F x MAPT mice. We probed the sleep-cognition linkage demonstrating hippocampal electrophysiological slowing during cognitive processing in mid-stage App NL−G−F x MAPT mice, prior to cognitive decline. We provide evidence for a positive feedback loop in the autophagic-sleep relationship by demonstrating that disrupted sleep in MAPT mice led to arrhythmic sleep patterns and accumulations of autophagic aggregates in the hippocampus and hypothalamus, similar to as was seen in the early Alzheimer’s phenotype. We further probed the autophagy-sleep linkage by treating MAPT mice with trehalose to activate autophagy and demonstrate an improvement in sleep recovery following a sleep disruption. Conclusions These findings demonstrate the vulnerability of sleep-regulating neurons to proteostatic dysfunction and the sleep-autophagy linkage as an early, and treatable, Alzheimer’s disease mechanism. Graphical Abstract Morrone et al provide evidence for the linkage between sleep and autophagic disruptions in Alzheimer’s disease (AD) progression. At early AD stages, sleep-wake regulating neurons in the hypothalamus and locus coeruleus exhibit increased cytoplasmic inclusions concomitant with the onset of sleep disturbances. Early-stage autophagic aggregates in the hippocampus appear more prominently in neuronal processes and in the cortex linked to plaques. This pathology worsens over AD progression, including advanced sleep and cognitive deficits, autophagic aggregates in entorhinal cortex-hippocampus projecting neurons. Disrupting sleep in control mice mimics the hippocampal, hypothalamic and sleep patterns impairments observed in early-stage AD, and therapeutic activation of autophagy improves sleep recovery. See also Table 1 for a summary of changes along with sex differences in autophagy and behavioral readouts.

Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.

Comment cette classification a été obtenuedéplier

Prédiction distillée sur la base complète

Imitation des enseignants

Ni prévalence calibrée, ni vérité terrain. Validation humaine à venir. Apprise à partir de 10 348 étiquettes directes de Codex et de 10 348 étiquettes directes de Gemma. Le mode candidate est l'union des têtes enseignantes seuillées; le consensus est leur intersection. Ces sorties portent le statut machine_predicted_unvalidated et ne sont ni des étiquettes humaines ni des étiquettes directes de modèles de pointe.

score de la tête « metaresearch » (Codex)0,000
score de la tête « metaresearch » (Gemma)0,000
Version: codex-gemma-dda1882f352aStatut de validation: machine_predicted_unvalidated
Catégories candidatesaucune
Catégories consensuellesaucune
DomaineSignal candidat: aucune · Signal consensuel: aucune
Devis d'étudeSignal candidat: Expérimental (laboratoire) · Signal consensuel: Expérimental (laboratoire)
GenreSignal candidat: Empirique · Signal consensuel: Empirique
Score de désaccord entre enseignants0,094
Score d'incertitude au seuil0,739

Scores Codex et Gemma par catégorie

CatégorieCodexGemma
Métarecherche0,0000,000
Méta-épidémiologie (sens strict)0,0000,000
Méta-épidémiologie (sens large)0,0000,000
Bibliométrie0,0000,001
Études des sciences et des technologies0,0000,000
Communication savante0,0000,000
Science ouverte0,0000,000
Intégrité de la recherche0,0000,000
Charge utile insuffisante (le modèle a refusé de juger)0,0000,000

Scores machine (provisoires)

Les deux têtes enseignantes du modèle étudiant, lues sur ce travail. Un score ordonne la base pour la relecture; il n'affirme jamais une catégorie, et le statut de validation accompagne chaque rangée tel quel.

Scores de référence d'un modèle non mature (critères de maturité non atteints, 7 itérations). Un score ordonne; il n'affirme jamais une catégorie.

Tête enseignante Opus0,026
Tête enseignante GPT0,298
Écart entre enseignants0,272 · la distance entre les deux têtes enseignantes sur ce seul travail
Statut de validationscore_only:v0-immature-baseline · tel quel depuis la passe de notation : score_only signifie que le nombre peut ordonner les travaux, et qu'aucune étiquette de catégorie n'en découle

Classification

machine, non validée

Prédiction automatique; un appel candidat d’une seule tête enseignante, pas un consensus.

Les modèles n’ont appliqué aucune catégorie : rien dans la taxonomie ne correspondait à ce travail.
Devis d'étudeExpérimental (laboratoire)
Domainenon disponible
GenreEmpirique

Le détail, modèle par modèle et score par score, se trouve en fin de page sous « Comment cette classification a été obtenue ».

En bref

Citations3
Publié2025
Routes d'admission1
Résumé présentoui

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