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Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Metabolic syndrome impacts the central nervous system to cause neurodegenerative and neurological diseases. If the blood-brain barrier is broken down for any reason, there can be release of cytokines and inflammatory mediators, diapedesis across the endothelium, and destruction of the cells of the blood-brain barrier. Inflammation is closely linked with neuropathologies. There can be various types of CNS dysfunction, memory deficits, visuospatial deficits, executive function deficits, slowed processing speed, and reduced intellectual function. Autopsy studies show that diabetic patients with dementia have more microvascular lesions than diabetic patients without dementia. The lesions are not the primary reason for cognitive deficits, but they are related to widespread vascular dysfunction, while contributing to cerebral dysfunction. Treatment of metabolic syndrome and insulin resistance may improve memory as well as slow down age-related declines in cognition.
Hybrid Nanosystems
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Pablo Vicente Torres-Ortega, Laura Saludas, Jon Eneko Idoyaga, Carlos Rodríguez-Nogales, Elisa Garbayo, María José Blanco-Prieto
Treatments aiming to stop the progression of brain-related disorders are often nonspecific and focused on the resolution of short-term symptoms. The delivery of therapeutics across the blood-brain barrier represents another limiting challenge in the treatment of these diseases. Hybrid nanosystems (HNs), defined as the combination of inorganic and organic compounds in a single nanocarrier, offer a new generation of multifunctional nanoparticles (NPs) with superior biological and structural properties. HNs could contribute not only to the design of more effective therapies for brain disorders but also to the development of new theranostic strategies which combine therapeutic and diagnostic functions in a single system.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The blood–brain barrier is an important structure that prevents harmful substances in the bloodstream from entering brain tissue. The blood–brain barrier has two main components: a thick capillary basement membrane and tight junctions between the endothelial cells of the capillaries. Capillaries in other parts of the body have gaps between the endothelial cells that allow substances to diffuse across the capillary wall and enter the interstitial space. Tight junctions in brain capillaries and the thick basement membrane prevents diffusion, the brain relies on astrocytes to control the movement of substances from blood to brain. The foot processes of astrocytes press tightly against the endothelial wall of brain capillaries, secreting chemicals that control the permeability of the capillary. This structure is semipermeable to some water-soluble substances like glucose, but not others, for example, proteins and antibiotics. However, it is permeable to fat-soluble substances, e.g., oxygen, carbon dioxide, alcohol and most anaesthetic agents (Tortora and Derrickson 2017). The blood–brain barrier is affected by trauma and inflammation and can malfunction.
Effectiveness of ALK inhibitors in treatment of CNS metastases in NSCLC patients
Published in Annals of Medicine, 2023
Michał Gil, Magdalena Knetki-Wróblewska, Przemysław Niziński, Maciej Strzemski, Paweł Krawczyk
The blood-brain barrier consists of 3 components: endothelial cells of capillaries, astrocytes and pericytes. Endothelial cells are specialized epithelium lining the lumen of a capillary vessel in the brain [6]. This epithelium has unique features, i.e. no fenestration, a large number of mitochondria due to high cellular metabolism, low pinocytic activity, the presence of tight junctions and selective permeability to molecules [6,7]. Astrocytes mediate between capillaries and neurons in the brain. Their parts additionally protect the brain against substances that have passed through endothelial cells. The final component are pericytes, small cells that surround the endothelial cells of the epithelium. They control immunological processes, have the ability to phagocytose and control the diameter of capillaries [6,8].
Combination of tetrandrine and 3-n-butylphthalide protects against cerebral ischemia-reperfusion injury via ATF2/TLR4 pathway
Published in Immunopharmacology and Immunotoxicology, 2021
Cunfang Li, Aijun Chai, Yongchao Gao, Xuan Qi, Xuguang Zheng
TTD is bisbenzyl isoquinoline alkaloid, which has significant anti-inflammatory, anti-cancer, and cytoprotective effects. TTD is clinically applicable in treating arrhythmia, silicosis, inflammation, and obliterative cardiovascular disease [14–17]. Previous studies reveal that TTD reduces I/R damage of the liver, heart, and cerebrum [21–23]. In this study, the combination treatment of TTD decreased infarct volume and alleviated cerebral I/R injury in vivo and in vitro via suppressing the apoptosis and inflammatory response. However, the existing blood–brain barrier may reduce clinical results. Previous studies reveal that the combination of TTD and vincristine exerts more potent in suppressing the progression of brain glioma [24]. Itraconazole or voriconazole alone and in combination with tetrandrine are more efficiently in protecting brain tissues from aspergillus fumigatus. Recent studies have reported that NBP has efficacy in treat cerebral infarction, including improving microcirculation, and inhibiting thrombus formation, oxidative stress damage and the apoptosis of neuronal cells [25–27]. NBP upregulates VEGF expression and HIF-1α and promotes angiogenesis [28]. Meanwhile, NBP treatment reduces cerebral damage caused by cerebral I/R injury [27,29]. In this study, TTD + NBP more efficient in suppressing cerebral I/R injury. Therefore, the combination of TTD and NBP may be a efficient therapy for cerebral I/R injury. However, the underlying molecular mechanism is still unclear.
Targeting neuroprotective functions of astrocytes in neuroimmune diseases
Published in Expert Opinion on Therapeutic Targets, 2021
The heterogeneity of astrocytes is not limited to their immune responses. It is important to point out that astrocytes contribute to diverse physiological processes by modulating concentrations of ions and neurotransmitters in the extracellular space, secreting antioxidant molecules, and participating in synapse formation and elimination. They interact closely with neurons through metabolic coupling involving the astrocyte-neuron lactate shuttle, and also participate in the glutamate–glutamine cycle supporting glutamatergic and GABAergic neurotransmission. In addition, astrocytes are part of the neurovascular unit that regulates cerebral blood flow and maintains the integrity of the blood-brain barrier. Astrocytes adapt to different CNS environments, leading to significant spatial heterogeneity of the astrocyte population within a healthy brain. Furthermore, during brain development and aging, varying CNS environments result in temporal changes in astrocyte morphology and most, if not all, of their diverse functions listed above (for recent comprehensive reviews of astrocyte functions and heterogeneity see [3–7]). Due to their active contribution to a broad range of nervous system pathologies, astrocytes have been proposed as targets for therapeutic interventions (reviewed in [4,7–9]). Although most homeostatic functions of astrocytes become dysregulated in pathological states, this article only considers modulation of astrocyte neuroimmune functions as a therapeutic strategy.