Alzheimer Disease, Sleep Apnea
Conditions
Brief summary
Age-related sleep changes and common sleep disorders like obstructive sleep apnea (OSA) may increase amyloid burden and represent risk factors for cognitive decline in the elderly. We will directly interrogate the brain using a 2-night nocturnal polysomnography (NPSG) and amyloid deposition using C-PiB PET/MR both at baseline and at the 24-month follow-up. This study has the potential to identify the mechanisms by which age-related sleep changes contribute to AD neurodegeneration in cognitively normal elderly, the group that could profit the most from sleep preventive strategies.
Interventions
DIAGNOSTIC_TESTPET Scan and nocturnal polysomnography
Amyloid PET scans will be used to assess amyloid burden in the brain, and nocturnal polysomnography will be used to assess sleep and cardiopulmonary variables
Sponsors
NYU Langone Health
National Institute on Aging (NIA)
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
55 Years to 75 Years
Healthy volunteers
Yes
Inclusion criteria
To be eligible to participate in this study, an individual must meet all of the following criteria: * Male and female subjects with normal cognition and 55-75 years. * Within normal limits on neurological and psychiatric examinations. All subjects enrolled will have a CDR=0. * All subjects will have had a minimum of 12 years of education. Among minority subjects \>80% of the elderly individuals coming to the NYU-ADC meet this criterion. The education restriction reduces performance variance on cognitive test measures and improves the sensitivity for detecting pathology and disease progression using the robust norms available at NYU. Given most subjects will meet this criterion we do not consider this a major selection bias or generalization limitation for this study. * An informed family member or life-partner (preferably bed-partner) will be interviewed to confirm the reliability of the subject interview.
Exclusion criteria
An individual who meets any of the following criteria will be excluded from participation in this study: * History of brain tumor, MRI evidence of brain damage or brain disease including significant trauma, hydrocephalus, seizures, mental retardation or other serious neurological disorder (e.g. Parkinson's disease or other movement disorders). * Significant history of alcoholism or drug abuse. * History of psychiatric illness (e.g., schizophrenia, bipolar, PTSD, or life-long history of major depression). * Geriatric Depression Scale (short form)\>6. * Insulin dependent diabetes. * Evidence of clinically relevant cardiac, pulmonary, endocrine or hematological conditions. * Physical impairment of such severity as to adversely affect the validity of psychological testing. * Any prosthetic devices (e.g., pacemaker or surgical clips) that constitutes a hazard for MRI imaging. * Medications affecting cognition: Narcotic analgesics, chronic use of medications with anticholinergic activity, anti-Parkinsonian medications (carbidopa/levodopa, amantadine, bromocriptine, selegiline). Others: amphetamines, amphetamine-like compounds, appetite suppressants, phenothiazines, reserpine, buspirone, clonidine, disulfiram, guanethidine, MAO inhibitors, theophylline, tricyclic antidepressants, salicylates, cholinesterase inhibitors and memantine. * History of a first-degree family member with early onset (age \<60 years) dementia. * Irregular sleep-wake rhythms (based on the actigraphy recordings) or severe OSA (AHI4%≥30). * Chronic use of antidepressants and melatonin are allowed. * Excessive daytimes sleepiness (Epworth Sleepiness Scale \>10) or history of CVE (arrhythmias, heart valve disease, cardiomyopathy, carotid or coronary artery disease and chest pain) will not be allowed in the OSA groups.
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Establishing how mild-to-moderate OSA increases AD risk will inform novel preventive therapies for AD. | 2.5 years |
Secondary
| Measure | Time frame |
|---|---|
| Establishing that SWS quality is associated with longitudinal amyloid deposition will identify a key mechanism by which age increases AD risk. | 2.5 years |
Countries
United States
Contacts
PRINCIPAL_INVESTIGATORRicardo Osorio, MD
New York Langone Medical Center
Outcome results
None listed