Von Economo’s encephalitis
Avindra Nath, Joseph R. Berger in Clinical Neurovirology, 2020
The gross pathology of chronic encephalitis lethargica is characterized by modest findings of atrophy either focal or generalized. Microscopic pathology shows a coincidence of old and recent inflammation suggesting persistence of virus with the principal changes in corpus striatum, thalamus, hypothalamus, posterior wall of III ventricle, and substantial nigra. Microscopic findings included neuronophagia, astrogliosis, hemosiderin staining perivascularly, and pigment degeneration in substantia nigra and locus ceruleus. The astrogliosis may be overwhelming involving widespread areas of the brain and occur in the absence of significant other pathologies [80]. Neurofibrillary tangles have been reported in the substantia nigra, locus ceruleus, and raphe nuclei.
Mapping the Injured Brain
Yu Chen, Babak Kateb in Neurophotonics and Brain Mapping, 2017
Much of what has been learned regarding structural alterations following trauma have come from experimental models of TBI in rodent studies. Pathophysiology results from these studies suggest initially the axons swell up in response to injury due to the loss of integrity of ionic transport channels located on the axon. While some swelling resolves, extensive unresolved swelling often results in broken axons with terminal axon bulbs. Accompanying damage may also involve loss of the integrity of the myelin sheath known as demyelination. This demyelination often progresses over time which results in reduced axonal integrity in the chronic stages of injury. In addition to direct axonal damage, the injury also results in a transient increase in numbers of astrocytes and microglial cells (Chen et al., 2003). The atypical increase in the number of astrocytes in a region due to the death of nearby neurons is referred to as astrogliosis. Reactive astrogliosis are believed to play essential roles in preserving healthy neurons and minimizing inflammation within the surrounding brain tissue (Myer et al., 2006).
Understanding Brain Delivery
Carla Vitorino, Andreia Jorge, Alberto Pais in Nanoparticles for Brain Drug Delivery, 2021
Before examining BBB alterations underlying ageing, it is important to define physiological or normal ageing as a deterioration of functions without cognitive decline or dementia [112]. Briefly, some of the age-related differences observed in humans encompass a decrease of capillary density and surface area; an increase in capillary wall thickness, accompanied by a decrease in the number of BECs and respective mitochondria; a reduced expression of tight junctions and P-gp; accumulation of extracellular matrix components and an increase of the thickness of the basal lamina; production of neurotoxic pro-inflammatory mediators by microglia; pericyte degeneration; and deterioration of neuronal plasticity with increased apoptosis [112, 113]. Reports on astrocytic modifications during ageing are varied. Some authors affirm that astrogliosis takes place with ageing, that is, an augmented proliferation and reactivity of astrocytes characterised by a higher expression of glial fibrillary acidic protein as a response to an inflammatory and oxidative state [114]. In parallel, other authors describe a loss of astrocytic endfeet contact with BECs in aged mice caused by a depletion of AQP4 [115] as well as an accumulation of iron in astrocytes which can generate free radicals and harm cells [116]. Although there are controversial data, ageing has been associated with a higher permeability of the human BBB, according to a meta-analysis of 31 studies with 1953 individuals [117]. Indeed, albumin extravasation has been observed, together with increased brain leakage. It is believed that this leakiness may play a role in the development of age-related dementias [118].
Novel nano-carriers with N-formylmethionyl-leucyl-phenylalanine-modified liposomes improve effects of C16-angiopoietin 1 in acute animal model of multiple sclerosis
Published in Drug Delivery, 2023
Xiao-Xiao Fu, Han Qu, Jing Wang, Hua-Ying Cai, Hong Jiang, Hao-Hao Chen, Shu Han
Following inflammation in the CNS, astrocytes can be activated through hypertrophy and/or proliferation, resulting in reactive astrogliosis. Generally, activated astrocytes prefer to accumulate within and at the margins of demyelinated regions, produce proinflammatory cytokines and chemokines, present antigens to T-lymphocytes, and participate in the inflammatory response during the pathological development of MS and EAE (Gaillard et al., 2012). As a transcription factor mediating CNS inflammation, NF-κB is positively involved in the transcriptional regulation of multiple genes, such as those encoding pro-inflammatory cytokines (like IL-1β) and proinflammatory enzymes (like COX-2), which are critical regulators of the inflammatory process and promote chronic inflammation (Jiang et al., 2014). Chronic inflammation induced by the reaction of astrocytes could produce glial scars at the site of lesions, which may further suppress the regeneration of axons. Data presented herein revealed that the C + A compounds could decrease the GFAP + reactive astroglia, and suppress the production of ROS, NF-κB, IL-1β, and COX-2 in serum or tissue, while upregulating anti-inflammatory IL-10 in serum. Importantly, reduced inflammatory cell infiltration and activation may be related to a more rapid recovery of locomotor function.
The therapeutic effect of nano-zinc on the optic nerve of offspring rats and their mothers treated with lipopolysaccharides
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Eman Mohammed Emara, Hassan Ih El-Sayyad, Amr M Mowafy, Heba a El-Ghaweet
The optic nerve (cranial nerve II) is a central nervous system (CNS) tract that passes through the optic canal to leave the orbit. It is made up of the retinal ganglion cells (RGCs) axons. It allows vision by transmitting neural impulses from the retina to the brain. It is divided into four sections: the intraocular nerve head, the intraorbital, the intracanalicular and the intracranial [6]. The types of glial cells in the optic nerve are oligodendrocytes, astrocytes and microglia. Oligodendrocytes are responsible for producing the myelin sheaths that protect the CNS axons and contact nodes of Ranvier as well as they are the locations where action potentials are propagated and axonal integrity. Astrocytes are responsible for numerous physiological and pathological activities such as potassium homeostasis and metabolism as well as reactive astrogliosis in response to CNS trauma. Microglia are immune cells in CNS and have a significant impact on inflammation and infections [7].
The potential of curcumin for treating spinal cord injury: a meta-analysis study
Published in Nutritional Neuroscience, 2023
Mahnaz Kahuripour, Zahra Behroozi, Behnaz Rahimi, Michael R. Hamblin, Fatemeh Ramezani
Sensory and motor disability due to injury to the central nervous system, especially the spinal cord, is one of the most critical issues annoying medical professionals and patients. To date, advances in pharmacology and surgery in neuroscience have not provided any definitive treatment for the sensory, motor, and autonomic disorders for spinal cord injury (SCI). The causes of the inability of the damaged CNS area to repair itself include loss of the ability of nerve cells to divide and proliferate, and the creation of an unfavorable environment for axonal growth. Inflammation and oxidative stress following primary mechanical injury is the most important factor causing secondary neurological disorders. Studies have shown that inflammation induces astrogliosis and prevents the healing and repair of the affected axons [1,2]. Astrogliosis changes in the morphology and function of astrocytes. The degree of astrogliosis and proliferation of active astrocytes is shown by increased GFAP (Glial fibrillary acidic protein) expression [3,4]. Following the growth and division of astrocytes, astrogliosis prevents the repair of lesions by creating a physical barrier to prevent axonal growth. Recent studies that prevent inflammation (such as photobiomodulation therapy [5,6]) and create an environment conducive to axonal growth and avoid astrogliosis have been considered more to repair the CNS.
Related Knowledge Centers
- Autoimmunity
- Central Nervous System
- Gliosis
- Ischemia
- Stroke
- Infection
- Astrocyte
- Neuron
- Injury
- Neurodegenerative Disease