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Medial temporal lobe and obstructive sleep apnea: Effect of sex, age, cognitive status and free-water

Medial temporal structures, namely the hippocampus, the entorhinal cortex and the parahippocampal gyrus, are particularly vulnerable to Alzheimer’s disease and hypoxemia. Here, we tested the associations between obstructive sleep apnea (OSA) severity and medial temporal lobe volumes in 114 participa...

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Detalles Bibliográficos
Autores principales: Martineau-Dussault, Marie-Ève, André, Claire, Daneault, Véronique, Baril, Andrée-Ann, Gagnon, Katia, Blais, Hélène, Petit, Dominique, Montplaisir, Jacques Y., Lorrain, Dominique, Bastien, Célyne, Hudon, Carol, Descoteaux, Maxime, Boré, Arnaud, Theaud, Guillaume, Thompson, Cynthia, Legault, Julie, Martinez Villar, Guillermo E., Lafrenière, Alexandre, Lafond, Chantal, Gilbert, Danielle, Carrier, Julie, Gosselin, Nadia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9668668/
https://www.ncbi.nlm.nih.gov/pubmed/36272339
http://dx.doi.org/10.1016/j.nicl.2022.103235
Descripción
Sumario:Medial temporal structures, namely the hippocampus, the entorhinal cortex and the parahippocampal gyrus, are particularly vulnerable to Alzheimer’s disease and hypoxemia. Here, we tested the associations between obstructive sleep apnea (OSA) severity and medial temporal lobe volumes in 114 participants aged 55–86 years (35 % women). We also investigated the impact of sex, age, cognitive status, and free-water fraction correction on these associations. Increased OSA severity was associated with larger hippocampal and entorhinal cortex volumes in women, but not in men. Greater OSA severity also correlated with increased hippocampal volumes in participants with amnestic mild cognitive impairment, but not in cognitively unimpaired participants, regardless of sex. Using free-water corrected volumes eliminated all significant associations with OSA severity. Therefore, the increase in medial temporal subregion volumes may possibly be due to edema. Whether these structural manifestations further progress to neuronal death in non-treated OSA patients should be investigated.