BACKGROUND: Since discovering the glymphatic system, there has been a looming interest in exploring its relationship with psychiatric disorders. Recently, increasing evidence suggests an involvement of the glymphatic system in the pathophysiology of psychiatric disorders. However, clear data are still lacking. In this context, this rapid comprehensive PRISMA-ScR (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews) scoping review aims to identify and analyze current evidence about the relation between the glymphatic system and psychiatric disorders.
METHODS: We conducted a comprehensive review of the literature and then proceeded to discuss the findings narratively. Tables were then constructed and articles were sorted according to authors, year, title, location of study, sample size, psychiatric disorder, the aim of the study, principal findings, implications.
RESULTS: Twenty papers were identified as eligible, among which 2 articles on Schizophrenia, 1 on Autism Spectrum Disorders, 2 on Depression, 1 on Depression and Trauma-related Disorders, 1 on Depression and Anxiety, 2 on Anxiety and Sleep Disorders, 8 on Sleep Disorders, 2 on Alcohol use disorder and 1 on Cocaine Use Disorder.
CONCLUSIONS: This review suggests a correlation between the glymphatic system and several psychiatric disorders: Schizophrenia, Depression, Anxiety Disorders, Sleep Disorders, Alcohol Use Disorder, Cocaine Use Disorder, Trauma-Related Disorders, and Autism Spectrum Disorders. Impairment of the glymphatic system could play a role in Trauma-Related Disorders, Alcohol Use Disorders, Cocaine Use Disorders, Sleep Disorders, Depression, and Autism Spectrum Disorders. It is important to implement research on this topic and adopt standardized markers and radio diagnostic tools.

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Several risk factors contribute to the development of Alzheimer\'s disease (AD), including genetics, metabolic health, cardiovascular history, and diet. It has been observed that women appear to face a higher risk of developing AD. Among the various hypotheses surrounding the gender disparity in AD, one pertains to the potential neuroprotective properties of estrogen. Compared to men, women are believed to be more susceptible to neuropathology due to the significant decline in circulating estrogen levels following menopause. Studies have shown, however, that estrogen replacement therapies in post-menopausal women do not consistently reduce the risk of AD. While menopause and estrogen levels are potential factors in the elevated incidence rates of AD among women, this review highlights the possible roles estrogen has in other pathways that may also contribute to the sex disparity observed in AD such as olfaction, sleep, and glymphatic functionality.

Currently, there is unavailability of disease-modifying medication for Alzheimer\'s disease (AD), a debilitating neurological disorder. The pathogenesis of AD appears to be complex and could be influenced by the glymphatic system present in the central nervous system (CNS). Amyloid-beta (Aβ) and other metabolic wastes are eliminated from the brain interstitium by the glymphatic system, which encompasses perivascular channels and astroglial cells. Dysfunction of the glymphatic system, which could occur due to decreased aquaporin 4 (AQP4) expression, aging-related alterations in the human brain, and sleep disruptions, may contribute to the pathogenesis of AD and also accelerate the development of AD by causing a buildup of harmful proteins like Aβ. Promising approaches have been examined for reducing AD pathology, including non-pharmacological therapies that target glymphatic function, like exercise and sleep regulation. In addition, preclinical research has also demonstrated the therapeutic potential of pharmaceutical approaches targeted at augmenting AQP4-mediated glymphatic flow. To identify the precise processes driving glymphatic dysfunction in AD and to find new treatment targets, more research is required. Innovative diagnostic and treatment approaches for AD could be made possible by techniques such as dynamic contrast-enhanced MRI, which promises to evaluate glymphatic function in neurodegenerative diseases. Treatment options for AD and other neurodegenerative diseases may be improved by comprehending and utilizing the glymphatic system\'s function in preserving brain homeostasis and targeting the mechanisms involved in glymphatic functioning. This review intends to enhance the understanding of the complex link between AD and the glymphatic system and focuses on the function of AQP4 channels in promoting waste clearance and fluid exchange.

OBJECTIVE: The glioblastomas, aggressive brain tumors with a poor prognosis, have drawn interest in their interaction with the glymphatic system-an emerging brain drainage network. This review explores the relationship between glioblastomas and the glymphatic system, aiming to elucidate their impact on disease progression. The aim of the study was to address the alterations in the glymphatic system in the presence of glioblastoma, and their implications for disease pathogenesis and prognosis.
METHODS: Following PRISMA guidelines, we conducted a systematic literature review, identifying studies on the glymphatic system in glioblastomas. Four high-quality studies were selected based on stringent criteria. Data extraction involved categorizing key findings, and thematic analysis uncovered recurring patterns in glymphatic alterations associated with glioblastomas.
RESULTS: Out of 356 studies, four meeting the high-quality criteria were included. These studies revealed modifications in lymphatic outflow, factors contributing to glymphatic dysfunction, impediments to cerebrospinal fluid drainage, and emerging roles in glioma management. The findings allow a comprehensive understanding of alterations within the glymphatic system in the presence of glioblastoma.
CONCLUSIONS: The glymphatic system in glioblastomas exhibits changes, including diminished lymphatic outflow, disruptions and obstacles to fluid drainage, which represent new dimensions in glioma management. These alterations affect drug delivery, immunotherapy, and imaging interpretation. Future research should prioritize elucidating molecular mechanisms, developing therapeutic strategies, optimizing drug delivery, exploring immunotherapy, and translating findings into clinical practice.

BACKGROUND: Idiopathic intracranial hypertension (IIH) remains a poorly understood condition with no standardized treatment. Treatment is therefore generally individualized. Recent isolated reports have begun to describe the use of third ventriculostomy (open or closed) for the treatment of IIH. This review aims to communicate the current evidence for the use of third ventriculostomy in IIH.
METHODS: A systemic review, using PubMed, was performed of studies describing the use of third ventriculostomy, either open or closed, for the treatment of idiopathic intracranial hypertension.
RESULTS: Only 3 studies for a total of 3 patients were found in which a third ventriculostomy was performed for the treatment of IIH.
CONCLUSIONS: Despite very plausible proposed mechanisms of action, there is currently a paucity of both studies and, therefore, evidence for the use of either endoscopic or open third ventriculostomy for the treatment of IIH. The studies done to date do strongly suggest that further consideration is warranted.

BACKGROUND: This meta-analysis aimed to explore the association of perivascular spaces (PVS) burden with the risks of future stroke events and mortality in patients with ischemic stroke and transient ischemic attack (TIA).
METHODS: We systematically searched PubMed, Embase, and Cochrane database from inception to December 31, 2023. We included eligible studies that reported adjusted estimated effects for future intracranial hemorrhage (ICH), ischemic stroke, and mortality with baseline PVS burden in patients with ischemic stroke and TIA. Data were pooled using an inverse-variance method for the fixed effects (FE) model and a restricted maximum likelihood method for the random effects (RE) model.
RESULTS: Thirteen observational studies (5 prospective, 8 retrospective) were included, comprising 20,256 patients. Compared to 0-10 PVS at basal ganglia (BG-PVS), a higher burden (>10) of BG-PVS was significantly associated with an increased risk of future ICH (adjusted hazards ratio [aHR] 2.79, 95% confidence interval [CI]: 1.16-6.73, RE model; aHR 2.14, 95% CI: 1.34-3.41, FE model; I2 = 64%, n = 17,084 from four studies) followed up for at least 1 year. There was no significant association between >10 BG-PVS and ICH within 7 days after reperfusion therapy (adjusted odds ratio [aOR] 1.69, 95% CI: 0.74-3.88, RE model; aOR 1.43, 95% CI: 0.89-2.88, FE model; I2 = 67%, n = 1,176 from four studies). We did not detect a significant association of recurrent ischemic stroke, mortality, or disability with BG-PVS burden. Neither >10 PVS at centrum semiovale (CSO-PVS) nor increasing CSO-PVS burden was significantly associated with the risk of future intracranial hemorrhage or ischemic stroke recurrence.
CONCLUSIONS: Current evidence suggests that a higher BG-PVS burden may be associated with an increased risk of future ICH in patients with ischemic stroke and TIA.

The existence of a previously unrecognized subarachnoid lymphatic-like membrane (SLYM) was reported in a recent study. SLYM is described as an intermediate leptomeningeal layer between the arachnoid and pia mater in mouse and human brains, which divides the subarachnoid space (SAS) into two functional compartments. Being a macroscopic structure, having missed detection in previous studies is surprising. We systematically reviewed the published reports in animals and humans to explore whether prior descriptions of this meningeal layer were reported in some way. A comprehensive search was conducted in PubMed/Medline, EMBASE, Google Scholar, Science Direct, and Web of Science databases using combinations of MeSH terms and keywords with Boolean operators from inception until 31 December 2023. We found at least eight studies that provided structural evidence of an intermediate leptomeningeal layer in the brain or spinal cord. However, unequivocal descriptions for this layer all along the central nervous system were scarce. Obscure names like the epipial, intermediate meningeal, outer pial layers, or intermediate lamella were used to describe it. Its microscopic/ultrastructural details closely resemble the recently reported SLYM. We further examined the counterarguments in current literature that are skeptical of the existence of this layer. The potential physiological and clinical implications of this new meningeal layer are significant, underscoring the urgent need for further exploration of its structural and functional details.

Research into magnetic resonance imaging (MRI)-visible perivascular spaces (PVS) has recently increased, as results from studies in different diseases and populations are cementing their association with sleep, disease phenotypes, and overall health indicators. With the establishment of worldwide consortia and the availability of large databases, computational methods that allow to automatically process all this wealth of information are becoming increasingly relevant. Several computational approaches have been proposed to assess PVS from MRI, and efforts have been made to summarise and appraise the most widely applied ones. We systematically reviewed and meta-analysed all publications available up to September 2023 describing the development, improvement, or application of computational PVS quantification methods from MRI. We analysed 67 approaches and 60 applications of their implementation, from 112 publications. The two most widely applied were the use of a morphological filter to enhance PVS-like structures, with Frangi being the choice preferred by most, and the use of a U-Net configuration with or without residual connections. Older adults or population studies comprising adults from 18 years old onwards were, overall, more frequent than studies using clinical samples. PVS were mainly assessed from T2-weighted MRI acquired in 1.5T and/or 3T scanners, although combinations using it with T1-weighted and FLAIR images were also abundant. Common associations researched included age, sex, hypertension, diabetes, white matter hyperintensities, sleep and cognition, with occupation-related, ethnicity, and genetic/hereditable traits being also explored. Despite promising improvements to overcome barriers such as noise and differentiation from other confounds, a need for joined efforts for a wider testing and increasing availability of the most promising methods is now paramount.

Cortical spreading depression (CSD) is a slow wave of cortical depolarization closely associated with migraines with an aura. Previously, it was thought that CSD depolarization was mainly driven by neurons, with characteristic changes in neuronal swelling and increased extracellular potassium (K+) and glutamate. However, the role of astrocytes, a member of the neurovascular unit, in migraine with CSD has recently received increasing attention. In the early stages of CSD, astrocytes provide neurons with energy support and clear K+ and glutamate from synaptic gaps. However, in the late stages of CSD, astrocytes release large amounts of lactic acid to exacerbate hypoxia when the energy demand exceeds the astrocytes\' compensatory capacity. Astrocyte endfoot swelling is a characteristic of CSD, and neurons are not similarly altered. It is primarily due to K+ influx and abnormally active calcium (Ca2+) signaling. Aquaporin 4 (AQP-4) only mediates K+ influx and has little role as an aquaporin. Astrocytes endfoot swelling causes perivascular space closure, slowing the glymphatic system flow and exacerbating neuroinflammation, leading to persistent CSD. Astrocytes are double-edged swords in migraine with CSD and may be potential targets for CSD interventions.