Frontiers in Neuroscience最新文献

Aim: The objective of this study was to gain insight into the nature of cognitive fatigue and to identify future trends of objective assessment techniques in this field.

Methods: One thousand and eighty-five articles were retrieved from the Web of Science Core Collection database. R version 4.3.1, VOSviewer 1.6.20, CiteSpace 6.2.R4, and Microsoft Excel 2019 were used to perform the analysis.

Results: A total of 704 institutes from 56 countries participated in the relevant research, while the People's Republic of China contributed 126 articles and was the leading country. The most productive institute was the University of Gothenburg. Johansson Birgitta from the University of Gothenburg has posted the most articles (n = 13). The PLOS ONE published most papers (n = 38). The Neurosciences covered the most citations (n = 1,094). A total of 3,116 keywords were extracted and those with high frequency were mental fatigue, performance, quality-of-life, etc. Keywords mapping analysis indicated that cognitive fatigue caused by continuous work and traumatic brain injury, as well as its rehabilitation, have become the current research trend. The most co-cited literature was published in Sports Medicine. The strongest citation burst was related to electroencephalogram (EEG) event-related potential and spectral power analysis.

Conclusion: Publication information of related literature on the objective assessment of cognitive fatigue from 2007 to 2024 was summarized, including country and institute of origin, authors, and published journal, offering the current hotspots and novel directions in this field.

Background: Previous studies have demonstrated widespread brain neurodegeneration in Alzheimer's disease (AD). However, the neurobiological and pathogenic substrates underlying this structural atrophy across the AD spectrum remain largely understood.

Methods: In this study, we obtained structural MRI data from ADNI datasets, including 83 participants with early-stage cognitive impairments (EMCI), 83 with late-stage mild cognitive impairments (LMCI), 83 with AD, and 83 with normal controls (NC). Our goal was to explore structural atrophy across the full clinical AD spectrum and investigate the genetic mechanism using gene expression data from the Allen Human Brain Atlas.

Results: As a result, we identified significant volume atrophy in the left thalamus, left cerebellum, and bilateral middle frontal gyrus across the AD spectrum. These structural changes were positively associated with the expression levels of genes such as ABCA7, SORCS1, SORL1, PILRA, PFDN1, PLXNA4, TRIP4, and CD2AP, while they were negatively associated with the expression levels of genes such as CD33, PLCG2, APOE, and ECHDC3 across the clinical AD spectrum. Further gene enrichment analyses revealed that the positively associated genes were mainly involved in the positive regulation of cellular protein localization and the negative regulation of cellular component organization, whereas the negatively associated genes were mainly involved in the positive regulation of iron transport.

Conclusion: Overall, these results provide a deeper understanding of the biological mechanisms underlying structural changes in prodromal and clinical AD.

Background: Patients with traumatic brain injury (TBI) often experience post-injury anxiety and depression, which can persist over time. However, the relationships between anxiety and depression in TBI patients and delirium, sleep quality, self-efficacy, and serum inflammatory markers require further investigation.

Objective: This study aims to explore the associations of delirium, sleep quality, self-efficacy, and serum inflammatory markers with anxiety and depression in TBI patients, and to examine potential influencing factors.

Methods: We conducted a cohort study involving 127 patients with TBI. Delirium was assessed using the Confusion Assessment Method (CAM) and CAM-ICU, while anxiety, depression, sleep quality, self-efficacy, and pain were evaluated using the appropriate tools, respectively. Serum inflammatory markers (CRP, TNF-α, IL-6) were collected within 1 day post-injury. Generalized estimating equations (GEE) were used to analyze the relationships between delirium, sleep, self-efficacy, and anxiety/depression.

Results: The study identified 56 patients with delirium. Patients with delirium differed significantly from those without delirium in age, TBI classification, sleep duration, CRP levels, TNF-α levels, pain, self-efficacy, and insomnia (P < 0.05). The GEE analysis revealed that delirium, CRP levels, self-efficacy, underlying diseases, insomnia, TBI classification, age, and sleep duration were associated with anxiety symptoms in TBI patients at 6 months post-discharge (P < 0.05). Depression in TBI patients at 6 months post-discharge was not associated with delirium or insomnia but correlated with CRP levels, TBI classification, and self-efficacy (P < 0.05).

Conclusion: TBI patients who experience delirium, insomnia, and low self-efficacy during the acute phase are likely to exhibit more anxiety at the 6-month follow-up. Depression in TBI patients is not associated with delirium or insomnia but is negatively correlated with self-efficacy. CRP levels post-TBI may serve as a biomarker to identify patients at risk of emotional symptoms and potentially accelerate patient recovery.

The role of myeloid cells (granulocytes and monocytes) in neurodegeneration and neurodegenerative disorders (NDD) is indisputable. Here we discuss the roles of myeloid cells in neurodegenerative diseases, and the recent advances in biofluid and imaging myeloid biomarker research with a focus on methods that can be used in the clinic. For this review, evidence from three neurodegenerative diseases will be included, Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). We discuss the potential for these biomarkers to be used in humans with suspected NDD as prognostic, diagnostic, or monitoring tools, identify knowledge gaps in literature, and propose potential approaches to further elucidate the role of myeloid cells in neurodegeneration and better utilize myeloid biomarkers in the understanding and treatment of NDD.

Therapeutic hypothermia inhibits organ damage by suppressing metabolism, which makes it a therapy of choice for treating various diseases. Specifically, it is often used to treat conditions involving central nervous system disorders where it is expected to positively impact functional prognosis. Although keeping the body temperature at a hypothermic level has been conventionally used, how to manage the body temperature correctly remains a topic of debate. Recently, the concept of temperature management has been proposed to improve the quality of body temperature control and avoid hyperthermia. This review focuses on the effect of temperature on the central nervous system in conditions involving central nervous system disorders and the practice of temperature management in clinical situations.

Chronic prostatitis/chronic pelvic pain syndrome is a prevalent condition affecting the male urinary system. The urinary dysfunction resulting from this disorder has a direct or indirect impact on the patient's quality of life. Recent studies have suggested that organ cross-sensitization between the prostate and bladder may elucidate this phenomenon; however, the specific molecular mechanisms remain unclear. In this study, we simulated the urinary symptoms of prostatitis patients using an animal model and examined the expression of relevant proteins within the prostate-bladder sensitized neural pathway. We found that transient receptor potential vanilloid 1 (TRPV1) protein is highly expressed in the dorsal root ganglia (DRG) that co-innervate both the prostate and bladder, potentially increasing the sensitivity of TRPV1 channels via the substance P-neurokinin 1 (SP-NK-1) pathway, which may exacerbate micturition symptoms. Furthermore, in the absence of bladder inflammation, elevated levels of neurogenic substances in bladder tissue were found to sensitize bladder sensory afferents. Collectively, these results underscore the significant role of TRPV1 in bladder sensitization associated with prostatitis, suggesting that the inhibition of TRPV1 along this sensitization pathway could be a promising approach to treating urinary dysfunction linked to prostatitis in the future.

There are well-documented gender differences in the risk and severity of sleep disorders and associated comorbidities. While fundamental sex differences in sleep regulatory mechanisms may contribute to gender disparities, biological responses to sleep loss and stress may underlie many of the risks for sleep disorders in women and men. Some of these sex differences appear to be dependent on sex chromosome complement (XX or XY) and the organizational effects of reproductive hormones. Reproductive development plays a critical role in the ability of sex chromosomes and reproductive hormones to produce sex differences in sleep and wakefulness. Rodent models reveal that reproductive hormones drive many but not all sex differences in sleep-wake architecture. The ability of reproductive hormones to alter sleep are often dependent on responses to sleep loss and stress. However, in the absence of reproductive hormones (in gonadectomized rodents) sex differences in sleep amount and the ability to recover from sleep loss persist. The suprachiasmatic nucleus (SCN) and the ventrolateral preoptic nucleus (VLPO) of the hypothalamus play crucial regulatory roles in mediating the effects of reproductive hormones on the sleep-wake cycle. Taken together, the work reviewed here reveals that the reproductive hormone environment and sex chromosome complement may underlie gender disparities in sleep patterns and the risk for sleep disorders.

Olfactory dysfunction has emerged as a hallmark feature shared among several neurological conditions, including both neurodevelopmental and neurodegenerative disorders. While diseases of both categories have been extensively studied for decades, their association with olfaction has only recently gained attention. Olfactory deficits often manifest already during prodromal stages of these diseases, yet it remains unclear whether common pathophysiological changes along olfactory pathways cause such impairments. Here we probe into the intricate relationship between olfactory dysfunction and neurodegenerative and neurodevelopmental disorders, shedding light on their commonalities and underlying mechanisms. We begin by providing a brief overview of the olfactory circuit and its connections to higher-associated brain areas. Additionally, we discuss olfactory deficits in these disorders, focusing on potential common mechanisms that may contribute to olfactory dysfunction across both types of disorders. We further debate whether olfactory deficits contribute to the disease propagation or are simply an epiphenomenon. We conclude by emphasizing the significance of olfactory function as a potential pre-clinical diagnostic tool to identify individuals with neurological disorders that offers the opportunity for preventive intervention before other symptoms manifest.

Introduction: Cancer patients have a heightened susceptibility to anxiety and depressive disorders, which significantly impact the effectiveness of cancer treatments and long-term quality of life. This study aimed to compare the efficacy of different antidepressants in cancer and non-cancer patients.

Methods: A total of 610 patients diagnosed with depressive episodes and/or anxiety disorders were retrospectively included and divided into a cancer group and a non-cancer control group. Antidepressants used included escitalopram, duloxetine, sertraline, venlafaxine, and vortioxetine, combined with trazodone or not. The Patient Health Questionnaire-9 (PHQ-9) and the Generalized Anxiety Disorder Questionnaire-7 (GAD-7) scores were used to evaluate the efficacy after 4 weeks and 8 weeks of systematic antidepressants treatment.

Results: Compared to the non-cancer group, the cancer group had higher proportions of females, older individuals, and patients with poor sleep quality, while reporting fewer somatic symptoms at baseline (all p < 0.05). PHQ-9 and GAD-7 scores in cancer patients treated with antidepressants were significantly lower than baseline at week 4 and week 8 (all p < 0.05). The sertraline group demonstrated significantly less improvement in GAD-7 scores at week 4 and in both GAD-7 and PHQ-9 scores at week 8 compared to the escitalopram group, while duloxetine, venlafaxine, and vortioxetine showed comparable efficacy to escitalopram. Antidepressants combined with trazodone showed significant improvement in PHQ-9 scores at week 4 compared to those without trazodone. The gynecological cancer group showed significantly more improvement in GAD-7 and PHQ-9 scores at week 4 and 8 compared to breast cancer patients.

Conclusion: Antidepressant treatment in cancer patients with anxiety and depression is as effective as in non-cancer patients. The efficacy of escitalopram is comparable to duloxetine, venlafaxine, and vortioxetine, all of which outperformed sertraline in cancer patients.