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000282288 0247_ $$2doi$$a10.1177/13872877251379466
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000282288 037__ $$aDZNE-2025-01259
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000282288 1001_ $$aTanaka, Emi$$b0
000282288 245__ $$aModulation of middle-latency somatosensory evoked magnetic field waveforms associated with the pathophysiological states of Alzheimer's disease.
000282288 260__ $$aAmsterdam$$bIOS Press$$c2025
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000282288 520__ $$aBackgroundAlzheimer'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.
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000282288 650_7 $$2Other$$aAlzheimer's disease
000282288 650_7 $$2Other$$aamyloid-β protein
000282288 650_7 $$2Other$$acortical excitability
000282288 650_7 $$2Other$$aevoked potentials
000282288 650_7 $$2Other$$aglucose metabolism
000282288 650_7 $$2Other$$amagnetoencephalography
000282288 650_7 $$2Other$$asomatosensory
000282288 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000282288 650_2 $$2MeSH$$aHumans
000282288 650_2 $$2MeSH$$aAlzheimer Disease: physiopathology
000282288 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000282288 650_2 $$2MeSH$$aMale
000282288 650_2 $$2MeSH$$aEvoked Potentials, Somatosensory: physiology
000282288 650_2 $$2MeSH$$aAged
000282288 650_2 $$2MeSH$$aFemale
000282288 650_2 $$2MeSH$$aMagnetoencephalography
000282288 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000282288 650_2 $$2MeSH$$aPositron-Emission Tomography
000282288 650_2 $$2MeSH$$aAged, 80 and over
000282288 650_2 $$2MeSH$$aCognitive Dysfunction: physiopathology
000282288 650_2 $$2MeSH$$aCognitive Dysfunction: diagnostic imaging
000282288 650_2 $$2MeSH$$aMedian Nerve: physiopathology
000282288 650_2 $$2MeSH$$aMiddle Aged
000282288 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000282288 650_2 $$2MeSH$$aSomatosensory Cortex: physiopathology
000282288 7001_ $$aNihashi, Takashi$$b1
000282288 7001_ $$aKato, Takashi$$b2
000282288 7001_ $$00000-0001-7810-8984$$aArahata, Yutaka$$b3
000282288 7001_ $$aTakeda, Akinori$$b4
000282288 7001_ $$aSakurai, Keita$$b5
000282288 7001_ $$aYokoi, Katsunori$$b6
000282288 7001_ $$aIwata, Kaori$$b7
000282288 7001_ $$0P:(DE-2719)2812059$$aDiers, Kersten$$b8$$udzne
000282288 7001_ $$aMaess, Burkhard$$b9
000282288 7001_ $$00000-0002-4259-1297$$aNakamura, Akinori$$b10
000282288 773__ $$0PERI:(DE-600)2070772-1$$a10.1177/13872877251379466$$gVol. 108, no. 2, p. 862 - 872$$n2$$p862 - 872$$tJournal of Alzheimer's disease$$v108$$x1387-2877$$y2025
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