Pathogenesis, Assessments, and Management of Chemotherapy-Related Cognitive Impairment (CRCI): An Updated Literature Review

There are various cancer treatments at present, and chemotherapy is one of the main methods. Chemotherapy-related cognitive impairment (CRCI), as one of the side effects of chemotherapy, has gradually attracted the attention of more and more researchers. CRCI has been verified by subjective reports and objective neuropsychological tests so far. But oncologists’ understanding of it and its treatments are still incomplete. In this review, we mainly give a comprehensive overview of the mechanism of CRCI, then describe a variety of evaluation methods, and finally summarize the treatment approaches under current medical conditions and compare it with an excellent article published in 2015 with the aim of providing directions for future research and better understanding of CRCI for clinicians

The Interrelation between Reactive Oxygen Species and Autophagy in Neurological Disorders

Neurological function deficits due to cerebral ischemia or neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) have long been considered a thorny issue in clinical treatment. Recovery after neurologic impairment is fairly limited, which poses a major threat to health and quality of life. Accumulating evidences support that ROS and autophagy are both implicated in the onset and development of neurological disorders. Notably, oxidative stress triggered by excess of ROS not only puts the brain in a vulnerable state but also enhances the virulence of other pathogenic factors, just like mitochondrial dysfunction, which is described as the culprit of nerve cell damage. Nevertheless, autophagy is proposed as a subtle cellular defense mode against destructive stimulus by timely removal of damaged and cytotoxic substance. Emerging evidence suggests that the interplay of ROS and autophagy may establish a determinant role in the modulation of neuronal homeostasis. However, the underlying regulatory mechanisms are still largely unexplored. This review sets out to afford an overview of the crosstalk between ROS and autophagy and discusses relevant molecular mechanisms in cerebral ischemia, AD, and PD, so as to provide new insights into promising therapeutic targets for the abovementioned neurological conditions

Cognition Deficits in Parkinson’s Disease: Mechanisms and Treatment

Parkinson’s disease (PD) is the second most common progressive neurodegenerative disorder mainly in middle-elderly population, which represents diverse nonmotor symptoms (NMS) besides such well-documented motor symptoms as bradykinesia, resting tremor, rigidity, and postural instability. With the advancement of aging trend worldwide, the global prevalence of PD is mounting up year after year. Nowadays, accumulating lines of studies have given a comprehensive and thorough coverage of motor symptoms in PD. Yet much less attention as compared has been paid to the nonmotor symptoms of PD, such as cognition deficits. Of note, a patient with PD who suffers from cognitive impairment may harbour a statistically significantly higher risk of progressing toward dementia, which negatively affects their life expectancy and daily functioning and overall lowers the global quality of life. Furthermore, it is a widely held view that cognitive dysfunction does not just occur in the late stage of PD. On the basis of numerous studies, mild cognitive impairment (MCI) is a harbinger of dementia in PD, which is observed as an intermediate state with considerable variability; some patients remain stable and some even revert to normal cognition. Considered that the timing, profile, and rate of cognitive impairment vary greatly among PD individuals, it is extremely urgent for researchers and clinicians alike to identify and predict future cognitive decline in this population. Simultaneously, early screening and canonical management of PD with cognitive deficits are very imperative to postpone the disease progression and improve the prognosis of patients. In our review, we focus on a description of cognitive decline in PD, expound emphatically the pathological mechanisms underlying cognition deficits in PD, then give a comprehensive overview of specific therapeutic strategies, and finally dissect what fresh insights may bring new exciting prospect for the subfield

CMA1 is potent prognostic marker and associates with immune infiltration in gastric cancer

Background: Chymase 1 (CMA1), a gene known to be expressed in mast cells (MCs), is largely linked to immunity. However, the relationship between CMA1 and prognosis of multiple tumours and tumour-infiltrating lymphocytes (TILs) remains elusive. Methods: The differential expressions of CMA1 in different tumours and their corresponding normal tissues were evaluated via exploring Tumour Immune Estimation Resource (TIMER) and Oncomine database; the correlation within expression level of CMA1 and outcome of cancer patients was evaluated via Kaplan–Meier plotter and Gene Expression Profiling Interactive Analysis (GEPIA) database; the correlation between CMA1 and tumour immune cell infiltration was further investigated by TIMER; additionally, the correlation between CMA1 and gene signature pattern of immune infiltration were checked using TIMER and GEPIA. Results: There were significant differences in CMA1 expression levels between gastric cancer (GC) tissues and adjacent normal tissues. The high expression of CMA1 was closed related to poor overall survival (OS) and progression-free survival (PFS) in patients with GC (OS HR = 1.50, p = .00015; PFS HR = 1.33, p = .016). Especially, in GC patients at N1, N2 and N3 stages, high CMA1 expression was correlated with poor OS and PFS, but not with NO (p = .15, .09). The expression of CMA1 was positively associated with the levels of infiltrated CD4+, CD8+ T cells, neutrophils, macrophages, and dendritic cells (DCs) in GC. Whereas, CMA1 expression was considerably associated with various immune markers. Conclusion: CMA1 is a key gene whose expression level is significantly correlated with GC prognosis and infiltration levels of CD8+, CD4+ T cells, neutrophils, macrophages, and DCs in GC. In addition, the expression of CMA1 may be involved in regulating tumour-associated macrophages (TAMs), dendritic cells, exhausted T cells and regulatory T cells in GC. It suggests that CMA1 could be utilized as a prognostic marker and a sign of immune infiltration in GC