櫻井 圭太

BackgroundArgyrophilic grain disease (AGD) is a common yet underrecognized tauopathy that often mimics Alzheimer's disease (AD) in clinical and imaging presentations. While regional atrophy in AGD has been reported on magnetic resonance imaging (MRI), network-level structural changes remain poorly understood.ObjectiveWe aimed to explore a gray matter volume network related to AGD.MethodsStructural MRI data were collected from 12 patients with pathologically confirmed AGD (age at MRI, 87.7 ± 5.5 years; male, 4), 12 patients with pathologically confirmed AD (83.4 ± 10.0 years; male, 4), and 9 healthy controls (HCs; 82.4 ± 1.9 years; male, 2) at Fukushimura Hospital in Japan. Scaled Subprofile Model with principal component analysis was applied to preprocessed gray matter volume data of AGD and HCs to identify an AGD-related network.ResultsAn AGD-related network involving relative reduction in the ambient gyrus, entorhinal cortex, hippocampus, amygdala, and thalamus was identified. Represented by principal components 1, 2, and 3, this network showed significantly higher expression in patients with AGD than HCs (p < 0.0001, permutation test). The expression of the network was also higher in patients with AD than HCs (p < 0.0001, t-test).ConclusionsThis exploratory study identified a gray matter volume network related to AGD, providing a basis for future research of network-based imaging approaches.

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.