Interplay between the Glymphatic System and the Endocannabinoid System: Implications for Brain Health and Disease

Osuna-Ramos, Juan F.; Camberos-Barraza, Josué; Torres-Mondragón, Laura E.; Rábago-Monzón, Ángel R.; Camacho-Zamora, Alejandro; Valdez-Flores, Marco A.; Angulo-Rojo, Carla E.; Guadrón-Llanos, Alma M.; Picos-Cárdenas, Verónica J.; Calderón-Zamora, Loranda; Magaña-Gómez, Javier A.; Norzagaray-Valenzuela, Claudia D.; Cárdenas-Torres, Feliznando I.; De la Herrán-Arita, Alberto K.

doi:10.3390/ijms242417458

Cited by 3 publications

(3 citation statements)

References 99 publications

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“…In addition, astrocytes actively participate in clearing excess synaptic glutamate through transporters. This uptake mechanism helps prevent spillover and maintains the balance of neurotransmitters in the synaptic cleft [ 59 , 60 , 61 , 62 ].…”

Section: Glial Cells: the Orchestrators Of Neural Symphonymentioning

confidence: 99%

“…Importantly, astrocytes contribute to the maintenance of the blood–brain barrier (BBB) and regulate the influx of immune cells into the CNS ( Figure 1 and Figure 2 ). In the context of neuroinflammation, astrocytes undergo astrogliosis, a process characterized by hypertrophy and increased expression of GFAP [ 59 , 73 , 74 ].…”

Section: Glial Cells: the Orchestrators Of Neural Symphonymentioning

confidence: 99%

“…2024, 25, x FOR PEER REVIEW 8 of 30through transporters. This uptake mechanism helps prevent spillover and maintains the balance of neurotransmitters in the synaptic cleft[59][60][61][62].…”

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confidence: 99%

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Sleep, Glial Function, and the Endocannabinoid System: Implications for Neuroinflammation and Sleep Disorders

Camberos-Barraza,

Camacho-Zamora,

Bátiz-Beltrán

et al. 2024

IJMS

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The relationship between sleep, glial cells, and the endocannabinoid system represents a multifaceted regulatory network with profound implications for neuroinflammation and cognitive function. The molecular underpinnings of sleep modulation by the endocannabinoid system and its influence on glial cell activity are discussed, shedding light on the reciprocal relationships that govern these processes. Emphasis is placed on understanding the role of glial cells in mediating neuroinflammatory responses and their modulation by sleep patterns. Additionally, this review examines how the endocannabinoid system interfaces with glia-immune signaling to regulate inflammatory cascades within the central nervous system. Notably, the cognitive consequences of disrupted sleep, neuroinflammation, and glial dysfunction are addressed, encompassing implications for neurodegenerative disorders, mood disturbances, and cognitive decline. Insights into the bidirectional modulation of cognitive function by the endocannabinoid system in the context of sleep and glial activity are explored, providing a comprehensive perspective on the potential mechanisms underlying cognitive impairments associated with sleep disturbances. Furthermore, this review examines potential therapeutic avenues targeting the endocannabinoid system to mitigate neuroinflammation, restore glial homeostasis, and normalize sleep patterns. The identification of novel therapeutic targets within this intricate regulatory network holds promise for addressing conditions characterized by disrupted sleep, neuroinflammation, and cognitive dysfunction. This work aims to examine the complexities of neural regulation and identify potential avenues for therapeutic intervention.

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Section: Glial Cells: the Orchestrators Of Neural Symphonymentioning

confidence: 99%

Section: Glial Cells: the Orchestrators Of Neural Symphonymentioning

confidence: 99%

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Sleep, Glial Function, and the Endocannabinoid System: Implications for Neuroinflammation and Sleep Disorders

Camberos-Barraza,

Camacho-Zamora,

Bátiz-Beltrán

et al. 2024

IJMS

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Accumulation of Cerebrospinal Fluid, Ventricular Enlargement, and Cerebral Folate Metabolic Errors Unify a Diverse Group of Neuropsychiatric Conditions Affecting Adult Neocortical Functions

Ikeda,

Capel,

Doddaballapur

et al. 2024

IJMS

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Cerebrospinal fluid (CSF) is a fluid critical to brain development, function, and health. It is actively secreted by the choroid plexus, and it emanates from brain tissue due to osmolar exchange and the constant contribution of brain metabolism and astroglial fluid output to interstitial fluid into the ventricles of the brain. CSF acts as a growth medium for the developing cerebral cortex and a source of nutrients and signalling throughout life. Together with perivascular glymphatic and interstitial fluid movement through the brain and into CSF, it also acts to remove toxins and maintain metabolic balance. In this study, we focused on cerebral folate status, measuring CSF concentrations of folate receptor alpha (FOLR1); aldehyde dehydrogenase 1L1, also known as 10-formyl tetrahydrofolate dehydrogenase (ALDH1L1 and FDH); and total folate. These demonstrate the transport of folate from blood across the blood–CSF barrier and into CSF (FOLR1 + folate), and the transport of folate through the primary FDH pathway from CSF into brain FDH + ve astrocytes. Based on our hypothesis that CSF flow, drainage issues, or osmotic forces, resulting in fluid accumulation, would have an associated cerebral folate imbalance, we investigated folate status in CSF from neurological conditions that have a severity association with enlarged ventricles. We found that all the conditions we examined had a folate imbalance, but these folate imbalances were not all the same. Given that folate is essential for key cellular processes, including DNA/RNA synthesis, methylation, nitric oxide, and neurotransmitter synthesis, we conclude that ageing or some form of trauma in life can lead to CSF accumulation and ventricular enlargement and result in a specific folate imbalance/deficiency associated with the specific neurological condition. We believe that addressing cerebral folate imbalance may therefore alleviate many of the underlying deficits and symptoms in these conditions.

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The Gut Microbiome-Neuroglia Axis: Implications for Brain Health, Inflammation, and Disease

Camberos-Barraza,

Guadrón-Llanos,

De la Herrán-Arita

2024

Neuroglia

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The human central nervous system is convolutedly connected to the gut microbiome, a diverse community of microorganisms residing in the gastrointestinal tract. Recent research has highlighted the bidirectional communication between the gut microbiome and neuroglial cells, which include astrocytes, microglia, oligodendrocytes, and ependymal cells. These neuroglial cells are essential for maintaining CNS homeostasis, supporting neuronal function, and responding to pathological conditions. This review examines the interactions between the gut microbiome and neuroglia, emphasizing their critical roles in brain health and the development of neurological disorders. Dysbiosis, or imbalance in the gut microbiome, has been associated with various neurological and psychiatric conditions, such as autism spectrum disorder, anxiety, depression, and neurodegenerative diseases like Alzheimer’s and Parkinson’s. The microbiome influences brain function through microbial metabolites, immune modulation, and neuroinflammatory responses. Understanding these interactions paves the way for new therapeutic targets and strategies for preventing and treating CNS disorders. This scoping review aims to highlight the mechanisms of the microbiome-neuroglia axis in maintaining brain health and its potential as a therapeutic target.

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Interplay between the Glymphatic System and the Endocannabinoid System: Implications for Brain Health and Disease

Cited by 3 publications

References 99 publications

Sleep, Glial Function, and the Endocannabinoid System: Implications for Neuroinflammation and Sleep Disorders

Sleep, Glial Function, and the Endocannabinoid System: Implications for Neuroinflammation and Sleep Disorders

Accumulation of Cerebrospinal Fluid, Ventricular Enlargement, and Cerebral Folate Metabolic Errors Unify a Diverse Group of Neuropsychiatric Conditions Affecting Adult Neocortical Functions

The Gut Microbiome-Neuroglia Axis: Implications for Brain Health, Inflammation, and Disease

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