Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.
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Zhang Shaoshi, Roemer-Cassiano Sebastian N, Chong Joyce Ruifen, Fang Tian, Li Yan, Wang Ziwen, Zeng Tianchu, Li Xin, Deco Gustavo, Venketasubramanian Narayanaswamy, Zhou Juan Helen, Chen Christopher Li-Hsian, Alzheimer's Disease Neuroimaging Initiative, Lai Mitchell K P, Franzmeier Nicolai, Yeo B T Thomas
Аннотация
INTRODUCTION: Excitation-inhibition (E/I) imbalance has been proposed as an early circuit-level mechanism in Alzheimer's disease (AD), but its relationship to molecular pathology and cognition in humans remains unclear.
METHODS: We integrated biophysical modeling of resting-state functional magnetic resonance imaging with cerebrospinal fluid (CSF) and plasma biomarkers to examine whether E/I ratio links amyloid pathophysiology to memory in non-demented individuals across two cohorts from North America (N = 302; CSF amyloid beta 42 [Aβ42]) and Singapore (N = 240; plasma phosphorylated tau 217 [p-tau217]).
RESULTS: Elevated E/I ratio was associated with lower CSF Aβ42 and higher plasma p-tau217, with greater sensitivity in sensory-motor regions. In contrast, elevated E/I ratio in association cortices was more strongly related to worse memory function. Mediation analyses indicated E/I ratio partially accounted for the AD biomarker-memory relationship.
DISCUSSION: E/I imbalance represents an intermediate, systems-level circuit mechanism that links AD pathophysiology to cognitive impairment, offering novel insight into early neurophysiological changes along the AD continuum.
METHODS: We integrated biophysical modeling of resting-state functional magnetic resonance imaging with cerebrospinal fluid (CSF) and plasma biomarkers to examine whether E/I ratio links amyloid pathophysiology to memory in non-demented individuals across two cohorts from North America (N = 302; CSF amyloid beta 42 [Aβ42]) and Singapore (N = 240; plasma phosphorylated tau 217 [p-tau217]).
RESULTS: Elevated E/I ratio was associated with lower CSF Aβ42 and higher plasma p-tau217, with greater sensitivity in sensory-motor regions. In contrast, elevated E/I ratio in association cortices was more strongly related to worse memory function. Mediation analyses indicated E/I ratio partially accounted for the AD biomarker-memory relationship.
DISCUSSION: E/I imbalance represents an intermediate, systems-level circuit mechanism that links AD pathophysiology to cognitive impairment, offering novel insight into early neurophysiological changes along the AD continuum.