Modulation of middle-latency somatosensory evoked magnetic field waveforms associated with the pathophysiological states of Alzheimer's disease

Background Alzheimer's disease (AD) frequently causes epilepsy and myoclonus. These symptoms are thought to be associated with neuronal hyperexcitability, highlighting the need for biomarkers that reflect synaptic functional alterations. Objective We aimed to examine changes in neuronal excitability associated with AD progression using magnetoencephalography (MEG). Furthermore, we investigated the relationship between alterations in electromagnetic signals and other neuroimaging biomarkers. Methods We measured middle-latency somatosensory evoked magnetic fields (m-SEFs) following right median nerve stimulation in 45 individuals, comprising 6, 8, and 31 individuals with AD dementia (ADD), mild cognitive impairment (MCI), and cognitively healthy older adults, respectively. Cortical reactivity relative to the primary somatosensory response (N20 m) was assessed using normalized m-SEF waveforms. Additionally, we analyzed associations between these waveforms and amyloid-β (Aβ) deposition, regional glucose metabolism, and gray matter volume using positron-emission tomography and magnetic resonance imaging. Results The m-SEF waveform exhibited six components (M2–M7) within 150 ms of the N20 m (M1) response. The m-SEF waveforms tended to be enlarged in ADD and MCI, with a significant enhancement of M2 in ADD. The amplitude of M7 at approximately 100 ms latency was significantly and positively correlated with local Aβ deposition in the sensorimotor cortex. Moreover, regional glucose hypometabolism in the hippocampus and pulvinar was significantly associated with enlargement of the M4, M6, and M7 components. Conclusions These findings indicate that cortical responses to somatosensory stimulation are modulated by AD progression. M-SEF may serve as a potential marker for evaluating cortical excitability in the sensorimotor cortex.