Mild Cognitive Impairment (MCI) is a border or precursor state of dementia. To optimize implemented interventions for MCI, it is essential to clarify the underlying neural mechanisms. However, knowledge regarding the brain regions responsible for MCI is still limited. Here, we implemented the Montreal Cognitive Assessment (MoCA) test, a screening tool for MCI, in 20 healthy elderly participants (mean age, 67.5 years), and then recorded magnetoencephalograms (MEG) while they performed a visual sequential memory task. In the task, each participant memorized the four possible directions of seven sequentially presented arrow images. Recall accuracy for beginning items of the memory sequence was significantly positively related with MoCA score. Meanwhile, MEG revealed stronger alphaband (8-13 Hz) rhythm desynchronization bilaterally in the precuneus (PCu) for higher MoCA (normal) participants. Most importantly, this PCu desynchronization response weakened in correspondence with lower MoCA score during the beginning of sequential memory encoding, a time period that should rely on working memory and be affected by declined cognitive function. Our results suggest that deactivation of the PCu is associated with early MCI, and corroborate pathophysiological findings based on post-mortem tissue which have implicated hypoperfusion of the PCu in early stages of Alzheimer disease. Our results indicate the possibility that cognitive decline can be detected early and non-invasively by monitoring PCu activity with electrophysiological methods.
Electrophysiological studies have demonstrated that theta-band activity is useful for investigating neural mechanisms of memory. However, mechanisms specifically driving memory performance remain poorly understood. In sequential memory, performance can be artificially attenuated by shortening the inter-stimulus interval (ISI) between memory item presentations. Therefore, we sought to clarify the mechanisms of sequential memory performance by analyzing theta-band (4–8 Hz) activity recorded via magnetoencephalogram in 33 participants during performance of a sequential memory task where memory items were presented at either slow or fast rates in accordance with longer or shorter ISIs, respectively. Particularly in the slow task, theta activity clearly modulated in accordance with the presentation of memory items. Common cortical target regions in the occipital and frontal cortex were identified in both tasks and related to visual encoding and memory maintenance, respectively. Compared to the slow task, occipital-theta activity was significantly lower in the fast task from the midterm until the ending of encoding, in correspondence with significantly lower recall for memory items in this same period. Meanwhile, despite a loss of clarity in responsiveness to individual memory items in the fast task, frontal-theta activity was not different between tasks and exhibited particularly strong responses in both tasks during the holding period prior to recall. Our results indicate that shorter processing time erodes sequential memory performance beginning at the level of visual encoding.
Studies on evoked responses in Parkinson's disease (PD) may be useful for elucidating the etiology and quantitative evaluation of PD. However, in previous studies, the association between evoked responses and detailed motor symptoms or cognitive functions has not been clear. This study investigated the characteristics of the visual (VEF), auditory (AEF), and somatosensory (SEF) evoked magnetic fields in patients with Parkinson’s disease (PD), and the correlations between evoked fields and the patient’s clinical characteristics, motor symptoms, and cognitive functions. Twenty patients with PD and 10 healthy controls (HCs) were recruited as participants. We recorded VEF, AEF, and SEF, collected clinical characteristics, performed physical examinations, and administered 10 cognitive tests. We investigated differences in the latencies of the evoked fields between patients with PD and HCs. We also evaluated the correlation of the latencies with motor symptoms and cognitive functioning. There were significant differences between the two groups in 6 of the cognitive tests, all of which suggested mild cognitive impairment in patients with PD. The latencies of the VEF N75m, P100m, N145m, AEF P50m, P100m, and SEF P60m components were greater in the patients with PD than in the HCs. The latencies mainly correlated with medication and motor symptoms, less so with cognitive tests, with some elements of the correlations remaining significant after Bonferroni correction. In conclusion, the latencies of the VEF, AEF, and SEF were greater in PD patients than in HCs and were mainly correlated with medication and motor symptoms rather than cognitive functioning. Findings from this study suggest that evoked fields may reflect basal ganglia functioning and are candidates for assessing motor symptoms or the therapeutic effects of medication in patients with PD.
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