This study indicated a strong correlation between hirsutism and metabolic abnormalities. Hirsutism is the most common cutaneous finding in PCOS women. Acne and AGA are associated with other manifestations of clinical hyperandrogenism, but not obvious markers of biochemical hyperandrogenemia and metabolic dysfunction.

Objective. We investigated combined cognitive and exercise interventions in the literature and summarized their effectiveness in improving poststroke cognitive impairment (PSCI). Data Sources. Electronic databases and trial registries were searched from their inception until July 2020. Study Selection. Trials were collected with the following study inclusion criteria: (1) patients over 18 years of age who were diagnosed with PSCI; (2) combined cognitive-exercise interventions, regardless of the order of the two types of interventions or whether they were administered simultaneously; (3) any control group studied at the same time that was deemed acceptable, including no intervention/routine care, delayed intervention, sham intervention, and passive training; (4) the use of any validated cognitive neuropsychological test to evaluate cognitive function; and (5) clinically administered random trials with controls. Data Extraction. Five randomized controlled trials met the inclusion criteria. Two reviewers independently assessed the eligibility of the full texts and methodological quality of the included studies using the Cochrane risk of bias tool. Inconsistent results were resolved by additional discussion or decided by a third examiner, if necessary. Data Analysis. Meta-analysis demonstrated that the combined interventions had a significant effect on executive function and working memory [Stroop test (time), standardized mean difference SMD = 0.42 , 95% confidence interval (CI): 0.80–0.04, p = 0.02 ; Trail Making Test, SMD = 0.49 , 95% CI: 0.82–0.16, p = 0.004 ; Forward Digit Span Test, SMD = 0.91 , 95% CI: 0.54–1.29, p ≤ 0.001 ]. While it was impossible to conduct a meta-analysis of global cognitive function and other cognitive domains, individual experiments demonstrated that the combined interventions played a significant role in global cognition, reasoning ability, logical thinking, and visual-spatial memory function. Conclusions. Our analyses demonstrated that the combined interventions had a significant effect on the improvement of PSCI, particularly in terms of executive function. However, the moderate risk of bias in the included trials and the small number of relevant studies indicated a need for more uniform diagnostic and evaluation criteria, and larger trials would provide stronger evidence to better understand the effectiveness of the combined interventions. This trial is registered with trial registration number INPLASY202160090.

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Parkinson’s disease remains one of the leading neurodegenerative diseases in developed countries. Despite well-defined symptomology and pathology, the complexity of Parkinson’s disease prevents a full understanding of its’ etiological mechanism. Mechanistically, α-synuclein misfolding and aggregation appears central for disease progression, but mitochondrial dysfunction, dysfunctional protein clearance and ubiquitin/proteasome systems, and neuroinflammation have also been associated with Parkinson’s disease. Particularly neuroinflammation, which was initially thought to be a side effect of Parkinson’s disease pathogenesis, has now been recognized as driver of Parkinson’s disease exacerbation. Next-generation sequencing identified a plethora of long noncoding RNAs (lncRNA) with important transcriptional regulatory functions. Moreover, a myriad of lncRNA are known regulators of inflammatory signaling and neurodegenerative diseases including IL-1β secretion and Parkinson’s disease. Here lncZFAS1 was identified as a regulator of inflammasome activation and pyroptosis in human neuroblast SH-SY5Y cells following MPP+ treatment, a common in vitro Parkinson’s disease cell model. Mechanistically, TXNIP ubiquitination through MIB1 E3 ubiquitin ligase regulates NLRP3 inflammasome activation in neuroblast cells. In contrast MPP+ activates the NLPR3 inflammasome through miR590-3p up-regulation, and direct interference with MIB1-dependent TXNIP ubiquitination. LncZFAS overexpression inhibits this entire pathway through direct interference with miR590-3p exposing a novel therapeutic target to prevent excessive inflammasome activation and pyroptosis in neuroblast cells during Parkinson's disease.

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Parkinson’s disease remains one of the leading neurodegenerative diseases in developed countries. Despite well-defined symptomology and pathology, the complexity of Parkinson’s disease prevents a full understanding of its etiological mechanism. Mechanistically, α-synuclein misfolding and aggregation appear to be central for disease progression, but mitochondrial dysfunction, dysfunctional protein clearance and ubiquitin/proteasome systems, and neuroinflammation have also been associated with Parkinson’s disease. Particularly, neuroinflammation, which was initially thought to be a side effect of Parkinson’s disease pathogenesis, has now been recognized as driver of Parkinson’s disease exacerbation. Next-generation sequencing has been used to identify a plethora of long noncoding RNAs (lncRNA) with important transcriptional regulatory functions. Moreover, a myriad of lncRNAs are known to be regulators of inflammatory signaling and neurodegenerative diseases, including IL-1β secretion and Parkinson’s disease. Here, LncZFAS1 was identified as a regulator of inflammasome activation, and pyroptosis in human neuroblast SH-SY5Y cells following MPP+ treatment, a common in vitro Parkinson’s disease cell model. Mechanistically, TXNIP ubiquitination through MIB1 E3 ubiquitin ligase regulates NLRP3 inflammasome activation in neuroblasts. In contrast, MPP+ activates the NLPR3 inflammasome through miR590-3p upregulation and direct interference with MIB1-dependent TXNIP ubiquitination. LncZFAS overexpression inhibits this entire pathway through direct interference with miR590-3p, exposing a novel research idea regarding the mechanism of Parkinson’s disease.

Background: Aging induces degenerative changes in the body and causes cognitive dysfunction, which has a significant negative impact on the daily lives of older adults. At present, there are limited effective interventions to slow the incidence of Aging-related cognitive impairment or even dementia. Among them, exercise and cognitive training are worthy of further research, especially the research on mechanisms. Studies have shown that LncRNA and miRNA play an important role in the occurrence, development, and rehabilitation of aging-related cognitive impairment. We aimed to identify the effect of cognitive-exercise dual-task training on cognitive function in naturally aged rats and to investigate the mechanism by which the LncRNA NEAT1/miR124-3p/caveolin-1-PI3K/Akt/GSK3β pathway plays a role in the improvement of cognitive function with dual-task training. Methods: Forty SD rats at 18 months of age were randomly divided into four groups (n=10 for each group): exercise training group, cognitive training group, cognitive-exercise dual-task training group, and aging control group. Each group underwent 12 weeks of intervention according to their corresponding training protocols. New object recognition tests were performed on all rats after the completion of the intervention. The expressions of related pathway proteins, LncRNA, and miRNA in the hippocampus were examined by Western blotting (WB) and/or Quantitative real-time polymerase chain reactions (qRT-PCR) after euthanasia of the rats. HT22 mouse hippocampal neuronal cells were cultured and miR-124-3p and lncRNA NEAT1 were over-expressed/down-expressed, respectively. WB and/or qRT-PCR were used to determine the levels of caveolin-1-PI3K/Akt/GSK3 pathway, miR-124-3p, and lncRNA NEAT1 expression in the neurons. Results: The results showed that compared with the aging control group, the cognitive-exercise dual-task training group had better performance on novelty recognition (P < 0.01), and their expressions of lncRNA NEAT1, caveolin-1, and p-GSK3β were significantly decreased (P < 0.05), while miR124-3p, p-PI3K, and p-Akt were significantly increased (P < 0.05). Conclusion: Our study showed that cognitive-exercise dual-task training improved cognitive function in aging rats better than no training or single training. The mechanism of cognitive function improvement could be related to the regulation of LncRNA NEAT1/miR124-3p- caveolin1/PI3K/Akt/GSK3β pathway.