Bushen-Tiansui Formula Improves Cognitive Functions in an Aβ1–42 Fibril-Infused Rat Model of Alzheimer’s DiseaseRead the full article
Neural Plasticity is an interdisciplinary journal dedicated to the publication of articles related to all aspects of neural plasticity, with special emphasis on its functional significance as reflected in behavior and in psychopathology.
Chief Editor, Professor Baudry, is currently University Professor at Western University of Health Sciences in Pomona, CA. His research focuses on understanding the molecular/cellular mechanisms of learning and memory and neurodegeneration.
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Targeted Engagement of the Action Selection Network during Task-Oriented Arm Training after Stroke
Action selection (AS), or selection of an action from a set of alternatives, is an important movement preparation process that engages a frontal-parietal network. The addition of AS demands to arm training after stroke could be used to engage this motor planning process and the neural network that supports it. The purpose of this case series is to describe the feasibility and outcomes associated with task-oriented arm training aimed at engaging the AS behavioral process and the related neural network in three individuals with chronic stroke. Three participants with mild to moderate motor deficits completed 13 to 15 sessions of task-oriented arm training that included AS cues for each movement repetition; cues dictated movement direction, height, or distance. Before and after training, individuals completed an AS brain-behavior probe during functional MRI. AS behavioral performance improved after training (increased accuracy, decreased reaction time) in all participants while brain activation in the AS network (dorsal premotor, parietal, dorsolateral prefrontal cortices) decreased in two participants. Gains in motor function were also found in all three participants, especially on patient-reported measures of perceived difficulty and confidence to complete upper extremity functional tasks. It was feasible to target the AS behavioral process and the related neural network through the addition of AS demands to functional, task-oriented arm training in three individuals with mild to moderate motor dysfunction poststroke.
Brain Functional Network in Chronic Asymptomatic Carotid Artery Stenosis and Occlusion: Changes and Compensation
Asymptomatic carotid artery stenosis (CAS) and occlusion (CAO) disrupt cerebral hemodynamics. There are few studies on the brain network changes and compensation associated with the progression from chronic CAS to CAO. In the current study, our goal is to improve the understanding of the specific abnormalities and compensatory phenomena associated with the functional connection in patients with CAS and CAO. In this prospective study, 27 patients with CAO, 29 patients with CAS, and 15 healthy controls matched for age, sex, education, handedness, and risk factors underwent neuropsychological testing and resting-state functional magnetic resonance (rs-fMRI) imaging simultaneously; graph theoretical analysis of brain networks was performed to determine the relationship between changes in brain network connectivity and the progression from internal CAS to CAO. The global properties of the brain network assortativity (), hierarchy (), network efficiency (), and small-worldness () were significantly more abnormal in the CAS group than in the control and CAO groups. In patients with CAS and CAO, the nodal efficiency of key nodes in multiple brain regions decreased, while the affected hemisphere lost many key functional connections. In this study, we found that patients with CAS showed grade reconstruction, invalid connections, and other phenomena that impaired the efficiency of information transmission in the brain network. A compensatory functional connection in the contralateral cerebral hemisphere of patients with CAS and CAO may be an important mechanism that maintains clinical asymptomatic performance. This study not only reveals the compensation mechanism of cerebral hemisphere ischemia but also validates previous explanations for brain function connectivity, which can help provide interventions in advance and reduce the impairment of higher brain functions. This trial is registered with Clinical Trial Registration-URL http://www.chictr.org.cn and Unique identifier ChiCTR1900023610.
Direct Evidence of Plasticity within Human Primary Motor and Somatosensory Cortices of Patients with Glioblastoma
Glioblastoma multiforme (GBM) is a devastating disease without cure. It is also the most common primary brain tumor in adults. Although aggressive surgical resection is standard of care, these operations are limited by tumor infiltration of critical cortical and subcortical regions. A better understanding of how the brain can recover and reorganize function in response to GBM would provide valuable clinical data. This ability, termed neuroplasticity, is not well understood in the adult human brain. A better understanding of neuroplasticity in GBM could allow for improved extent of resection, even in areas classically thought to have critical, static function. The best evidence to date has demonstrated neuroplasticity only in slower growing tumors or through indirect measures such as functional MRI or transcranial magnetic stimulation. In this novel study, we utilize a unique experimental paradigm to show direct evidence of plasticity via serial direct electrocortical stimulation (DES) within primary motor (M1) and somatosensory (S1) cortices in GBM patients. Six patients with glioblastoma multiforme in or near the primary motor or somatosensory cortex were included in this retrospective observational study. These patients had two awake craniotomies with DES to map cortical motor and sensory sites in M1 and S1. Five of six patients exhibited at least one site of neuroplasticity within M1 or S1. Out of the 51 total sites stimulated, 32 (62.7%) demonstrated plasticity. Of these sites, 14 (43.7%) were in M1 and 18 (56.3%) were in S1. These data suggest that even in patients with GBM in or near primary brain regions, significant functional reorganization is possible. This is a new finding which may lead to a better understanding of the fundamental factors promoting or inhibiting plasticity. Further exploration may aid in treatment of patients with brain tumors and other neurologic disorders.
Aβ-Induced Repressor Element 1-Silencing Transcription Factor (REST) Gene Delivery Suppresses Activation of Microglia-Like BV-2 Cells
Compelling evidence from basic molecular biology has demonstrated the crucial role of microglia in the pathogenesis of Alzheimer’s disease (AD). Microglia were believed to play a dual role in both promoting and inhibiting Alzheimer’s disease progression. It is of great significance to regulate the function of microglia and make them develop in a favorable way. In the present study, we investigated the function of repressor element 1-silencing transcription factor (REST) in Aβ1-42-induced BV-2 cell dysfunction. We concluded that Aβ1-42 could promote type I activation of BV-2 cells and induce cell proliferation, migration, and proinflammation cytokine TNF-α, IL-1β, and IL-6 expression. Meanwhile, REST was upregulated, and nuclear translocalization took place due to Aβ1-42 stimulation. When REST was knocked down by a specific short hairpin RNA (sh-RNA), BV-2 cell proliferation, migration, and proinflammation cytokine expression and secretion induced by Aβ1-42 were increased, demonstrating that REST may act as a repressor of microglia-like BV-2 cell activation.
No Effect of Anodal tDCS on Verbal Episodic Memory Performance and Neurotransmitter Levels in Young and Elderly Participants
Healthy ageing is accompanied by cognitive decline that affects episodic memory processes in particular. Studies showed that anodal transcranial direct current stimulation (tDCS) to the left dorsolateral prefrontal cortex (DLPFC) may counteract this cognitive deterioration by increasing excitability and inducing neuroplasticity in the targeted cortical region. While stimulation gains are more consistent in initial low performers, relying solely on behavioural measures to predict treatment benefits does not suffice for a reliable implementation of this method as a therapeutic option. Hence, an exploration of the underlying neurophysiological mechanisms regarding the differential stimulation effect is warranted. Glutamatergic metabolites (Glx) and γ-aminobutyric acid (GABA) are involved in learning and memory processes and can be influenced with tDCS; wherefore, they present themselves as potential biomarkers for tDCS-induced behavioural gains, which are affiliated with neuroplasticity processes. In the present randomized, double-blind, sham-controlled, crossover study, 33 healthy young and 22 elderly participants received anodal tDCS to their left DLPFC during the encoding phase of a verbal episodic memory task. Using MEGA-PRESS edited magnetic resonance spectroscopy (MRS), Glx and GABA levels were measured in the left DLPFC before and after the stimulation period. Further, we tested whether baseline performance and neurotransmitter levels predicted subsequent gains. No beneficial group effects of tDCS emerged in either verbal retrieval performances or neurotransmitter concentrations. Moreover, baseline performance levels did not predict stimulation-induced cognitive gains, nor did Glx or GABA levels. Nevertheless, exploratory analyses suggested a predictive value of the Glx : GABA ratio, with lower ratios at baseline indicating greater tDCS-related gains in delayed recall performance. This highlights the importance of further studies investigating neurophysiological mechanisms underlying previously observed stimulation-induced cognitive benefits and their respective interindividual heterogeneity.
Autophagy-Associated lncRNAs: Promising Targets for Neurological Disease Diagnosis and Therapy
Neurological diseases are a major threat to global public health and prosperity. The number of patients with neurological diseases is increasing due to the population aging and increasing life expectancy. Autophagy is one of the crucial mechanisms to maintain nerve cellular homeostasis. Numerous studies have demonstrated that autophagy plays a dual role in neurological diseases. Long noncoding RNAs (lncRNAs) are a vital class of noncoding RNAs with a length of more than 200 nucleotides and cannot encode proteins themselves but are expressed in most neurological diseases. An early phase, emerging knowledge has revealed that long noncoding RNAs (lncRNAs) are crucial in autophagy regulation. Furthermore, autophagy-associated lncRNAs can promote the development of neurological diseases or slow their progression. In this review, we introduce a general overview of lncRNA functional mechanisms and summarizes the recent progress of lncRNAs on autophagy regulation in neurological diseases to reveal possible novel therapeutic targets or useful biomarkers.