Journal Article

DZNE-2025-01259

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Modulation of middle-latency somatosensory evoked magnetic field waveforms associated with the pathophysiological states of Alzheimer's disease.

Tanaka, E. ; Nihashi, T. ; Kato, T. ; Arahata, Y. ; Takeda, A. ; Sakurai, K. ; Yokoi, K. ; Iwata, K. ; Diers, K.DZNE* ; Maess, B. ; Nakamura, A.

2025
IOS Press Amsterdam

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Please use a persistent id in citations: doi:10.1177/13872877251379466

Abstract: BackgroundAlzheimer'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.ObjectiveWe 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.MethodsWe 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.ResultsThe 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.ConclusionsThese 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.

Keyword(s): Humans (MeSH) ; Alzheimer Disease: physiopathology (MeSH) ; Alzheimer Disease: diagnostic imaging (MeSH) ; Male (MeSH) ; Evoked Potentials, Somatosensory: physiology (MeSH) ; Aged (MeSH) ; Female (MeSH) ; Magnetoencephalography (MeSH) ; Magnetic Resonance Imaging (MeSH) ; Positron-Emission Tomography (MeSH) ; Aged, 80 and over (MeSH) ; Cognitive Dysfunction: physiopathology (MeSH) ; Cognitive Dysfunction: diagnostic imaging (MeSH) ; Median Nerve: physiopathology (MeSH) ; Middle Aged (MeSH) ; Amyloid beta-Peptides: metabolism (MeSH) ; Somatosensory Cortex: physiopathology (MeSH) ; Alzheimer's disease ; amyloid-β protein ; cortical excitability ; evoked potentials ; glucose metabolism ; magnetoencephalography ; somatosensory ; Amyloid beta-Peptides

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Contributing Institute(s):

1. Artificial Intelligence in Medicine (AG Reuter)

Research Program(s):

1. 354 - Disease Prevention and Healthy Aging (POF4-354) (POF4-354)

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Database coverage:
; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; Essential Science Indicators ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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