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Associations between peripheral mitochondrial energetics and cortical neurophysiological alterations in Alzheimer’s disease

Poster Session F - Tuesday, March 10, 2026, 8:00 – 10:00 am PDT, Fairview/Kitsilano Ballroom

Sean L Kriwokon1 (), Santiago I Flores-Alonso1, Brianne A Kent1, Tony W Wilson2,3, Rachel K Spooner2, Alex I Wiesman1; 1Simon Fraser University, 2Boys Town National Research Hospital, 3Creighton University

Alzheimer’s disease is associated with both mitochondrial dysfunction and altered neurophysiological signalling. Peripheral measures of mitochondrial function have been established as effective predictors of mitochondrial performance in the healthy brain, and more recently, altered neurophysiological signalling has been associated with aberrant mitochondrial function. This indicates that peripheral mitochondrial energetics and altered neural signalling in Alzheimer’s disease may be related, but to date, no studies have directly tested their relationship. We collected neuroimaging and mitochondrial energetics data from biomarker-confirmed patients on the Alzheimer’s disease continuum (69.21 [6.91] years; n = 38) and healthy older adults (72.20 [4.73] years; n = 20). Each participant provided a blood sample for analysis of mitochondrial respiration using Seahorse Analyzer and task-free neurophysiological data using magnetoencephalography. We used region-wise linear models to test the relationship between ATP-linked respiration and neurophysiological changes in patients relative to controls, finding that mitochondrial respiration linked to ATP production is associated with altered alpha and theta band cortical rhythms in Alzheimer’s disease (α: pFDR < 0.05, r = -0.7; θ: pFDR < 0.05, r = -0.6). We then tested colocalization of mitochondria-neurophysiological relationships with a human brain atlas of respiratory capacity and found that brain regions with greater mitochondrial respiratory capacity exhibited a stronger relationship between aperiodic signalling and peripheral ATP-linked respiration (pFDR = 0.003, r = 0.35). Our findings suggest that peripheral blood measures of mitochondrial function can offer insight into the neurophysiological alterations associated with energetic changes in Alzheimer’s disease.

Topic Area: METHODS: Neuroimaging

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March 7 – 10, 2026