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Sleep disorders have a harmful impact on our brain and under certain conditions are thought to be linked to an increased risk of Alzheimer’s disease. A link which had until now been poorly understood by the scientific community. For the first time, a study based on multiple brain imaging techniques conducted by Inserm researcher Géraldine Rauchs at two laboratories hosted at GIP CYCERON – the Physiopathology and Imaging of Neurological Disorders laboratory (Inserm/ Université de Caen-Normandie) and the Neuropsychology and Imaging of Human Memory laboratory (Inserm/Université de Caen-Normandie/Ecole Pratique des Hautes Etudes – PSL/CHU Caen) – has revealed, among other forms of impairment, the appearance of amyloid plaques characteristic of Alzheimer’s disease in the brains of older adults with sleep apnea but no cognitive disorders. The results of this research were published in JAMA Neurology on March 23, 2020.
Obstructive sleep apnea syndrome is the most common sleep breathing disorder, affecting more than 30% of the population over the age of 65. It consists of uncontrolled and repeated pauses in breathing during sleep, linked to the temporary obstruction of the upper airways, in the throat, and is linked to numerous health problems – primarily cardiovascular diseases. However, given that the condition remains silent for a long time, it is probably underestimated in the general population.
In order to do this, Inserm researcher Géraldine Rauchs conducted a study at the Physiopathology and Imaging of Neurological Disorders laboratory (Inserm/ Université de Caen-Normandie) in collaboration with the Neuropsychology and Imaging of Human Memory laboratory (Inserm/Université de Caen-Normandie/Ecole Pratique des Hautes Etudes – PSL). This study, published in JAMA Neurology, used a variety of brain imaging techniques to map cerebral changes in people with untreated sleep apnea, on the structural, molecular and functional levels.
Changes in the brain
The researchers began by recruiting 127 participants over the age of 65, in good health and with no cognitive disorders. Using a portable home device to record their sleep and breathing overnight, the researchers detected the presence of varying degrees of sleep apnea in 75% of them.
In addition, the participants all underwent a battery of tests to evaluate their cognitive function, particularly executive functions and memory. They answered questionnaires about how they perceived their cognitive function and sleep quality. Several brain imaging examinations were then conducted in order to study their brain from every angle and detect any changes potentially linked to Alzheimer’s disease. Although no differences were observed among the participants in terms of cognitive performance, the imaging did reveal several notable changes in the brains of those with sleep apnea.
In these participants, there is a more marked accumulation of beta-amyloid protein in the brain. Characteristic of Alzheimer’s disease, this protein accumulates in the form of plaque which, depending on its density and distribution in the brain, may lead to the onset of clinical signs of the disease. Furthermore, the researchers observed increases in gray matter mass and glucose consumption, suggesting the presence of inflammatory processes in the brain.
To continue this research, Rauchs and her team will now look at the impact of treating apnea on changes in brain lesions and analyze the differences between the brains of male and female sleep apnea patients.
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Association of sleep-disordered breathing with Alzheimer’s disease biomarkers in community-dwelling older adults Claire André1,2, PhD; Stéphane Rehel1,2, MSc; Elizabeth Kuhn1, MSc; Brigitte Landeau1, MSc; Inès Moulinet1, MSc; Edelweiss Touron1, MSc; Valentin Ourry2, MSc; Gwendoline Le Du1, MSc; Florence Mézenge1, BA; Clémence Tomadesso1, PhD; Robin de Flores1, PhD; Alexandre Bejanin1, PhD; Siya Sherif1, PhD; Nicolas Delcroix3, PhD; Alain Manrique4, MD, PhD; Ahmed Abbas2, PharmD; Natalie L. Marchant5, PhD; Antoine Lutz6, PhD; Olga M. Klimecki7, PhD; Fabienne Collette8, PhD; Eider M. Arenaza-Urquijo1, PhD; Géraldine Poisnel1, PhD; Denis Vivien1,9, PhD; Françoise Bertran10, MD; Vincent de la Sayette2,11, MD; Gaël Chételat1*, PhD; Géraldine Rauchs2*, PhD; for the Medit-Ageing Research Group. 1 Normandie Univ, UNICAEN, INSERM, U1237, PhIND “Physiopathology and Imaging of Neurological Disorders”, Institut Blood and Brain @ Caen-Normandie, Cyceron, 14000 Caen, France. 2 Normandie Univ, UNICAEN, PSL Université, EPHE, INSERM, U1077, CHU de Caen, GIP Cyceron, NIMH, Caen, France. 3 CNRS, UMS-3048, GIP Cyceron, Bd Henri Becquerel, Caen, France. 4 Normandie Univ, UNICAEN, EA 4650 SEILIRM, GIP Cyceron, Caen, France. 5 Division of Psychiatry, University College London, London, United Kingdom. 6 Lyon Neuroscience Research Center INSERM U1028, CNRS UMR5292, Lyon University, Lyon, France. 7 Swiss Center for Affective Sciences, Department of Medicine, University of Geneva, Geneva, Switzerland. 8 GIGA-CRC, In Vivo Imaging and Psychology and Cognitive Neuroscience Unit, Liège University, Belgium. 9 Département de Recherche Clinique, CHU Caen-Normandie, Caen, France. 10 Unité d’exploration et de traitement des troubles du sommeil, CHU de Caen, Caen, France. 11 Service de Neurologie, CHU de Caen, Caen, France. JAMA Neurology, Mars 2020 DOI : 10.1001/jamaneurol.2020.0311