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The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
Damage to the CNS is invariably accompanied by hypertrophy and hyperplasia of astrocytes, a process known as astrocytosis or gliosis (Figure 12.5), in which numerous intracellular fibres of GFAP are laid down in an irregular manner.
Nervous System
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Mark T. Butt, Alys Bradley, Robert Sills
This diagnosis is appropriate whenever there is an increase in the number and size of astrocytes, especially when in the proximity of an identified structural alteration in some component of the central portion of the nervous system. Reactive astrocytosis, gemistocytosis (a gemistocyte is a term for an enlarged/reactive astrocyte), and astrogliosis are synonymous terms.
The neurobiology of traumatic brain injury
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Thomas C. Glenn, Richard L. Sutton, David A. Hovda
In most clinical neuropathological studies, there is an inference that the resulting CTE is related to the exposure of individuals to repeated concussions. In a recent experimental study using mice, this hypothesis was addressed.91 Using a weight drop method without a craniotomy, mice were exposed to various combinations of repeated insults that varied from 5 days to 5 months with combinations of concussive insults (daily, weekly, biweekly, or monthly). Mice subjected to repeat mild TBI daily or weekly, but not biweekly or monthly, had persistent cognitive deficits as long as 1 year after their last injury. Although these deficits were associated with astrocytosis, they were not related to tau phosphorylation or amyloid β as measured by ELISA. Interestingly, these deficits were also unrelated to the formation of plaques or tangles (by immunohistochemistry), changes in brain volume, or changes in white matter integrity as measured using magnetic resonance imaging. From these experiments, it would appear that when repeat mild TBI occurs over a short period of time, subjects may be more susceptible to prolonged cognitive decline, and this may not be related to tau accumulation. Such a mild TBI-induced vulnerability has been reported in a rat model of closed head injury;76 however, from an experimental perspective, the mechanism(s) related to the phosphorylation of tau (CTE) may not be restricted to the exposure of repeated mild blows to the head.
4-(3-Nitrophenyl)thiazol-2-ylhydrazone derivatives as antioxidants and selective hMAO-B inhibitors: synthesis, biological activity and computational analysis
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Daniela Secci, Simone Carradori, Anél Petzer, Paolo Guglielmi, Melissa D’Ascenzio, Paola Chimenti, Donatella Bagetta, Stefano Alcaro, Gokhan Zengin, Jacobus P. Petzer, Francesco Ortuso
Previous studies have also shown the correlation between MAO-B and Alzheimer’s disease (AD) due to (i) the increase of MAO-B activity in brain and platelets in AD patients, (ii) the MAO-B specific ligand 11C-deuterium-l-deprenyl showed enhanced binding in presymptomatic familial AD patients, and (iii) AD patients are characterised by enhanced astrocytosis. Moreover, MAO-B was reported to be associated with γ-secretase in the regulation of intraneuronal Aβ levels especially in pyramidal neurons as well as glia cells in the frontal cortex and hippocampus17. However, the main pathogenic feature linked with the progression of AD is the weakening of the cholinergic system in the brain and inhibitors of AChE and BuChE are approved as a therapeutic strategy to limit the symptoms and progression of AD. The role of BuChE is not completely known yet.
Pathogenesis of epileptic seizures and epilepsy after stroke
Published in Neurological Research, 2018
Huajun Yang, Gary Rajah, Anchen Guo, Yongjun Wang, Qun Wang
In the later stages of cerebral vascular disease, epilepsy can be caused by the proliferation of glial cells [46]. Kharlamov et al. [47] assessed astroglial response in the brains of both epileptic and non-epileptic rats following photothrombosis after the six-month monitoring period. Activated astroglia were detected in the cortex and hippocampus, following lesioning and the development of seizure activity. Morphological and functional abnormalities following abnormal proliferation of glial cells is known as reactive astrocytosis. Normal astrocytes can actively ingest K+ and synthesize inhibitory neurotransmitters such as GABA, which is important in stabilizing neuronal excitability [46]. However, in reactive astrocytes, changes in the modulation of ion channels can lead to decline in the ability of reactive astrocytes to ingest K+, making the neuron easy to depolarize and over-discharge [48]. Meanwhile, changes in the expression of various astrocytic enzymes, such as adenosine kinase and glutamine synthetase, resulting in increasing of glutamate and decrease of GABA, thus increasing the excitability of neurons [49]. In addition to astroglial proliferation, recent evidence suggests that oligodendrocyte cell density is also increased in the white matter of the hippocampus and the neocortices in patients with epilepsy [50]. Microglia is involved in inflammatory pathways which contribute to the pathogenesis of seizures in various forms of epilepsy [51]. However, few studies were focused on the specific mechanisms for the role of oligodendrocyte and microglia in the pathogenesis of post-stroke epilepsy. The impact of gliocyte proliferation on epileptogenesis in patients after stroke needs further validation.
Vulnerability of glia and vessels of rat substantia nigra in rotenone Parkinson model
Published in Ultrastructural Pathology, 2018
Sanaa A. M. Elgayar, Amel A. M. Abdel-hafez, Asmaa M. S. Gomaa, Raghda Elsherif
Therefore, it can be deduced that the astrocytes have been influenced by rotenone in a way similar to that on neurons, but to a lesser extent. Astrocyte proliferation could occur as a consequence of the neuronal loss; therefore, astrocytosis does not participate in rotenone toxicity but astrocyte dysfunction might lead to their death and consequently to increased neuronal death. Neurons are more susceptible to injury than astrocytes, as they have limited antioxidant capacity, and rely heavily on their metabolic coupling with astrocytes to combat oxidative stress.26