China
Africa
Explore chapters and articles related to this topic
Von Economo’s encephalitis
Published in Avindra Nath, Joseph R. Berger, 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.
Neonatal Bacterial Infection
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Koilmani Emmanuvel Rajan, Christopher Karen
During inflammation, both microglia and astrocytes get activated, and their morphology changes in a process called astrogliosis. Microglia interacts with neurons and astrocytes to neutralize infections as quickly as possible and acts as a first immune defense against infections. Additionally, macrophages can phagocytose the pathogens present in the brain and spinal cord and present them to T cells. It can also travel to the site of infection and release proinflammatory cytokines. Astrocytes (astroglia) are star-shaped abundant cells found in the brain (Lovino et al. 2013).
Mapping the Injured Brain
Published in Yu Chen, Babak Kateb, Neurophotonics and Brain Mapping, 2017
Chandler Sours, Jiachen Zhuo, Rao P. Gullapalli
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).
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.
In vivo neural tissue engineering using adipose-derived mesenchymal stem cells and fibrin matrix
Published in The Journal of Spinal Cord Medicine, 2023
Krishnapriya Chandrababu, Harikrishnan Vijayakumar Sreelatha, Tara Sudhadevi, Arya Anil, Sabareeswaran Arumugam, Lissy Kalliyana Krishnan
Transplanted cells survived despite the presence of a delivery matrix. We observed an increase in cavitation, ED1 cell infiltration, and astrogliosis in OPC-SFM and NPC-SFM treated tissues. Substantial numbers of PKH26-MBP dual positive cells in OPC-NPC-Fib cryosections indicate a favorable outcome. The loco-motor functions assessed by BBB scoring were similar in all groups but showed an improvement tendency in C-Fib-treated animals. We assessed the development of astrogliosis based on GFAP staining alone. However, in future studies, the exact type of reactive astrocytes present at the injury site could be assessed using a panel of markers suggested by Ben Barres.29,30 One-time administration of cells to the injury site has limited the number of cells transplanted (1 × 104 cells). Hence the effect of more cells as a single dose or in multiple doses needs to be assessed for better regeneration. The insufficiency of cell numbers and the shorter assessment period could be the reasons for not achieving normal loco-motor functions. Exploring a minimally invasive route for cell transplantation holds the potential for future research. Multiple doses may cause needle insertion injury to the spinal cord. Schwann cells (5 × 104/5 µl) delivered to the subarachnoid space have shown improved locomotory functions in rat SCI models in 60 days.31 There is a scope for a long-term study with a higher cell number and less invasive cell delivery strategy to evaluate proposed cell-based therapy.31
What is the gold standard model for Alzheimer’s disease drug discovery and development?
Published in Expert Opinion on Drug Discovery, 2021
Ramón Cacabelos, Iván Carrera, Olaia Martínez-Iglesias, Natalia Cacabelos, Vinogran Naidoo
To bridge the gap between AD animal models and human studies, three-dimensional (3D) cell culture models have been developed. 3D cell culture models attempt to replicate some aspects of the brain microenvironment, mimicking neuronal-glial cell interactions, and blood flow [78]. The development of 3D cell culture systems (organoids, neurospheroids, matrix-embedded 3D cultures) are useful to recapitulate extracellular pathologies such as plaque formation in vitro [78]. Microphysiological human mini-brain models are another attractive modality of dynamic cell-culture systems for AD research and drug development [80]. Astrogliosis is a common phenomenon in AD pathology. In a newly developed model of reactive astrocytes (GiD), the excessive production of hydrogen peroxide (H2O2) originated from MAO-B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death; this phenotype can be prevented by AAD-2004, a potent H2O2 scavenger [81].