Neuroscience
-
Rodent models of cerebral ischemia provide a valuable contribution to a better understanding of stroke pathophysiology, to validate diagnostic methods, and to enable testing of new treatments for ischemia-reperfusion damage and comorbidities. However, ethical concerns have led to increased attention to the welfare aspects of such models. Supportive therapies are an essential part of the overall animal care and use program and should be tailored to the experimental model being studied, the regulatory requirements, and research objectives to achieve high-quality preclinical studies and ethical research practices. ⋯ This report provides a systematic review of the scientific literature covering the relevant period from years 1988 to September 2024, with the aim to investigating veterinary medical interventions useful to minimize suffering in rodent models of stroke without producing experimental bias. The research findings, consolidated from 181 selected studies, published from 1991 to 2023, indicate the feasibility of implementing personalized protocols of anesthesia, analgesics, antibiotics, and other supportive therapies in rodent models of stroke, while avoiding scientific interferences. These data fill a gap in current knowledge and could be of interest for an interdisciplinary audience working with rodent models of stroke, stimulating further refinements to safeguard both animal welfare and the validity of experimental findings, and may promote the culture of ethical conduct in various research fields and disciplines.
-
Mitochondrial dysfunction is a pivotal factor in the pathogenesis of neurodegenerative disorders, driving neuronal degeneration through mechanisms involving oxidative stress, impaired energy production, and dysregulated calcium homeostasis. Agmatine, an endogenous polyamine derived from arginine, has garnered attention for its neuroprotective properties, including anti-inflammatory, anti-oxidative, and antiapoptotic effects. Recent studies have highlighted the potential of agmatine in preserving mitochondrial function and mitigating neurodegeneration, making it a promising candidate for therapeutic intervention. ⋯ Despite promising findings, challenges such as optimizing agmatine's pharmacokinetics, determining optimal dosing regimens, and elucidating its precise molecular targets within mitochondria remain to be addressed. Future research directions should focus on developing targeted delivery systems for agmatine, investigating its interactions with mitochondrial proteins, and conducting well-designed clinical trials to evaluate its therapeutic efficacy and safety profile in neurodegenerative disorders. Overall, agmatine emerges as a novel therapeutic agent with the potential to modulate mitochondrial homeostasis and alleviate neurodegenerative pathology, offering new avenues for treating these debilitating conditions.
-
For a long time, traditional medicine has acknowledged the gut's impact on general health. Contemporary science substantiates this association through investigations of the gut microbiota, the extensive community of microorganisms inhabiting our gastrointestinal system. These microscopic residents considerably improve digestive processes, nutritional absorption, immunological function, and pathogen defense. ⋯ We also conducted a thorough examination of the existing understanding in the area of how microbiota affects social behaviors, including emotions, stress responses, and cognitive functions. We also explored the potential of interventions that focus on the connection between the gut and the brain, such as using probiotics to treat diseases of the CNS. This research opens up new possibilities for addressing mental health and neurological conditions in an innovative manner.
-
Review
Multifaceted roles of DLG3/SAP102 in neurophysiology, neurological disorders and tumorigenesis.
DLG3, also known as Synapse-associated protein 102 (SAP102), is essential for the organization and plasticity of excitatory synapses within the central nervous system (CNS). It plays a critical role in clustering and moving key components necessary for learning and memory processes. Mutations in the DLG3 gene, which result in truncated SAP102 proteins, have been associated with a range of neurological disorders, including X-linked intellectual disability (XLID), autism spectrum disorders (ASD), and schizophrenia, all of which can disrupt synaptic structure and cognitive functions. ⋯ Moreover, SAP102 has been demonstrated to regulate tumor-induced bone pain through activating NMDA receptors. These findings highlight SAP102 as a promising therapeutic target for both neurological disorders and cancer. Therefore, further investigation into the regulatory roles of SAP102 in neural development and disease may lead to novel therapeutic approaches for treating synaptic disorders and managing cancer progression.
-
Review
Emerging biophysical techniques for probing synaptic transmission in neurodegenerative disorders.
Plethora of research has shed light on the critical role of synaptic dysfunction in various neurodegenerative disorders (NDDs), including Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD). Synapses, the fundamental units for neural communication in the brain, are highly vulnerable to pathological conditions and are central to the progression of neurological diseases. The presynaptic terminal, a key component of synapses responsible for neurotransmitter release and synaptic communication, undergoes structural and functional alterations in these disorders. ⋯ The review articles highlighted provide a comprehensive overview of how synaptic vulnerability and pathology are shared mechanisms across a spectrum of neurological disorders. In major neurodegenerative diseases, synaptic dysfunction is a common thread linking these conditions. The intricate molecular machinery involved in neurotransmitter release, synaptic vesicle dynamics, and presynaptic protein regulation are key areas of focus for understanding synaptic alterations in neurodegenerative diseases.