TY - JOUR
T1 - EEG spectral power abnormalities and their relationship with cognitive dysfunction in patients with Alzheimer’s disease and type 2 diabetes
AU - Benwell, Christopher S. Y.
AU - Davila-Perez, Paula
AU - Fried, Peter J.
AU - Jones, Richard N.
AU - Travison, Thomas G.
AU - Santarnecchi, Emiliano
AU - Pascual-Leone, Alvaro
AU - Shafi, Mouhsin M.
N1 - This study was primarily funded by the National Institutes of Health (NIH R21 NS082870). A.P.- L. was also supported in part by the Sidney R. Baer Jr. Foundation, the NIH (R01HD069776, R01NS073601, R21 MH099196, R21 NS085491, R21 HD07616), Harvard Catalyst | The Harvard Clinical and Translational Science Center (NCRR and the NCATS NIH, UL1 RR025758), the Football Players Health Study at Harvard University, and by the Defense Advanced Research Projects Agency (DARPA) via HR001117S0030. C.S.Y.B. was also supported by the Economic and Social Research Council (UK) (ES/I02395X/1), the Experimental Psychology Society (UK) and the Guarantors of Brain (UK). E.S. is partially supported by the Office of the Director of National Intelligence (ODNI), Intelligence Advanced Research Projects Activity (IARPA), via 2014-13121700007, by the Beth Israel Deaconess Medical Center (BIDMC) via the Chief Academic Officer (CAO) grant 2017, and by the Defense Advanced Research Projects Agency (DARPA) via HR001117S0030, and the NIH (P01 AG031720-06A1, R01 MH117063-01, R01 AG060981-01). M.M.S. is supported by the CURE (Citizens United for Research in Epilepsy) foundation, the Football Players Health Study (FPHS) at Harvard University, and the NIH (R01 MH115949, R01AG060987, R01 NS073601, P01 AG031720-06A1). The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard Catalyst, Harvard University and its affiliated academic health care centers, the National Institutes of Health, DARPA, IARPA, ODNI, BIDMC, or the Sidney R. Baer Jr. Foundation. The authors thank E. Seligson, N. Atkinson, and S. Saxena for their assistance in data collection, and A. Connor and J. Macone for regulatory and compliance oversight and assistance with evaluation of participant health and medical history.
PY - 2020/1
Y1 - 2020/1
N2 - Rhythmic neural activity has been proposed to play a fundamental role in cognition. Both healthy and pathological aging are characterized by frequency-specific changes in oscillatory activity. However, the cognitive relevance of these changes across the spectrum from normal to pathological aging remains unknown. We examined electroencephalography (EEG) correlates of cognitive function in healthy aging and 2 of the most prominent and debilitating age-related disorders: type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD). Relative to healthy controls (HC), patients with AD were impaired on nearly every cognitive measure, whereas patients with T2DM performed worse mainly on learning and memory tests. A continuum of alterations in resting-state EEG was associated with pathological aging, generally characterized by reduced alpha (α) and beta (β) power (AD < T2DM < HC) and increased delta (δ) and theta (θ) power (AD > T2DM > HC), with some variations across different brain regions. There were also reductions in the frequency and power density of the posterior dominant rhythm in AD. The ratio of (α + β)/(δ + θ) was specifically associated with cognitive function in a domain- and diagnosis-specific manner. The results thus captured both similarities and differences in the pathophysiology of cerebral oscillations in T2DM and AD. Overall, pathological brain aging is marked by a shift in oscillatory power from higher to lower frequencies, which can be captured by a single cognitively relevant measure of the ratio of (α + β) over (δ + θ) power.
AB - Rhythmic neural activity has been proposed to play a fundamental role in cognition. Both healthy and pathological aging are characterized by frequency-specific changes in oscillatory activity. However, the cognitive relevance of these changes across the spectrum from normal to pathological aging remains unknown. We examined electroencephalography (EEG) correlates of cognitive function in healthy aging and 2 of the most prominent and debilitating age-related disorders: type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD). Relative to healthy controls (HC), patients with AD were impaired on nearly every cognitive measure, whereas patients with T2DM performed worse mainly on learning and memory tests. A continuum of alterations in resting-state EEG was associated with pathological aging, generally characterized by reduced alpha (α) and beta (β) power (AD < T2DM < HC) and increased delta (δ) and theta (θ) power (AD > T2DM > HC), with some variations across different brain regions. There were also reductions in the frequency and power density of the posterior dominant rhythm in AD. The ratio of (α + β)/(δ + θ) was specifically associated with cognitive function in a domain- and diagnosis-specific manner. The results thus captured both similarities and differences in the pathophysiology of cerebral oscillations in T2DM and AD. Overall, pathological brain aging is marked by a shift in oscillatory power from higher to lower frequencies, which can be captured by a single cognitively relevant measure of the ratio of (α + β) over (δ + θ) power.
KW - Alzheimer's disease
KW - Cognitive aging
KW - EEG
KW - Neuropsychology
KW - Oscillations
KW - Type-2 diabetes mellitus
UR - http://www.scopus.com/inward/record.url?scp=85075390029&partnerID=8YFLogxK
U2 - 10.1016/j.neurobiolaging.2019.10.004
DO - 10.1016/j.neurobiolaging.2019.10.004
M3 - Article
C2 - 31727363
SN - 0197-4580
VL - 85
SP - 83
EP - 95
JO - Neurobiology of Aging
JF - Neurobiology of Aging
ER -
