Notes

Evaluating proper flexible operations like a process of company learning.
Structural MRI (sMRI) has been widely used to examine the cerebral changes that occur in Parkinson's disease (PD). However, previous studies have aimed for brain changes at the group level rather than at the individual level. Additionally, previous studies have been inconsistent regarding the changes they identified. It is difficult to identify which brain regions are the true biomarkers of PD. To overcome these two issues, we employed four different feature selection methods [ReliefF, graph-theory, recursive feature elimination (RFE), and stability selection] to obtain a minimal set of relevant features and nonredundant features from gray matter (GM) and white matter (WM). Then, a support vector machine (SVM) was utilized to learn decision models from selected features. Based on machine learning technique, this study has not only extended group level statistical analysis with identifying group difference to individual level with predicting patients with PD from healthy controls (HCs), but also identified moshese brain regions are related to the pathological brain changes characteristic of PD and can be regarded as potential biomarkers of PD. Besides, we also found the brain abnormality of superior frontal gyrus (dorsolateral, SFGdor) and lingual gyrus (LING), which have been confirmed in other studies of PD. This further demonstrates that machine learning models are beneficial for clinicians as a decision support system in diagnosing PD.Simultaneous bimanual movements are not merely the sum of two unimanual movements. Here, we considered the unimanual/bimanual motor system as comprising three components unimanual-specific, bimanual-specific, and overlapping (mobilized during both unimanual and bimanual movements). If the force-generating system controlling the same limb differs between unimanual and bimanual movements, unimanual exercise would be expected to fatigue the unimanual-specific and overlapping parts in the force-generating system but not the bimanual-specific part. Therefore, we predicted that the decrease in bimanual force generation induced by unimanual neuromuscular fatigue would be smaller than the decrease in unimanual force generation. Sixteen healthy right-handed adults performed unimanual and bimanual maximal handgrip measurements before and after a submaximal fatiguing handgrip task. In the fatigue task, participants were instructed to maintain unimanual handgrip force at 50% of their maximal handgrip force until the time to task failure. Each participant performed this task in a left-hand fatigue (LF) condition and a right-hand fatigue (RF) condition, in a random order. Although the degree of neuromuscular fatigue was comparable in both conditions, as expected, the decrease in bimanual right handgrip force was significantly smaller than those during unimanual right performance in the RF condition, but not in the LF condition. These results indicate that for the right-hand, neuromuscular fatigue in unimanual handgrip does not completely affect simultaneous bimanual handgrip. Regarding the underlying mechanisms, we propose that although neuromuscular fatigue caused by unimanual handgrip reduces the motor output of unimanual-specific and overlapping parts in the force-generating system, when simultaneous bimanual handgrip is performed, the overlapping part (which is partially fatigued) and the bimanual-specific part (which is not yet fatigued) generate motor output, thus decreasing the force reduction.Freezing of gait (FOG) is a common and challenging clinical symptom in Parkinson's disease. In this review, we summarise the recent insights into freezing of gait and highlight the strategies that should be considered to improve future treatment. There is a need to develop individualised and on-demand therapies, through improved detection and wearable technologies. Whilst there already exist a number of pharmacological (e.g., dopaminergic and beyond dopamine), non-pharmacological (physiotherapy and cueing, cognitive training, and non-invasive brain stimulation) and surgical approaches to freezing (i.e., dual-site deep brain stimulation, closed-loop programming), an integrated collaborative approach to future research in this complex area will be necessary to systematically investigate new therapeutic avenues. A review of the literature suggests standardising how gait freezing is measured, enriching patient cohorts for preventative studies, and harnessing the power of existing data, could help lead to more effective treatments for freezing of gait and offer relief to many patients.Day-active tree shrews have a well-developed internal capsule (ic) that clearly separates the caudate nucleus (Cd) and putamen (Pu). The striatum consists of the Cd, ic, Pu, and accumbens nucleus (Acb). Here, we characterized the cytoarchitecture of the striatum and the whole-brain inputs to the Cd, Pu, and Acb in tree shrews by using immunohistochemistry and the retrograde tracer Fluoro-Gold (FG). CP-690550 ic50 Our data show the distribution patterns of parvalbumin (PV), nitric oxide synthase (NOS), calretinin (CR), and tyrosine hydroxylase (TH) immunoreactivity in the striatum of tree shrews, which were different from those observed in rats. The Cd and Pu mainly received inputs from the thalamus, motor cortex, somatosensory cortex, subthalamic nucleus, substantia nigra, and other cortical and subcortical regions, whereas the Acb primarily received inputs from the anterior olfactory nucleus, claustrum, infralimbic cortex, thalamus, raphe nucleus, parabrachial nucleus, ventral tegmental area, and so on. The Cd, Pu, and Acb received inputs from different neuronal populations in the ipsilateral (60, 67, and 63 brain regions, respectively) and contralateral (23, 20, and 36 brain regions, respectively) brain hemispheres. Overall, we demonstrate that there are species differences between tree shrews and rats in the density of PV, NOS, CR, and TH immunoreactivity in the striatum. Additionally, we mapped for the first time the distribution of whole-brain input neurons projecting to the striatum of tree shrews with FG injected into the Cd, Pu, and Acb. The similarities and differences in their brain-wide input patterns may provide new insights into the diverse functions of the striatal subregions.Genetically encoded voltage indicators (GEVIs) expressed pan-neuronally were able to optically resolve bicuculline induced spontaneous oscillations in brain slices of the mouse motor cortex. Three GEVIs were used that differ in their timing of response to voltage transients as well as in their voltage ranges. The duration, number of cycles, and frequency of the recorded oscillations reflected the characteristics of each GEVI used. Multiple oscillations imaged in the same slice never originated at the same location, indicating the lack of a "hot spot" for induction of the voltage changes. Comparison of pan-neuronal, Ca2+/calmodulin-dependent protein kinase II α restricted, and parvalbumin restricted GEVI expression revealed distinct profiles for the excitatory and inhibitory cells in the spontaneous oscillations of the motor cortex. Resolving voltage fluctuations across space, time, and cell types with GEVIs represent a powerful approach to dissecting neuronal circuit activity.Neurological disorders are mainly characterized by progressive neuron loss and neurological deterioration, which cause human disability and death. However, many types of neurological disorders have similar pathological mechanisms, including the neuroinflammatory response. Various microRNAs (miRs), such as miR-21, miR-124, miR-146a, and miR-132 were recently shown to affect a broad spectrum of biological functions in the central nervous system (CNS). Microglia are innate immune cells with important roles in the physiological and pathological activities of the CNS. Recently, abnormal expression of miR-124 was shown to be associated with the occurrence and development of various diseases in CNS via regulating microglia function. In addition, miR-124 is a promising biomarker and therapeutic target. Studies on the role of miR-124 in regulating microglia function involved in pathogenesis of neurological disorders at different stages will provide new ideas for the use of miR-124 as a therapeutic target for different CNS diseases.Myelination is essential for signal processing within neural networks. Emerging data suggest that neuronal activity positively instructs myelin development and myelin adaptation during adulthood. However, the underlying mechanisms controlling activity-dependent myelination have not been fully elucidated. Myelination is a multi-step process that involves the proliferation and differentiation of oligodendrocyte precursor cells followed by the initial contact and ensheathment of axons by mature oligodendrocytes. Conventional end-point studies rarely capture the dynamic interaction between neurons and oligodendrocyte lineage cells spanning such a long temporal window. Given that such interactions and downstream signaling cascades are likely to occur within fine cellular processes of oligodendrocytes and their precursor cells, overcoming spatial resolution limitations represents another technical hurdle in the field. link2 In this mini-review, we discuss how advanced genetic, cutting-edge imaging, and electrophysiological approaches enable us to investigate neuron-oligodendrocyte lineage cell interaction and myelination with both temporal and spatial precision.Metabolic syndromes are frequently associated with dementia, suggesting that the dysregulation of energy metabolism can increase the risk of neurodegeneration and cognitive impairment. In addition, growing evidence suggests the link between infections and brain disorders, including Alzheimer's disease. The immune system and energy metabolism are in an intricate relationship. Infection triggers immune responses, which are accompanied by imbalance in cellular and organismal energy metabolism, while metabolic disorders can lead to immune dysregulation and higher infection susceptibility. In the brain, the activities of brain-resident immune cells, including microglia, are associated with their metabolic signatures, which may be affected by central nervous system (CNS) infection. Conversely, metabolic dysregulation can compromise innate immunity in the brain, leading to enhanced CNS infection susceptibility. Thus, infection and metabolic imbalance can be intertwined to each other in the etiology of brain disorders, including dementia. Insulin and leptin play pivotal roles in the regulation of immunometabolism in the CNS and periphery, and dysfunction of these signaling pathways are associated with cognitive impairment. Meanwhile, infectious complications are often comorbid with diabetes and obesity, which are characterized by insulin resistance and leptin signaling deficiency. link3 Examples include human immunodeficiency virus (HIV) infection and periodontal disease caused by an oral pathogen Porphyromonas gingivalis. This review explores potential interactions between infectious agents and insulin and leptin signaling pathways, and discuss possible mechanisms underlying the relationship between infection, metabolic dysregulation, and brain disorders, particularly focusing on the roles of insulin and leptin.
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