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Title Authors PubMed ID
1 Longitudinal relationships among cerebrospinal fluid biomarkers, cerebral blood flow, and grey matter volume in individuals with a familial history of Alzheimer s disease Sanami S; Intzandt B; Huck J; Villeneuve S; Iturria-Medina Y; Gauthier CJ; Prevent-Ad Research Group None; 40347524
CONCORDIA
2 Sleep spindles and slow oscillations predict cognition and biomarkers of neurodegeneration in mild to moderate Alzheimer's disease Páez A; Gillman SO; Dogaheh SB; Carnes A; Dakterzada F; Barbé F; Dang-Vu TT; Ripoll GP; 39878233
CONCORDIA
3 The β2-adrenergic biased agonist nebivolol inhibits the development of Th17 and the response of memory Th17 cells in an NF-κB-dependent manner Hajiaghayi M; Gholizadeh F; Han E; Little SR; Rahbari N; Ardila I; Lopez Naranjo C; Tehranimeh K; Shih SCC; Darlington PJ; 39445009
BIOLOGY
4 Effects of early midlife ovarian removal on sleep: Polysomnography-measured cortical arousal, homeostatic drive, and spindle characteristics Brown A; Gervais NJ; Gravelsins L; O' Byrne J; Calvo N; Ramana S; Shao Z; Bernardini M; Jacobson M; Rajah MN; Einstein G; 39178647
HKAP
5 The β2-adrenergic receptor agonist terbutaline upregulates T helper-17 cells in a protein kinase A-dependent manner Carvajal Gonczi CM; Hajiaghayi M; Gholizadeh F; Xavier Soares MA; Touma F; Lopez Naranjo C; Rios AJ; Pozzebon C; Daigneault T; Burchell-Reyes K; Darlington PJ; 37438188
PERFORM
6 Cross-collection latent Beta-Liouville allocation model training with privacy protection and applications Luo Z; Amayri M; Fan W; Bouguila N; 36685642
ENCS
7 Estrogen receptors observed at extranuclear neuronal sites and in glia in the nucleus accumbens core and shell of the female rat: Evidence for localization to catecholaminergic and GABAergic neurons Almey A; Milner TA; Brake WG; 35397175
CSBN
8 Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex Olajide OJ; Chapman CA; 34144329
PSYCHOLOGY
9 Data-driven beamforming technique to attenuate ballistocardiogram artefacts in electroencephalography-functional magnetic resonance imaging without detecting cardiac pulses in electrocardiography recordings Uji M; Cross N; Pomares FB; Perrault AA; Jegou A; Nguyen A; Aydin U; Lina JM; Dang-Vu TT; Grova C; 34101939
PERFORM
10 How cerebral cortex protects itself from interictal spikes: The alpha/beta inhibition mechanism Pellegrino G; Hedrich T; Sziklas V; Lina JM; Grova C; Kobayashi E; 34002916
PERFORM
11 Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease. Olajide OJ, Suvanto ME, Chapman CA 33495355
PSYCHOLOGY
12 Topographical distribution of Aβ predicts progression to dementia in Aβ positive mild cognitive impairment Pascoal TA, Therriault J, Mathotaarachchi S, Kang MS, Shin M, Benedet AL, Chamoun M, Tissot C, Lussier F, Mohaddes S, Soucy JP, Massarweh G, Gauthier S, Rosa-Neto P, 32582834
PERFORM
13 Comparison of underivatized silica and zwitterionic sulfobetaine hydrophilic interaction liquid chromatography stationary phases for global metabolomics of human plasma Sonnenberg RA; Naz S; Cougnaud L; Vuckovic D; 31439439
CHEMBIOCHEM
14 Reciprocal modulation of helper Th1 and Th17 cells by the β2-adrenergic receptor agonist drug terbutaline. Carvajal Gonczi CM, Tabatabaei Shafiei M, East A, Martire E, Maurice-Ventouris MHI, Darlington PJ 28710773
PERFORM

 

Title:Sleep spindles and slow oscillations predict cognition and biomarkers of neurodegeneration in mild to moderate Alzheimer's disease
Authors:Páez AGillman SODogaheh SBCarnes ADakterzada FBarbé FDang-Vu TTRipoll GP
Link:https://pubmed.ncbi.nlm.nih.gov/39878233/
DOI:10.1002/alz.14424
Publication:Alzheimer s & dementia : the journal of the Alzheimer s Association
Keywords:Alzheimer's diseaseamyloid betabiomarkerscognitioncognitive declinesleepsleep spindlesslow oscillationstau
PMID:39878233 Category: Date Added:2025-01-29
Dept Affiliation: CONCORDIA
1 Sleep, Cognition and Neuroimaging Laboratory, Concordia University, Montreal, Canada.
2 Centre de Recherche de l'Institut Universitaire de Gériatrie de Montréal (CRIUGM), Montréal (Québec), Canada.
3 Nuffield Department for Primary Care Health Sciences, University of Oxford, Oxford, UK.
4 Unitat de Trastorns Cognitius, Cognition and Behavior Study Group, Hospital Universitari Santa Maria Universitat de Lleida, Lleida, Spain.
5 Translational Research in Respiratory Medicine (TRRM), Hospital Universitari Arnau de Vilanova-Santa Maria, Biomedical Research Institute of Lleida (IRBLleida), Lleida, Spain.
6 Alzheimer's Disease and Other Cognitive Disorders Unit, Neurology Service, Hospital Clínic de Barcelona, Fundació de Recerca Clínic - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.

Description:

Introduction: Changes in sleep physiology can predate cognitive symptoms by decades in persons with Alzheimer's disease (AD), but it remains unclear which sleep characteristics predict cognitive and neurodegenerative changes after AD onset.

Methods: Using data from a prospective cohort of mild to moderate AD (n = 60), we analyzed non-rapid eye movement sleep spindles and slow oscillations (SOs) at baseline and their associations with baseline amyloid beta (Aß) and tau and with cognition from baseline to 3-year follow-up.

Results: Higher spindle and SO activity predicted significant changes in Aß and tau at baseline, lower Alzheimer's Disease Assessment Scale Cognitive Subscale (better cognitive performance) score, and higher Mini-Mental State Examination score from baseline to 36 months. Spindles and SOs mediated the effect of phosphorylated tau 181 (pTau181)/Aß42 on cognition, while pTau181/aß42 moderated the effect of spindles and SOs on cognition.

Discussion: Our findings demonstrate that spindle and SO activity during sleep constitute predictive and non-invasive biomarkers of neurodegeneration and cognition in AD patients.

Highlights: Sleep spindles predict long-term cognitive performance in AD. Sleep spindle and SOs can be predictive, non-invasive biomarkers for AD. Sleep may be one of the most important modifiable risk factors for AD progression. Sleep microarchitecture is a novel therapeutic target for preserving brain heath. Sleep physiology can provide novel therapeutic targets to slow AD progression.





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