NeuroSci

Background: Patients with primary central nervous system (CNS) tumors often experience fatigue and sleep disturbances, significantly impacting their quality of life. Exercise has been shown to improve these symptoms in various cancer populations. The aim of this study is to evaluate the effects of different types of exercise on fatigue and sleep in less-investigated CNS tumor patients. Methods: A literature search was conducted in PubMed, Scopus, Cochrane Library, and CINAHL. Eligible randomized and non-randomized studies evaluating exercise interventions in patients diagnosed with primary brain tumors were systematically reviewed, primarily using a narrative synthesis approach. Cancer-related fatigue and sleep-related outcomes were extracted as variables of interest. Where possible [≥2 Randomized Control Trials (RCTs) available for glioma patients], meta-analyses were conducted to assess the overall effects of physical therapy on the above-mentioned outcomes. Results: A total of 15 relevant intervention studies were identified, either RCTs or other types of studies, such as prospective feasibility cohort studies and case studies. A total of 448 participants were enrolled, with the majority diagnosed with glioma. There were single reports on pituitary adenoma after surgery and meningioma patients. In glioma patients, the overall effect of various modality exercise interventions on fatigue was non-significant, reflecting the heterogeneous characteristics of studies with diverse outcomes. However, meta-analysis focusing on combined exercise interventions (aerobic and resistance training) showed a positive effect on reducing fatigue in these patients [Standardized Mean Difference (SMD) = 0.866, p = 0.03]. Fatigue in glioma patients may also improve through yoga and Pilates. Aerobic but not strength exercise seems to improve sleep in glioma patients (SMD = 1.14, p = 0.02). Sleep quality may also improve through yoga and combined exercise. Conclusions: Certain types of exercise appear to effectively reduce fatigue and improve sleep in patients with CNS tumors. Future, well–controlled, multi-arm, larger-scale studies are necessary to resolve discrepancies, as well as to explore long-term outcomes and define factors influencing individualized exercise responses.

Alzheimer’s disease (AD) remains an unmet medical challenge, as there are no effective therapies that alter the disease’s progression. While approaches have targeted molecules like acetylcholine (ACh) and glutamate, these strategies have provided only limited benefits and do not address the complex molecular mechanisms underlying AD development. This review suggests that β-alanine (3-aminopropanoic acid) is an underexplored neurotransmitter that could serve as a potential AD drug target. Existing evidence indicates that β-alanine modulates GABAergic and glutamatergic neurotransmission, thereby affecting neuronal hyperexcitability. Additionally, studies suggest that β-alanine has antioxidant effects, reducing oxidative stress caused by reactive oxygen species (ROS). We propose that β-alanine might bind to Aβ/tau proteins, possibly targeting the six-amino acid sequences EVHHQK/DDKKAK, which are involved in protein aggregation. β-Alanine may also influence the release of pro-inflammatory cytokines from microglia, potentially reducing neuroinflammation. We also hypothesize that β-alanine may help regulate metal dyshomeostasis, which leads to ROS production. Taurine, structurally like β-alanine, appears to influence comparable mechanisms. Although structural similarity doesn’t ensure therapeutic effectiveness, this evidence supports considering β-alanine as a treatment for AD. Furthermore, β-alanine and its analogues face challenges, including crossing the blood–brain barrier (BBB) and optimizing structure–activity relationships (SAR). This review includes articles through September 2025, sourced from four databases.

Hand representation maps of the primate primary motor (M1) and somatosensory (SI) cortices exhibit plasticity, with their spatial extent modifiable through training. While activation and map enlargement during tapping tasks are well documented, the directionality of information flow between these regions remains unclear. We applied Information Imbalance Gain Causality (IIG) to examine the propagation and temporal dynamic of BOLD activity among Area 4 (precentral gyrus), Area 3a (fundus of the central sulcus), and SI areas (postcentral gyrus). Data were collected from both hemispheres of nine participants performing alternating right–left hand finger tapping inside a 1.5T fMRI scan. The results revealed strong information flow from both the precentral and postcentral gyri toward the sulcus during tapping task, with weaker bidirectional exchange between the gyri. When not engaged in tapping, both gyri communicated with each other and the sulcus. During active tapping, flow bypassed the sulcus, favoring a more direct postcentral to precentral way. Overtime, postcentral to sulcus influence strengthened during non task periods, but diminished during tapping. These findings suggest that M1, Area 3a, and SI areas form a dynamic network that supports rapid learning processing, where Area 3a of the sulcus may contribute to maintaining representational plasticity during complex tapping tasks.