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Many central nervous system (CNS) disorders lack approved treatment options. Previous research demonstrated that peptide CAQK can bind to chondroitin sulfate proteoglycans (CSPGs) in the extracellular matrix of the CNS. In vivo studies have investigated CAQK conjugated to nanoparticles containing therapeutic agents with varying methodologies/outcomes. This paper presents the first systematic review assessing its properties, applications, and outcomes secondary to its use. Following PRISMA guidelines, a comprehensive search was performed across multiple databases. Studies utilizing CAQK as a therapeutic agent/homing molecule in animal/human models were selected. Sixteen studies met the inclusion criteria. Mice and rats were the predominant animal models. All studies except one used CAQK to deliver a therapeutic agent. The reviewed studies mostly included models of brain and spinal cord injuries. Most studies had intravenous administration of CAQK. All studies demonstrated various benefits and that CAQK conjugation facilitated localization to target tissues. No studies directly evaluated the effects of CAQK alone. The data are limited by the heterogeneity in study methodologies and the lack of direct comparison between CAQK and conjugated agents. Overall, these findings present CAQK utilization to deliver a therapeutic agent as a promising targeting strategy in the management of disorders where CSPGs are upregulated.

Despite ample experimental data indicating a role of inflammatory mediators in the behavioral and neurobiological manifestations elicited by exposure to physical and psychologic stressors, causative associations between systemic low-grade inflammation and central nervous system inflammatory processes in posttraumatic stress disorder (PTSD) patients remain largely conceptual. As in other stress-related disorders, pro-inflammatory activity may play an equivocal role in PTSD pathophysiology, one that renders indiscriminate employment of anti-inflammatory agents of questionable relevance. In fact, as several pieces of preclinical and clinical research convergingly suggest, timely and targeted potentiation rather than inhibition of inflammatory responses may actually be beneficial in patients who are characterized by suppressed microglia function in the face of systemic low-grade inflammation. The deleterious impact of chronic stress-associated inflammation on the systemic level may, thus, need to be held in context with the - often not readily apparent - adaptive payoffs of low-grade inflammation at the tissue level.

Introduction: Multiple Sclerosis (MS) is a chronic autoimmune disease of the central nervous system, marked by inflammation, demyelination, and neurodegeneration. It severely impacts quality of life with symptoms like spasticity, pain, and cognitive impairment. Conventional treatments often fail, necessitating alternative therapies. Purpose: This review evaluates the efficacy and safety of cannabis extracts in treating MS, enhancing understanding of their benefits and limitations. State of knowledge: Studies suggest that cannabinoids may alleviate MS symptoms, particularly spasticity and pain. Clinical trials have shown significant reductions in muscle stiffness and pain, along with improved sleep quality. Meta-analyses, by Whiting et al. and Cochrane, support these findings but highlight the risk of side effects, which may limit long-term use. Additionally, research on animal models and in vitro studies indicate that cannabinoids may have neuroprotective and immunomodulatory properties, potentially reducing neuroinflammation and demyelination. Conclusion: Cannabinoids exhibit potential as a complementary therapy for managing MS symptoms, especially spasticity and pain. However, evidence is mixed, with some studies showing limited efficacy and considerable risk of side effects. More long-term, high-quality studies are needed to fully understand the therapeutic potential and safety profile of cannabinoids in MS treatment. Despite the challenges, the growing availability and changing legal status of medical cannabis suggest it could be a viable option for some patients, provided its use is carefully monitored and adapted to individual needs. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis is a chronic disease of the central nervous system characterized by inflammation, neurodegeneration, and failure of the central nervous system's repair mechanisms. The role of infectious agents against the background of genetic predisposition is currently considered a possible pathogenesis factor of this disease. Case presentation: We report the case of a 52-year-old white (Russian) female musician with 15-year history of relapsing–remitting multiple sclerosis who had repeatedly received conventional therapy without much benefit. In 2017, she was admitted to the outpatient department of the Institute of Virology, where she was treated with erythromycin and acyclovir (tablet forms), which were not applied in the traditional way but through the "device for transfer of information from the drug to the human body." The received effect led to suppression of the disease activity, a significant reduction in the symptoms of the disease, prevention of further increase in neurological manifestations of the disease, and improvement in the dynamics of the manifestation of the disease according to brain magnetic resonance imaging. Conclusion: The described case report is innovative and presents for the first time the results of a noninvasive approach to the treatment of a patient with multiple sclerosis in whom information about various medications was introduced into different parts of the body, including the brain. The results obtained may indicate a possible role of infectious agents in the genesis of multiple sclerosis. It indicates a potential impact on them by using a "device for transfer of information from the drug to the human body." The study was conducted in accordance with the principles of the Declaration of Helsinki. It was approved by the Institutional Review Board of the Research Institute of Virology of Uzbekistan (no. 12/8–1500, 1/3/2017). [ABSTRACT FROM AUTHOR]

Neuroinflammation is a significant contributor to the pathology of glaucoma. Targeting key-mediators in this process is a realistic option to slow disease progression. Galectin-3 is a β-galactoside binding lectin that has been associated with inflammation in both systemic and central nervous system diseases. Elevated Galectin-3 has recently been detected in multiple animal models of glaucoma and inhibiting Galectin-3 using an intravitreal injection of TD139 (a Galectin-3 small molecule inhibitor) is neuroprotective. We queried whether this neuroprotective effect was translatable to another animal model and species. TD139 was intravitreally injected, in a rat ocular hypertensive model of glaucoma, 3 days after the induction of ocular hypertension (at peak intraocular pressure). Retinal ganglion cell survival and glial morphological markers were quantified. The degeneration of retinal ganglion cells was prevented by TD139 injection, but gross glial markers remained unaffected. These data confirm that the intravitreal injection of TD139 is neuroprotective in a rat ocular hypertensive model of glaucoma, while suggesting that the inhibition of Galectin-3 is not sufficient to alter the gross inflammatory outcome. [ABSTRACT FROM AUTHOR]

Despite clinical data stretching over millennia, the neurobiological basis of the effectiveness of acupuncture in treating diseases of the central nervous system has remained elusive. Here, using an established model of acupuncture treatment in Parkinson's disease (PD) model mice, we show that peripheral acupuncture stimulation activates hypothalamic melanin‐concentrating hormone (MCH) neurons via nerve conduction. We further identify two separate neural pathways originating from anatomically and electrophysiologically distinct MCH neuronal subpopulations, projecting to the substantia nigra and hippocampus, respectively. Through chemogenetic manipulation specifically targeting these MCH projections, their respective roles in mediating the acupuncture‐induced motor recovery and memory improvements following PD onset are demonstrated, as well as the underlying mechanisms mediating recovery from dopaminergic neurodegeneration, reactive gliosis, and impaired hippocampal synaptic plasticity. Collectively, these MCH neurons constitute not only a circuit‐based explanation for the therapeutic effectiveness of traditional acupuncture, but also a potential cellular target for treating both motor and non‐motor PD symptoms. [ABSTRACT FROM AUTHOR]