China
Africa
Explore chapters and articles related to this topic
Exploration of Nanonutraceuticals in Neurodegenerative Diseases
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Swati Pund, Amita Joshi, Vandana Patravale
Nature has bestowed multiple layers of barriers to protect brain from pathogens, toxins, and circulating blood cells. Major barriers include: blood cerebrospinal fluid barrier (BCSFB), the blood–brain barrier (BBB), the ependymal barrier, the blood retinal barrier, and the blood spinal cord barrier (Sun et al., 2017). BBB restrains the movement of molecules to brain parenchyma, while BCSFB restricts free diffusion of molecules from circulating blood to the cerebrospinal fluid (CSF) and ependymal barrier controls diffusion of molecules/ions from the CSF to the brain. Consequently, these three barriers collectively restrict the movement of drugs/molecules from blood and CSF to the brain.
The Microbiome—Its Role in Neuroinflammation
Published in David Perlmutter, The Microbiome and the Brain, 2019
Maria R. Fiorentino, Alessio Fasano
Defects in gut barrier function, often associated with defects in blood–brain barrier integrity, have been reported in many inflammatory neurological diseases. Severance et al. and Melkersson et al. suggested the role of an impaired gut and blood–brain barrier in schizophrenia, respectively [115,116]. In ALS patients, high levels of LPS have been detected in the serum, consistent with increased gut permeability [14,117] and both the blood–brain barrier and the blood–spinal-cord–barrier (BSCB) exhibited reduced expression of intercellular junctional proteins, a sign of reduced barrier integrity [118–120]. The blood–brain barrier defects correlated with infiltration of macrophages and mast cells into the brain and spinal cord and exacerbated brain inflammation [118,121]. Likewise, disruption of the blood–brain barrier has been reported in Parkinson’s Disease [14,122], MS [123,124], Alzheimer’s Disease [125,126], and in autism spectrum disorders [127].
Biomechanics and Tissue Injuries
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
Strain is the displacement of one point relative to another caused by stress (force). Different forces achieve a given type of deformation. The forms of strain are tensile strain, shear strain, compressive strain, and over-pressure (Hunt et al., 2004). Strain has been described as the “proximate cause” of tissue injury (Gennarelli & Graham, 1998). Slow application of strain is better tolerated than rapid strain, which leads to the brain becoming brittle and breaking (Teasdale & Mathew, 1996). In the spinal cord, tissue strain contributes to microvasculature pathology. Extravasation and physiological injury markers were more highly correlated to the rate of spinal cord compression than to the depth of compression. The microvasculature sensitivity to injury was affected by vessel caliber and the cells comprising the blood spinal cord barrier (Maikos & Schreiber, 2007).
Pharmacological management of secondary spinal cord injury
Published in Expert Opinion on Pharmacotherapy, 2021
Alice Baroncini, Nicola Maffulli, Jörg Eschweiler, Markus Tingart, Filippo Migliorini
Secondary SCI is characterized by a cascade of events which result in neural damage and impairment of the regeneration capabilities of the central nervous system (CNS), thus concurring to the amplification of spinal cord damage after the acute trauma. The mechanical damage induced by the trauma causes disruption in the blood – spinal cord barrier and an acute hemorrhage, which in turn leads to local ischemia [1,2]. The damage to the blood – spinal cord barrier causes a sudden increment of inflammatory cells and cytokines, which produce a pro-inflammatory and pro-apoptotic environment [6]. Furthermore, apoptosis results in the release of neurotransmitters, such as glutamate, and other toxic compounds such as reactive oxygen species and potassium ions, which in turn cause excitotoxic cell death and ischemia [2,7,8].
Effects of combined treatment of minocycline and methylprednisolone on the expression of tumor necrosis factor alpha and interleukine-6 in experimental spinal cord injury: a light and electron microscopic study
Published in Ultrastructural Pathology, 2020
Leman Sencar, Derviş Mansuri Yilmaz, Abdullah Tuli, Sait Polat
SCI consists of two steps which include primary and secondary damage mechanisms.9–11 Primary injury causes physical disruption of neurons and glial cells and also affects blood vessels. In turn, secondary injury initiates destructive cellular and molecular mechanisms and causes an enlargement of the initial area of trauma.12 Secondary injury leads to ionic dysregulation, edema, glutamate excitotoxicity, lipid peroxidation, inflammation, free radical-induced cell death causing demyelination and axonal degeneration at the lesion area.11,12 The blood-spinal cord barrier is also disrupted and the neutrophils migrate lesion area.11 Expressions of proinflammatory cytokines such as IL-1, IL-6 and TNF-α significantly increase13 and these cytokines induce activation, proliferation and migration of astrocytes and microglia into the lesion site. This inflammation cascade causes apoptosis of neurons and oligodendrocytes, glial scar formation and loss of neuronal functions.11
Therapeutic approaches of trophic factors in animal models and in patients with spinal cord injury
Published in Growth Factors, 2020
María del Carmen Díaz-Galindo, Denisse Calderón-Vallejo, Carlos Olvera-Sandoval, J. Luis Quintanar
Blood spinal cord barrier (BSCB) is formed by the spinal capillaries and it is responsible for regulating the molecules that can enter the tissue, protecting it from the neurotoxins in the systemic circulation . In fact, one of the first events after SCI is the alteration of the BSCB which is very detrimental for tissue recovery. A recent study revealed that 48 h after SCI, the permeability of BSCB increased significantly in the untreated mice compared to mice treated with intraperitoneal melatonin. In addition, it was found that melatonin can improve and restore the integrity of BSCB by regulating tight junction proteins (Wu et al. 2014). In another study, Jing et al. (2014) investigated the effect of melatonin on microvessels after SCI. In this study, they found that melatonin improved blood loss, possibly due to positive regulation of angiopoietin-1 in the pericytes. Angiopoietin-1 can attenuate inflammation and apoptosis and protect microvessels by increasing the coverage of pericytes. Therefore, the neuroprotective effects of melatonin can also be derived from its ability to promote repair of BSCB.