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Abstract Details

Validation of Sleep EEG-based Brain Age Index for Dementia-related Diseases
Aging, Dementia, and Behavioral Neurology
P5 - Poster Session 5 (8:00 AM-9:00 AM)
10-011

Using a dataset of 11,039 sleep studies, we aim to investigate the association between  brain ages index (BAI) and dementia and validate sleep EEG-based brain age as a biomarker for dementia. We hypothesize that patients with dementia-related diseases have significantly higher BAI than patients without dementia.

Dementia is a common neurodegenerative disease in the elderly population. The progressive damage to the neurons causes gradual loss of memory, communication, reasoning, as well as psychiatric disorders. The deviations from the normal aging, known as Brain Age Index (BAI), have shown potential to serve as biomarkers for cognitive impairment.
Using our previously developed model, brain ages were computed based on a sleep EEG-based brain age algorithm. Studies were categorized into dementia, mild cognitive impairment (MCI), ambiguous, and non-dementia groups based on patients' clinical diagnosis and MoCA/MMSE scores.
We found that the BAI of patients with dementia (4.11 ± 10.02 yrs) were significantly higher than those of patients with no dementia (0.516 ±10.40 yrs), with p-value of 0.002 for independent-samples t-test, and those of healthy patients (-0.67 ± 9.52 yrs), with p-value of 0.0002. The BAI of patients with MCI (2.29 ± 8.13 yrs) were also significantly higher than those of healthy patients. BAI and MoCA score were negatively correlated with correlation coefficient of -0.211 (p-value = 0.036) as expected. Binary classification of dementia vs. non-dementia patients with logistic regression using BAI features yielded AUROC of 0.85. Top BAI features for dementia were related to kurtosis of EEG signals in N3 and REM stages.
Our results support the validity of sleep EEG-based Brain Age Index as a biomarker of dementia and open new possibilities for using BAI as an assessment tool. Further research is required to investigate how cognitive deficits in different types of dementia-related diseases contribute to higher brain age index.
Authors/Disclosures

PRESENTER
No disclosure on file
Haoqi Sun, PhD (Massachusetts General Hospital) Dr. Sun has nothing to disclose.
Luis Paixao, BMBCh, MSc (University of Miami Miller School of Medicine) No disclosure on file
Robert J. Thomas, MD (Beth Israel Deaconess Medical Center) Dr. Thomas has received personal compensation in the range of $500-$4,999 for serving as a Consultant for GLG Councils. Dr. Thomas has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Guidepoint Global. Dr. Thomas has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Jazz Pharmaceuticals. Dr. Thomas has received intellectual property interests from a discovery or technology relating to health care. Dr. Thomas has received publishing royalties from a publication relating to health care.
Alice D. Lam, MD, PhD Dr. Lam has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for Neurona Therapeutics. Dr. Lam has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Acadia Pharmaceuticals. The institution of Dr. Lam has received research support from Neurona Therapeutics. The institution of Dr. Lam has received research support from NIH. The institution of Dr. Lam has received research support from Alzheimer's Association.
M. B. Westover, MD, PhD (MGH) Dr. Westover has received personal compensation in the range of $50,000-$99,999 for serving as a Consultant for Beacon Biosignals. Dr. Westover has stock in Beacon Biosignals. The institution of Dr. Westover has received research support from NIH. Dr. Westover has received publishing royalties from a publication relating to health care. Dr. Westover has a non-compensated relationship as a cofounder with Beacon Biosignals that is relevant to Âé¶¹´«Ã½Ó³»­ interests or activities.