Role of Hypoxia Ans Sleep Fragmentation in Alzheimer's Disease. and Sleep Fragmentation.
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|ClinicalTrials.gov Identifier: NCT02814045|
Recruitment Status : Completed
First Posted : June 27, 2016
Last Update Posted : March 22, 2021
Alzheimer's Disease (AD) is the most prevalent neurodegenerative disease, manifested as an initial deficit of episodic memory that evolves into a global cognitive and psychosocial dysfunction and which prevalence is increasing around the world. Sleep disturbance is frequent since early stages of the disease and sleep fragmentation had been demonstrated increase the production of amyloid peptide (AB) (main pathological hallmark) in non-demented population. Obstructive Sleep Apnea (OSA), which consist in intermittent hypoxia and sleep fragmentation, is a major health problem with multiple systemic effects and it's very prevalent in AD. However, the influence of this comorbidity on the cognitive evolution of AD patients remains unknown. The investigation of neurobiological markers and sleep recording may reveal potential mechanisms of neurodegeneration and explain the influence of sleep fragmentation and/or hypoxia on cognitive decline.
To fill those gaps, investigators will perform a multidisciplinary and translational project to assess the progression of symptoms in AD patients, diagnosis of sleep disturbance and new biomarkers of progression of the disease.
The present proposal is going to be developed by coordination of different expertises that will be range from the clinical research conducted by a medical neurologist, to the animal model and most molecular work, to be done by an experimented group in mouse work.
|Condition or disease|
|Alzheimer's Disease Obstructive Sleep Apnea|
|Study Type :||Observational|
|Actual Enrollment :||144 participants|
|Official Title:||Impact of Obstructive Sleep Apnea in the Evolution of Alzheimer Disease. Role of Hypoxia and Sleep Fragmentation|
|Actual Study Start Date :||November 2015|
|Actual Primary Completion Date :||June 2017|
|Actual Study Completion Date :||July 2017|
Alzheimer with OSA
Alzheimer with OSA after PSG
Alzheimer without OSA
Alzheimer without OSA after PSG
- Change from baseline in cognitive scores on the Disease Assessment Scale-cognitive at 12 months in patients with mild AD with and without OSA. [ Time Frame: One year ]For this objective we will recruit consecutively 72 patients with OSA and another 72 patients without OSA from the same population of patients with mild initial AD. We will use extensive neuropsychological battery at baseline and at 12 month and polysomnography (PSG) to select both groups of patients at baseline.
- Differential pattern of biomarkers at baseline in in patients with mild AD with and without OSA. [ Time Frame: One year ]For this objective we will use CSF (ELISA will be employed to detect the levels of hypoxia-inducible factor 1-alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF); and CSF biomarkers of AD as AB42, tau and phosphotau. Lipidaemic and metabolomic analyses will be performed on both, blood sample and CSF. Brain MRI (hippocampal volume, specific patterns of cerebral perfusion and spectroscopy) and actigraph registry. Blood samples to determine inflammatory markers (TNF-alpha, Interleukine-6 and Interleukine-8), the Thiobarbituric Acid Reactive Substances (TBARS) and genotyping APOE4 will be preformed. We will analyze the correlation of these biological biomarkers with cognitive and behavioural progression in OSA and non-OSA AD patients.
Biospecimen Retention: Samples With DNA
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Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02814045
|Hospital santa Maria|
|Lleida, Catalonia, Spain, 25198|
|Hospital Santa Maria Lleida|
|Lleida, Spain, 25198|
|Principal Investigator:||Gerard Piñol, Md;PhD||Hospital Santa Maria|