Neuroscience
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We examined whether aging with and without a cerebral lesion such as stroke affects modulation of reactive balance response for recovery from increasing intensity of sudden slip-like stance perturbations. Ten young adults, older age-match adults and older chronic stroke survivors were exposed to three different levels of slip-like perturbations, level 1 (7.75m/s(2)), Level II (12.00m/s(2)) and level III (16.75m/s(2)) in stance. The center of mass (COM) state stability was computed as the shortest distance of the instantaneous COM position and velocity relative to base of support (BOS) from a theoretical threshold for backward loss of balance (BLOB). ⋯ Stroke group on the other hand was unable to modulate compensatory step length or control trunk extension at higher perturbation intensities resulting in reduced stability on levels II and III compared with the other groups. The findings reflect impaired modulation of recovery response with increasing intensity of sudden perturbations among stroke survivors compared with their healthy counter parts. Thus, aging superimposed with a cortical lesion could further impair reactive balance control, potentially contributing toward a higher fall risk in older stroke survivors.
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Metastasis suppressor 1 (MTSS1) or missing in metastasis (MIM) is an actin- and membrane-binding protein with tumor suppressor functions. MTSS1 is important for cell morphology, motility, metastasis. The role of MTSS1 in cell morphology has been widely investigated in non-neuronal tissues; however the role of MTSS1 in neurite outgrowth remains unclear. ⋯ In accordance with the over-expression data, knockdown of MTSS1 in cerebellar granule neurons could increase the axon length but decrease the dendrite length and the number of dendrites. In addition, MTSS1 knock down in embryonic hippocampal neurons suppressed neurite branching and reduced dendrite length. Our findings have demonstrated that MTSS1 modulates neuronal morphology, possibly through a Rac1-PIPs signaling pathway.
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Recanalization of occluded vessels leads to ischemia-reperfusion injury (IRI), with oxidative stress as one of the main causes of injury, despite the fact that recanalization therapy is the most effective treatment for ischemic stroke. The nuclear factor erythroid 2-related factor 2 (Nrf2) is one of the transcription factors which has an essential role in protection against oxidative stress. RS9 is a novel Nrf2 activator obtained from bardoxolone methyl (BARD), an Nrf2 activator that has already been tested in a clinical trial, using a biotransformation technique. ⋯ RS9 also attenuated the phosphorylation of NF-κB p65 2 and 6h after reperfusion. Finally, RS9 improved the survival rate and neurological deficits 7days after MCAO. Our results suggest that the activation of Nrf2 by RS9 has a neuroprotective effect, mediated by attenuating both oxidative stress and neuroinflammation, and that RS9 is an effective therapeutic candidate for the treatment of IRI.