Neuroscience
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Motor variability is an intrinsic feature of human beings that has been associated with the ability for learning and adaptation to specific tasks. The purpose of this review is to examine whether there is a possible direct relationship between individuals' initial variability in their ability for learning and adaptation in motor tasks. Eighteen articles examined the relationship between initial motor variability and the ability for learning or adaptation. ⋯ While in error-based task associations were reported with both greater amount variability and more complexity temporal structure. Nevertheless, bias in initial performance related to the amount of variability was found, so the temporal structure of initial variability seems to be a better indicator of improvement in this type of task. Further research is needed for further research to better understand the potential relationship between initial motor variability and the ability for learning or adaptation in motor tasks.
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Multicenter Study
Deep learning-based segmentation of acute ischemic stroke MRI lesions and recurrence prediction within 1 year after discharge: A multicenter study.
To explore the performance of deep learning-based segmentation of infarcted lesions in the brain magnetic resonance imaging (MRI) of patients with acute ischemic stroke (AIS) and the recurrence prediction value of radiomics within 1 year after discharge as well as to develop a model incorporating radiomics features and clinical factors to accurately predict AIS recurrence. ⋯ The MRA-UNet model can effectively improve the segmentation accuracy of MRI. The model, which was established by combining radiomics features and clinical factors, held some value for predicting AIS recurrence within 1 year.
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Review
Emerging biophysical techniques for probing synaptic transmission in neurodegenerative disorders.
Plethora of research has shed light on the critical role of synaptic dysfunction in various neurodegenerative disorders (NDDs), including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD). Synapses, the fundamental units for neural communication in the brain, are highly vulnerable to pathological conditions and are central to the progression of neurological diseases. The presynaptic terminal, a key component of synapses responsible for neurotransmitter release and synaptic communication, undergoes structural and functional alterations in these disorders. ⋯ The review articles highlighted provide a comprehensive overview of how synaptic vulnerability and pathology are shared mechanisms across a spectrum of neurological disorders. In major neurodegenerative diseases, synaptic dysfunction is a common thread linking these conditions. The intricate molecular machinery involved in neurotransmitter release, synaptic vesicle dynamics, and presynaptic protein regulation are key areas of focus for understanding synaptic alterations in neurodegenerative diseases.
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Parkinson's disease (PD) is a prevalent neurodegenerative disorder caused by degeneration of dopaminergic neurons, originating from the substantia nigra pars compacta, and characterized by motor symptoms such as bradykinesia, muscle rigidity, resting tremor, and postural instability, as well as non-motor symptoms such as anxiety, depression, reduced sense of smell, cognitive impairment, and visual dysfunction. Emerging evidence highlights the retina as a promising site for non-invasive exploration of PD pathology, due to its shared embryonic origin with the central nervous system. ⋯ This review provides a comprehensive synthesis of retinal dysfunctions in PD, focusing on structural and functional changes as potential biomarkers for early diagnosis and clinical assessment. By integrating findings from advanced imaging and electrophysiological studies, this review introduces novel perspectives on the correlation between retinal changes and PD pathophysiology, offering innovative approaches for early detection, disease progression monitoring, and therapeutic stratification.
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Neurodegenerative diseases (ND) are complex diseases of still unknown etiology. Lately, long non-coding RNAs (lncRNAs) have become increasingly popular and implicated in several pathologies as they have several roles and appear to be involved in all biological processes such as cell signaling and cycle control as well as translation and transcription. MEG3 is one of these and acts by binding proteins or directly or competitively binding miRNAs. ⋯ This review examines the current state of knowledge concerning the level of expression and the regulatory function of MEG3 in relation to several NDs. In addition, we examined the relation of MEG3 with neurotrophic factors such as Tumor growth factor β (TGFβ) and its possible mechanism of action. A comprehensive and in-depth analysis of the role of MEG3 in ND could give a clearer picture about the initiation of the process of neuronal death and help develop an alternative therapy that targets MEG3.