Neuroscience
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Glymphatic system dysfunction in mood disorders: Evaluation by diffusion magnetic resonance imaging.
The glymphatic system, an expansive cerebral waste-disposal network, harbors myriad enigmatic facets necessitating elucidation of their nexus with diverse pathologies. Murine investigations have revealed a relationship between the glymphatic system and affective disorders. This study aimed to illuminate the interplay between bipolar disorder and the glymphatic system. ⋯ A free-water imaging analysis revealed a substantial elevation in the free-water index within the white-matter tracts, prominently centered on the corpus callosum, within the bipolar cohort relative to that in the control group. In analogous cerebral regions, a conspicuous affirmative correlation was observed between the free-water-corrected radial diffusivity and depression rating scales. Our results showed that the protracted course of bipolar disorder concomitantly exacerbated glymphatic system dysregulation.
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Spinocerebellar ataxia type 3 (SCA3) is a neurodegenerative disorder caused by mutant ataxin-3 with an abnormally expanded polyQ tract and is the most common dominantly inherited ataxia worldwide. There are no suitable therapeutic options for this disease. Autophagy, a defense mechanism against the toxic effects of aggregation-prone misfolded proteins, has been shown to have beneficial effects on neurodegenerative diseases. ⋯ Western blot and total antioxidant capacity assays suggested that trehalose had great therapeutic potential for treating SCA3, likely through its antioxidant activity. Our data indicate that trehalose plays a neuroprotective role in SCA3 by inhibiting the aggregation and reducing the protein level of ataxin-3, which is also known to protect against oxidative stress. These findings provide a new insight into the possibility of treating SCA3 with trehalose and highlight the importance of inducing autophagy in SCA3.
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Both alcohol misuse and sleep deficiency are associated with deficits in semantic processing. However, alcohol misuse and sleep deficiency are frequently comorbid and their inter-related effects on semantic processing as well as the underlying neural mechanisms remain to be investigated. ⋯ Alcohol misuse may lead to reduced MFG activation while sleep deficiency hinder semantic processing by suppressing PCG activity in women. The pathway model underscores the influence of sleep quality and alcohol consumption severity on semantic processing in women, suggesting that sex differences in these effects need to be further investigated.
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We recently showed that vestibular stimulation can produce a long-lasting alleviation of motor features in Parkinson's disease. Here we investigated whether components of the motor related cortical response that are commonly compromised in Parkinson's - the Bereitschaftspotential and mu-rhythm event-related desynchronization - are modulated by concurrent, low frequency galvanic vestibular stimulation (GVS) during repetitive limb movement amongst 17 individuals with idiopathic Parkinson's disease. Relative to sham, GVS was favourably associated with higher amplitudes during the late and movement phases of the Bereitschaftspotential and with a more pronounced decrease in spectral power within the mu-rhythm range during finger-tapping. These data increase understanding of how GVS interacts with the preparation and execution of voluntary movement and give added impetus to explore its therapeutic effects on Parkinsonian motor features.
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Without a functioning prefrontal cortex, humans and other animals are impaired in measures of cognitive control and behavioral flexibility, including attentional set-shifting. However, the reason for this is unclear with evidence suggesting both impaired and enhanced attentional shifting. We inhibited the medial prefrontal cortex (mPFC) of rats while they performed a modified version of an attentional set-shifting task to explore the nature of this apparent contradiction. ⋯ However, in the modified task, mPFC inactivation abolished ED shift-costs. The results support the suggestion that the mPFC is needed for the downregulation of attention that prevents learning about redundant and irrelevant stimuli. With mPFC inactivated, the rat learns more rapidly when previously redundant exemplars become the only relevant information.