TY - JOUR
T1 - Elevating understanding
T2 - Linking high-altitude hypoxia to brain aging through EEG functional connectivity and spectral analyses
AU - Coronel-Oliveros, Carlos
AU - Medel, Vicente
AU - Whitaker, Grace Alma
AU - Astudillo, Aland
AU - Gallagher, David
AU - Z-Rivera, Lucía
AU - Prado, Pavel
AU - El-Deredy, Wael
AU - Orio, Patricio
AU - Weinstein, Alejandro
N1 - Publisher Copyright:
© 2024 Massachusetts Institute of Technology.
PY - 2024/4/1
Y1 - 2024/4/1
N2 - High-altitude hypoxia triggers brain function changes reminiscent of those in healthy aging and Alzheimer’s disease, compromising cognition and executive functions. Our study sought to validate high-altitude hypoxia as a model for assessing brain activity disruptions akin to aging. We collected EEG data from 16 healthy volunteers during acute high-altitude hypoxia (at 4,000 masl) and at sea level, focusing on relative changes in power and aperiodic slope of the EEG spectrum due to hypoxia. Additionally, we examined functional connectivity using wPLI, and functional segregation and integration using graph theory tools. High altitude led to slower brain oscillations, that is, increased δ and reduced α power, and flattened the 1/f aperiodic slope, indicating higher electrophysiological noise, akin to healthy aging. Notably, functional integration strengthened in the θ band, exhibiting unique topographical patterns at the subnetwork level, including increased frontocentral and reduced occipitoparietal integration. Moreover, we discovered significant correlations between subjects’ age, 1/f slope, θ band integration, and observed robust effects of hypoxia after adjusting for age. Our findings shed light on how reduced oxygen levels at high altitudes influence brain activity patterns resembling those in neurodegenerative disorders and aging, making high-altitude hypoxia a promising model for comprehending the brain in health and disease.
AB - High-altitude hypoxia triggers brain function changes reminiscent of those in healthy aging and Alzheimer’s disease, compromising cognition and executive functions. Our study sought to validate high-altitude hypoxia as a model for assessing brain activity disruptions akin to aging. We collected EEG data from 16 healthy volunteers during acute high-altitude hypoxia (at 4,000 masl) and at sea level, focusing on relative changes in power and aperiodic slope of the EEG spectrum due to hypoxia. Additionally, we examined functional connectivity using wPLI, and functional segregation and integration using graph theory tools. High altitude led to slower brain oscillations, that is, increased δ and reduced α power, and flattened the 1/f aperiodic slope, indicating higher electrophysiological noise, akin to healthy aging. Notably, functional integration strengthened in the θ band, exhibiting unique topographical patterns at the subnetwork level, including increased frontocentral and reduced occipitoparietal integration. Moreover, we discovered significant correlations between subjects’ age, 1/f slope, θ band integration, and observed robust effects of hypoxia after adjusting for age. Our findings shed light on how reduced oxygen levels at high altitudes influence brain activity patterns resembling those in neurodegenerative disorders and aging, making high-altitude hypoxia a promising model for comprehending the brain in health and disease.
KW - 1/f aperiodic activity
KW - Aging
KW - EEG
KW - Functional connectivity
KW - High-altitude hypoxia
KW - Oxygen supply
KW - Power spectrum
UR - http://www.scopus.com/inward/record.url?scp=85187455414&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/61f20aaa-4bd6-3f7f-b12a-10a81ac38bba/
U2 - 10.1162/netn_a_00352
DO - 10.1162/netn_a_00352
M3 - Article
AN - SCOPUS:85187455414
SN - 2472-1751
VL - 8
SP - 275
EP - 292
JO - Network Neuroscience
JF - Network Neuroscience
IS - 1
ER -