But this latest study also poses an interesting question: Could AD in its "preclinical stages" also lead to SDB and explain the increased prevalence of SDB in the elderly?
The study will be presented at the ATS 2013 International Conference.
"It's really a chicken and egg story," said Ricardo S. Osorio, MD, a research assistant professor at NYU School of Medicine who led the study. "Our study did not determine the direction of the causality, and, in fact, didn't uncover a significant association between the two, until we broke out the data on lean and obese patients."
When the researchers did consider body mass, they found that lean patientswith SDB did possess several specific and non-specific biomarkers of AD risk. Among obese patients , glucose hypometabolism was also found in the medial temporal lobe, but was not significant in other AD-vulnerable regions.
"We know that about 10 to 20 percent of middle-aged adults in the United States have SDB [defined as an apnea-hypopnea index greater than 5] and that the number jumps dramatically in those over the age of 65," said Dr. Osorio, noting that studies put the percentage of people over the age of 65 with SDB between 30 and 60 percent. "We don't know why it becomes so prevalent, but one factor may be that some of these patients are in the earliest preclinical stages of AD."
According to Dr. Osorio, the biochemical harbingers of AD are present 15 to 20 years before any of its currently recognized symptoms become apparent.
The NYU study enrolled 68 cognitively normal elderly patients (mean age 71.4±5.6, range 64-87) who underwent two nights of home monitoring for SDB and were tested for at least one diagnostic indicator of AD. The researchers looked at P-Tau, T-Tau and Aβ42 in CSF, FDG-PET (to measure glucose metabolism), Pittsburgh compound B (PiB) PET to measure amyloid load, and/or structural MRI to measure hippocampal volume. Reduced glucose metabolism in AD-vulnerable regions, decreased hippocampal volume, changes in P-Tau, T-Tau and Aβ42, and increased binding of PiB-PET are recognized as markers of risk for AD and have been reported to be abnormal in healthy subjects before the disease onset.
Biomarkers for AD risk were found only among lean study participants with SDB. These patients showed a linear association between the severity of SDB and CSF levels of the biomarker P-Tau and between SDB and glucose hypometabolism using FDG-PET, in the medial temporal lobe, the posterior cingulate cortex/precuneus and a composite score of all AD-vulnerable regions . Lean SDB patients also showed smaller hippocampi when compared to lean controls, but no differences were found in measures of amyloid burden such as decreased Aβ42 in CSF or PiB positive scans.