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).
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.
Neuroanatomy of the Functional Aging Brain
José León-Carrión, Margaret J. Giannini in Behavioral Neurology in the Elderly, 2001
Findings obtained from studies of age-related changes in brain morphology and behavior of mice have demonstrated age-dependent cerebral atrophy and cognitive dysfunction. Shimada2 followed the apparently normal development of mice and found that mice developed brain atrophy with advancing age. The neocortex was diffusely atrophic in aged mice, with the frontal cortex the most affected. The enthorinal cortex, amygdala, and nucleus accumbens were also atrophic. Other subcortical structures were mildly atrophic, but the hippocampus was not atrophic. Mild to moderate hypertrophic astrocytosis was observed in the atrophied regions but no Alzheimer-type pathology was seen. The cortical atrophy was due to both loss of neurons and shrinkage. Brain atrophy was not remarkable in normal aging control mice. Because of the morphological changes observed, cognitive impairment was observed with advancing age. All these features of mice were inherited (Figure 4.1).
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.
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.
Neuroprotective effects of quercetin on the cerebellum of zinc oxide nanoparticles (ZnoNps)-exposed rats
Published in Tissue Barriers, 2023
Shaimaa A. Abdelrahman, Amal S. El-Shal, Abeer A. Abdelrahman, Ebtehal Zaid Hassen Saleh, Abeer A. Mahmoud
Every chemical, mechanical, or degenerative input to the brain causes astrocyte proliferation and hypertrophy, which lead to increased GFAP production and astrogliosis, according to Sofroniew and Vinters.87 The molecular mechanism of astrocyte activation has been proposed as oxidative stress, which is a result of the increased need for neural protection.88 So, antioxidants administration could play a crucial protective role against astrogliosis. This explains the significant increase in GFAP immunoexpression in ZnONPs-exposed rats of the present study and reversal after Quercetin supplementation. GFAP is an intermediate filament protein known to be specifically expressed in astrocytes; the glial cells that are responsible for repairing and scarring of the brain following injuries.89 The increase in GFAP expression has been identified as a biomarker of neurotoxicity.90 In the CNS, Quercetin reduced the activation of astrocytes and reduced neuroinflammation.91 The blood-brain barrier is crucial in relation to the toxicity of the nanoparticles in the brain tissue. This expanded membrane between the cerebral capillaries and surrounding endothelial cells contains tight junctions.92,93 When nanoparticles enter the circulation, they may change the permeability of the membrane or cause a cascade of chemicals that damage tight junctions, causing direct or indirect toxicity in the brain tissues. NPs may also stimulate the vesicular transport, to get entry inside the microenvironment of CNS where they further disrupt several molecular pathways.94,95
Related Knowledge Centers
- Autoimmunity
- Central Nervous System
- Gliosis
- Ischemia
- Stroke
- Infection
- Astrocyte
- Neuron
- Injury
- Neurodegenerative Disease