Neuroscience
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Alzheimer's disease (AD) is a prevalent and debilitating neurodegenerative disease that leads to substantial loss of quality of life. Therapies currently available for AD do not modify the disease course and have limited efficacy in symptom control. ⋯ Entropy, a novel analysis for better understanding the nonlinear nature of neurophysiological data, has demonstrated consistent accuracy in disease detection. This literature review characterizes the use of entropy-based analyses from functional neuroimaging tools, including electroencephalography (EEG) and magnetoencephalography (MEG), in patients with AD for disease detection, therapeutic response measurement, and providing clinical insights.
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Sensorimotor adaptation alters mappings between motor commands and their predicted outcomes. Such remapping has been extensively studied in the visual domain, but the degree to which it occurs in modalities other than vision remains less well understood. Here, we manipulated the modality of reach target presentation to compare sensorimotor adaptation in response to perturbations of visual and auditory feedback location. ⋯ Presentation durations for target stimuli (500 ms) and (non-veridical) endpoint feedback of reach direction (100 ms) were matched for visual and auditory modalities. For all three groups, when endpoint feedback was perturbed, adaptation was evident: reach-directions increased significantly in the direction opposite the clamped feedback, and a significant aftereffect persisted after participants were instructed that the perturbation had been removed. This study provides new evidence that implicit sensorimotor adaptation occurs in response to perturbed auditory feedback of reach direction, suggesting that an implicit neural process to recalibrate sensory to motor maps in response to sensory prediction errors may be ubiquitous across sensory modalities.
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Primary angle-closure glaucoma (PACG) is a severe and irreversible blinding eye disease characterized by progressive retinal ganglion cell death. However, prior research has predominantly focused on static brain activity changes, neglecting the exploration of how PACG impacts the dynamic characteristics of functional brain networks. This study enrolled forty-four patients diagnosed with PACG and forty-four age, gender, and education level-matched healthy controls (HCs). ⋯ Subsequently, a support vector machine (SVM) model leveraging functional connectivity (FC) and FNC was applied to differentiate PACG patients from HCs. Our study underscores the presence of modified functional connectivity within large-scale brain networks and abnormalities in dynamic temporal metrics among PACG patients. By elucidating the impact of changes in large-scale brain networks on disease evolution, researchers may enhance the development of targeted therapies and interventions to preserve vision and cognitive function in PACG.
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The Ribosomal S6 Kinase (RSK) family of serine/threonine kinases function as key downstream effectors of the MAPK signaling cascade. In the nervous system, RSK signaling plays crucial roles in neuronal development and contributes to activity-dependent neuronal plasticity. This study examined the role of RSK signaling in cell viability during neuronal development and in neuroprotection in the mature nervous system. ⋯ Finally, we used the endothelin 1 (ET-1) model of ischemia to examine the neuroprotective effects of RSK signaling in the mature hippocampus in vivo. Notably, in the absence of RSK inhibition, the granule cell layer (GCL) was resistant to the effects of ET-1; However, disruption of RSK signaling (via the microinjection of BiD1870) prior to ET-1 injection triggered cell death within the GCL, thus indicating a neuroprotective role for RSK signaling in the mature nervous system. Together these data reveal distinct, developmentally-defined, roles for RSK signaling in the nervous system.
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Schizophrenia (SCZ) is a highly heterogeneous, severe neuropsychiatric disorder of unknown etiopathology. Increasing data indicate an overlap between schizophrenia and pathological processes related to immunological dysregulation as well as inflammation, such as high levels of pro-inflammatory substances in patients' blood and cerebrospinal fluid and autoantibodies against synaptic and nerve cell membrane proteins. Autoantibodies against SFT2D2 have been reported in patients with SCZ. ⋯ Quantitative reverse transcription-polymerase chain reactions showed that the expression of pro-inflammatory genes was upregulated in the primary somatosensory cortex and hippocampus of the anti-SFT2D2-IgG-infused mice. Additionally, the mice exhibited defective sensorimotor gating, memory deficits, motor impairment, and anxiety-related behaviors without signs of depression. These findings indicate that anti-SFT2D2 autoantibodies can induce encephalitis, cause a series of behavioral changes associated with schizophrenia, and offer a model for testing novel therapies to improve treatment strategies for a subgroup of patients with SCZ.