Journal of Neurorestoratology最新文献

Background

Although dyskinesia is well recognized in Parkinson's disease, it is generally under acknowledged in multiple system atrophy (MSA). Reported cases of dyskinesia primarily manifest in patients with MSA with predominant parkinsonism (MSA-P), and characteristically present as orofacial dystonia. However, we have observed other manifestations of dyskinesia in our clinical practice. The current report aims to present the specific manifestations of dyskinesia in MSA-P, with videos.

Methods

We enrolled six patients with MSA-P with dyskinesia from Xuanwu Hospital. Of these, four had clinically established MSA-P and two had clinically probable MSA-P according to the 2022 Movement Disorder Society criteria for MSA diagnosis. All six patients underwent an acute levodopa challenge test, and videos were recorded during the process.

Results

Dyskinesia had a unilateral distribution in four patients. Three patients presented with peak-dose orofacial dystonia; of these, two were associated with blepharospasm and two were associated with limb dystonia. In addition, we observed that one patient had peak-dose distal lower limb dystonia with upper limb chorea, one patient had wearing-off dystonia of the eyelids, and one patient had diphasic generalized chorea mimicking that of Parkinson's disease.

Conclusions

In addition to orofacial dystonia, the topographic patterns of dyskinesia in MSA-P can manifest as limb dystonia, blepharospasm, and generalized chorea. Moreover, the temporal patterns of dyskinesia in MSA-P can be peak-dose, wearing-off, or diphasic.

Hypertrophic olivary degeneration (HOD) arises from lesions of the dentato-rubro-olivary pathway (Guillain–Mollaret triangle), and bilateral HOD is the rarest. Our patient, a 42-year-old man with bilateral HOD caused by unilateral midbrain infarction, had both increased dizziness and ataxia as the first symptoms. HOD has no effective treatment and is easily misdiagnosed as other diseases in clinical practice. Our case demonstrated unique HOD symptomatology and emphasizes the important role of magnetic resonance imaging in diagnosing HOD. The use of gabapentin relieved nystagmus in our patient and may provide a reference for the future treatment of such patients.

Objective

Inflammatory reactions are recognized as pivotal in spinal cord injury (SCI), with the anti-inflammatory role of polarized microglia crucial in mitigating such injury. The present study aimed to determine the protective effects of GsMTx4 on functional recovery in a mouse model of SCI and investigate the role of GsMTx4 in cytokine-induced microglial activation and associated molecular mechanisms.

Methods

We assessed the effects of GsMTx4 on motor function in a mouse model of SCI, including neuronal survival and activated microglia in the vicinity of the injury after SCI. We also investigated the effects of GsMTx4 on expression of relevant inflammatory factors involved in cytokine-induced microglial activation and the associated signaling pathways.

Results

GsMTx4 effectively promoted functional recovery in mice and alleviated nerve damage after SCI. Additionally, GsMTx4 facilitated the transition of microglia from the M1 phenotype to the M2 phenotype, suppressed microglial activation, and reduced the expression of corresponding inflammatory mediators. These effects may involve modulation of neurogenic inflammation through the Piezo1/NFκB/STAT6 pathway, at least in part.

Conclusion

GsMTx4 safeguards against SCI by regulating microglial polarization, potentially via the Piezo1/NFκB/STAT6 pathway, offering initial evidence supporting the potential therapeutic efficacy of GsMTx4 for treatment of SCI.

Background

Depression, also known as major depressive disorder, is a mental disorder caused by multiple factors. The cause of depression remains unclear, but a growing number of studies have reported a link between depression and long non-coding RNAs (lncRNAs). In the present study, we reviewed the relationships between depression and four lncRNAs, focusing on the differential expression of these lncRNAs in patients with depression, how to regulate depression, and how to use lncRNAs for the diagnosis, prevention, and treatment of clinical depression.

Methods

A systematic review of 23 studies published between 2011 and 2021 was conducted using Pubmed. Selection criteria included publication date and relevance to topic: Only articles published after 2010 were included to ensure the review reflects the most recent research, and all articles are selected strictly on their research topic.

Results

The short communication has summarized the relationships between depression and four lncRNAs, especially antisense lncRNAs and lincRNAs, and their potential in the diagnosis of depression and its targeted therapy.

Conclusions

The study found that these four lncRNAs, particularly antisense lncRNAs and lincRNAs, are closely associated with various aspects of depression. These findings suggest new therapeutic targets and could contribute to improving the accuracy of depression diagnosis.

Traumatic brain injury (TBI) and lifestyle habits such as Western diet (WD) consumption represent two risk factors that affect an individual's health outcome globally. Individuals with TBI have a greater risk of mortality from associated chronic diseases than the general population. WD has been shown to impair cognitive function, decrease the brain's capacity to compensate for insult by affecting recovery as well as induce metabolic syndrome (MetS) which may be a risk factor for poor TBI prognosis. Hence, this study aims to investigate the impact of WD on TBI behavioral outcomes and neuropathology. Eight-week-old male C57BL6 mice were fed either WD or normal chow for 4 weeks prior to TBI induction. At week four, mice underwent either an experimental open-head TBI or a sham procedure. Mice continued their respective diets for four weeks after brain injury. Metabolic, cognitive function, and molecular assessment were performed four weeks after TBI. Results showed that while WD significantly increased fat percentage and elevated plasma cholesterol, there was no change in blood glucose level or body weight, indicating an early stage of MetS. Nevertheless, this was associated with neuroinflammation and impaired cognitive functions. However, there was no significant impact on cardiovascular function and mitochondrial bioenergetics. Importantly, the mild MetS induced by WD triggered basal motor, cognitive deterioration and exacerbated the long-term neuropathology of TBI. Taken together, our work highlights the magnitude of the contribution of lifestyle factors including the type of diet, even in the absence of overt metabolic consequences, on the neurobehavioral prognosis following TBI.