Activation of neuronal Ras‐related C3 botulinum toxin substrate 1 (Rac1) improves post‐stroke recovery and axonal plasticity in mice

2020 ◽  
Author(s):  
Fan Bu ◽  
Yashasvee Munshi ◽  
J Weldon Furr ◽  
Jia‐wei Min ◽  
Li Qi ◽  
...  
Keyword(s):  
Botulinum Toxin ◽  
Stroke Recovery ◽  
Axonal Plasticity ◽  
Post Stroke

Abstract 58: Neuronal Activation of Ras-Related C3 Botulinum Toxin Substrate 1 (Rac1) Improves Post-Stroke Recovery and Axonal Plasticity in Mice

Stroke ◽  
2019 ◽  
Vol 50 (Suppl_1) ◽  
Author(s):  
Fan Bu ◽  
Yashasvee Munshi ◽  
Weldon J Furr ◽  
Jia-wei Min ◽  
Anthony Patrizz ◽  
...  
Keyword(s):  
Botulinum Toxin ◽  
Stroke Recovery ◽  
Neuronal Activation ◽  
Axonal Plasticity ◽  
Post Stroke

scholarly journals Activation of endothelial ras-related C3 botulinum toxin substrate 1 (Rac1) improves post-stroke recovery and angiogenesis via activating Pak1 in mice

2019 ◽  
Vol 322 ◽  
pp. 113059 ◽  
Author(s):  
Fan Bu ◽  
Jia-Wei Min ◽  
Yashasvee Munshi ◽  
Yun-Ju Lai ◽  
Li Qi ◽  
...  
Keyword(s):  
Botulinum Toxin ◽  
Stroke Recovery ◽  
Post Stroke

Post-stroke recovery updates

2018 ◽  
Vol 19 (1) ◽  
pp. 53-57
Author(s):  
Ana Maria Bumbea ◽  
Roxana Carmen Dumitraşcu ◽  
Bogdan Ştefan Bumbea ◽  
Anca Emanuela Muşetescu ◽  
Otilia Rogoveanu ◽  
...  
Keyword(s):  
Stroke Recovery ◽  
Post Stroke

LncRNAs a New Target for Post-Stroke Recovery

2020 ◽  
Vol 26 (26) ◽  
pp. 3115-3121
Author(s):  
Jun Yang ◽  
Jingjing Zhao ◽  
Xu Liu ◽  
Ruixia Zhu
Keyword(s):  
Ischemic Stroke ◽  
Microglial Activation ◽  
Vital Role ◽  
Stroke Recovery ◽  
Biological Processes ◽  
Current Development ◽  
Post Stroke ◽  
Cascade Processes ◽  
Non Coding Rnas ◽  
Neuron Injury

LncRNAs (long non-coding RNAs) are endogenous molecules, involved in complicated biological processes. Increasing evidence has shown that lncRNAs play a vital role in the post-stroke pathophysiology. Furthermore, several lncRNAs were reported to mediate ischemia cascade processes include apoptosis, bloodbrain barier breakdown, angiogenesis, microglial activation induced neuroinflammation which can cause neuron injury and influence neuron recovery after ischemic stroke. In our study, we first summarize current development about lncRNAs and post-stroke, focus on the regulatory roles of lncRNAs on pathophysiology after stroke. We also reviewed genetic variation in lncRNA associated with functional outcome after ischemic stroke. Additionally, lncRNA-based therapeutics offer promising strategies to decrease brain damage and promote neurological recovery following ischemic stroke. We believe that lncRNAs will become promising for the frontier strategies for IS and can open up a new path for the treatment of IS in the future.

scholarly journals Post-Stroke Social Isolation Reduces Cell Proliferation in the Dentate Gyrus and Alters miRNA Profiles in the Aged Female Mice Brain

2020 ◽  
Vol 22 (1) ◽  
pp. 99
Author(s):  
Aleah Holmes ◽  
Yan Xu ◽  
Juneyoung Lee ◽  
Michael E. Maniskas ◽  
Liang Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dentate Gyrus ◽  
Social Isolation ◽  
Census Data ◽  
Elderly Women ◽  
Stroke Recovery ◽  
Tissue Loss ◽  
Female Mice ◽  
Post Stroke ◽  
The Brain

Social isolation and loneliness are risk factors for stroke. Elderly women are more likely to be isolated. Census data shows that in homeowners over the age of 65, women are much more likely to live alone. However, the underlying mechanisms of the detrimental effects of isolation have not been well studied in older females. In this study, we hypothesized that isolation impairs post-stroke recovery in aged female mice, leading to dysregulated microRNAs (miRNAs) in the brain, including those previously shown to be involved in response to social isolation (SI). Aged C57BL/6 female mice were subjected to a 60-min middle cerebral artery occlusion and were randomly assigned to either single housing (SI) or continued pair housing (PH) immediately after stroke for 15 days. SI immediately after stroke led to significantly more brain tissue loss after stroke and higher mortality. Furthermore, SI significantly delayed motor and sensory recovery and worsened cognitive function, compared to PH. A decrease in cell proliferation was seen in the dentate gyrus of SI mice assessed by bromodeoxyuridine (BrdU) labeling. miRNAome data analysis revealed changes in several miRNAs in the brain, such as miR-297a-3p and miR-200c-3p, which are known to regulate pathways involved in cell proliferation. In conclusion, our data suggest that SI can lead to a poor post-stroke recovery in aged females and dysregulation of miRNAs and reduced hippocampal cell proliferation.

scholarly journals Rehabilitation strategy for post-stroke recovery using an innovative elbow exoskeleton

2019 ◽  
Vol 233 (6) ◽  
pp. 668-680 ◽  
Author(s):  
Soumya K Manna ◽  
Venketesh N Dubey
Keyword(s):  
Acute Stage ◽  
Joint Torque ◽  
Stroke Recovery ◽  
Structural Description ◽  
Post Stroke ◽  
Single Structure ◽  
Rate Of Recovery ◽  
Last Stage ◽  
Working Region ◽  
Rehabilitation Strategy

Intensive and adaptive rehabilitation therapy is beneficial for post-stroke recovery. Three modes of rehabilitation are generally performed at different stages after stroke: external force-based control in the acute stage, assistive force-based rehabilitation in the midway of recovery and resistive force-based rehabilitation in the last stage. To achieve the above requirements, an innovative elbow exoskeleton has been developed to incorporate the three modes of rehabilitation in a single structure. The structure of the exoskeleton has been designed in such a way that the whole working region is divided into three where each region can provide a different mode of rehabilitation. Recovery rate can be varied for individuals since it depends on various parameters. To evaluate the rate of recovery, three joint parameters have been identified: range of angular movement, angular velocity and joint torque. These parameters are incorporated into the framework of planning a novel rehabilitation strategy, which is discussed in this article along with the structural description of the designed exoskeleton.

Abstract W MP41: Potentiation of Gaba-Mediated Synaptic Inhibition in the Recovery Phase: A Novel Therapeutic Target for Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Takeshi Hiu ◽  
Tonya Bliss ◽  
Jeanne Paz ◽  
Eric Wang ◽  
Zoya Farzampour ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Recovery Phase ◽  
Synaptic Activity ◽  
Stroke Recovery ◽  
Functional Changes ◽  
Post Stroke ◽  
Array Tomography ◽  
Neuronal Inhibition ◽  
Gaba Signaling ◽  
Novel Therapeutic

Background: Stroke is a major cause of disability yet pharmacotherapy targeting the recovery phase is lacking. Cortical circuit reorganization adjacent to the stroke site promotes recovery, thus elucidating mechanisms that promote this plasticity could lead to new therapeutics. Tonic neuronal inhibition, mediated by extrasynaptic GABA A receptors,inhibits post-stroke recovery. However, effects of phasic (synaptic) GABA signaling - which promotes plasticity during development - are unknown. Here we use a combined approach of i) array tomography to determine the composition of GABA synapses in the post-stroke mouse brain, ii) electrophysiology to determine whether stroke leads to functional changes in GABA-mediated phasic inhibition, and (iii) treatment with zolpidem, an FDA-approved GABA agonist, to modulate recovery. Results: We found, using array tomography, a 1.7-fold increase in the number of GABAergic synapses containing the α1 receptor subunit in layer 5 of the peri-infarct cortex (synapse number/μm 3 : 0.039±0.006 (control) vs 0.064±0.006 (stroke); P<0.01), but not in layer 2/3. There was an associated increase in spontaneous inhibitory post-synaptic currents (sIPSC) specific to layer 5 pyramidal neurons (sIPSC charge (fC): -403±27.8 (control) vs -724±166 (stroke); p=0.03). This effect was transient, occurring during the onset of functional recovery. To test whether the increased phasic inhibitory GABAergic signaling promotes stroke recovery, we treated animals with zolpidem, an agonist with high affinity for α1 subunit-containing GABA A receptors. Low dose zolpidem increased GABA A phasic signaling in layer 5 pyramidal cells and notably increased the rate and extent of behavioral recovery without altering infarct size. Conclusions: These data provide the first evidence that enhanced GABA A -mediated synaptic activity during the recovery phase improves stroke outcome. These data identify modulation of phasic GABA signaling as a novel therapeutic strategy for stroke, indicate zolpidem as a potential drug to improve recovery, and underscore the necessity to distinguish the role of tonic and phasic GABA inhibition in stroke recovery.

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