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@ARTICLE{Tanaka:282288,
      author       = {Tanaka, Emi and Nihashi, Takashi and Kato, Takashi and
                      Arahata, Yutaka and Takeda, Akinori and Sakurai, Keita and
                      Yokoi, Katsunori and Iwata, Kaori and Diers, Kersten and
                      Maess, Burkhard and Nakamura, Akinori},
      title        = {{M}odulation of middle-latency somatosensory evoked
                      magnetic field waveforms associated with the
                      pathophysiological states of {A}lzheimer's disease.},
      journal      = {Journal of Alzheimer's disease},
      volume       = {108},
      number       = {2},
      issn         = {1387-2877},
      address      = {Amsterdam},
      publisher    = {IOS Press},
      reportid     = {DZNE-2025-01259},
      pages        = {862 - 872},
      year         = {2025},
      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.},
      keywords     = {Humans / Alzheimer Disease: physiopathology / Alzheimer
                      Disease: diagnostic imaging / Male / Evoked Potentials,
                      Somatosensory: physiology / Aged / Female /
                      Magnetoencephalography / Magnetic Resonance Imaging /
                      Positron-Emission Tomography / Aged, 80 and over / Cognitive
                      Dysfunction: physiopathology / Cognitive Dysfunction:
                      diagnostic imaging / Median Nerve: physiopathology / Middle
                      Aged / Amyloid beta-Peptides: metabolism / Somatosensory
                      Cortex: physiopathology / Alzheimer's disease (Other) /
                      amyloid-β protein (Other) / cortical excitability (Other) /
                      evoked potentials (Other) / glucose metabolism (Other) /
                      magnetoencephalography (Other) / somatosensory (Other) /
                      Amyloid beta-Peptides (NLM Chemicals)},
      cin          = {AG Reuter},
      ddc          = {610},
      cid          = {I:(DE-2719)1040310},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41004660},
      doi          = {10.1177/13872877251379466},
      url          = {https://pub.dzne.de/record/282288},
}