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Silica Nanoparticles for Drug Delivery
Published in Vladimir Torchilin, Handbook of Materials for Nanomedicine, 2020
Paik and co-workers used α-synuclein-coated gold nanoparticles to prepare protein mediated “raspberry-type” MSN nanocomposites for Ca2+ ion controlled drug release. α-Synuclein is an amyloidogenic protein that is responsible for the Lewy body formation in Parkinson’s disease. In this system, it also tightly capped the gold nanoparticles over the MSN pores in an acid-stable manner. In the presence of divalent cations the protein’s conformation changed, such that the hydrodynamic diameter of the gold-protein nanocomposites decreased by 2 nm, opening the MSN pores while remaining attached to the MSN surface. Calcium was chosen because there is a relatively high intracellular concentration of free ions within the cytoplasm and surges in calcium concentration have been implicated in cancer, neurodegenerative diseases, and cardiovascular diseases. No release was observed without Ca2+ or in the presence of ethylenediaminetetraacetic acid, Na+, or K+ ions. In vitro studies were done using DOX as a model drug in HeLa cells. The carriers were determined to be biocompatible; however, DOX-loaded nanoparticles were cytotoxic, especially in the presence of an endoplasmic reticulum Ca2+ pump inhibitor thapsigargin, which increases the intercellular Ca2+ concentration. When a membrane permeable Ca2+ chelator was added, very little cytotoxicity was observed [82].
Terpenoids: The Biological Key Molecules
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Moumita Majumdar, Dijendra Nath Roy
PD, another neurodegenerative disorder caused by genetic mutation or by some extracellular toxins, is characterised by abnormal movement due to motor impairment accompanied by corticobasal degeneration and dementia with Lewy bodies (Nuytemans et al. 2010). Misfolded α-synuclein proteins accumulate to form Lewy bodies, altering dopamine signalling and resulting in neural dysfunction and apoptosis. Cannabinoid (Figure 3.2j), a cannabis terpene, is influential in the treatment of PD. Cannabinoids are reported as competent alternative drugs targeting signalling pathways involved in development of PD. The anti-oxidant nature of cannabinoids make them suitable for managing mitochondrial oxidative stress (Borges et al. 2013; Velayudhan et al. 2014). Some cannabinoids are also found inside the body. Endogenous signalling involves receptors located in the brain, specifically in the globus pallidus and substantia nigra pars reticulata. These signalling cascades have been found to be partially or fully damaged during the course of infection. After treatment with exogenous cannabinoids, the expression of the receptor CB1 was found to be highest, along with another ionotropic receptor, Transient receptor potential vanilloid 1 (TRPV1). Cannabinoids are potent anti-inflammatories in the central nervous system and periphery. Counter effects of the endogenous cannabinoid system and exogenous ligands have also been explored in vitro. CB1-deficient mice show early onset of cognitive impairment and some molecular features that are found to be frequent in PD (Bilkei-Gorzo 2012).
The Human Microbiome: How Our Health is Impacted by Microorganisms
Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
However, removal of the appendix may have at least one benefit: according to a new study86 based on a large population of patients, it was that people who had had appendectomy in the early years had a 19.3% reduction in the risk of Parkinson’s disease, and the onset time was an average of 3.6 years later. Further studies have shown that this is due to the role of α-synuclein in the appendix. The pathological protein α-synuclein is suspected to trigger Parkinson’s disease.
An efficient method for recombinant production of human alpha synuclein in Escherichia coli using thioredoxin as a fusion partner
Published in Preparative Biochemistry & Biotechnology, 2020
Babak Saffari, Mehriar Amininasab, Sara Sheikhi, Jamshid Davoodi
Human α-Synuclein (hAS) is a highly conserved small polypeptide with 140 amino acid residues that in fibrillar form is considered to be the major component of highly insoluble intracellular aggregates known as Lewy bodies and Lewy neurites, the defining neuropathological hallmarks of Parkinson’s disease (PD) and other synucleinopathies.[1,2] PD is regarded as the most prevalent neurodegenerative movement disorder and the second most common central nervous system disorder after Alzheimer’s disease (AD), resulting primarily from the loss of dopaminergic neurons in the basal ganglia and related structures.[3]
Experimental models of chemically induced Parkinson’s disease in zebrafish at the embryonic larval stage: a systematic review
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Paola Briñez-Gallego, Dennis Guilherme da Costa Silva, Marcos Freitas Cordeiro, Ana Paula Horn, Mariana Appel Hort
Parkinson’s disease (PD) is the second most common neurodegenerative disorder characterized by progressive motor dysfunction, including tremor, stiffness, bradykinesia/akinesia, instability, and variable cognitive decline (Poewe et al. 2017; Simon, Tanner, and Brundin 2020; Vaccari et al. 2019). The key neuropathological features of PD are the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and, therefore, depletion of dopamine and tyrosine hydroxylase (TH), the rate-limiting enzyme for dopamine synthesis in the striatum, accompanied by increased presence of Lewy bodies, which are filamentary aggregates arising from the accumulation of α-synuclein (α-syn) protein (De Lau et al. 2004). Although the etiology of PD remains unclear, remarkable advances have been made to elucidate the mechanisms underlying the pathogenesis of this disease (Hu and Wang 2016). Several investigators demonstrated that oxidative stress, a rise in reactive oxygen and nitrogen species (ROS/RNS) levels and decrease in antioxidant defenses, mitochondrial disfunction and neuroinflammation play an important role in the degeneration of dopaminergic neurons (Niedzielska et al. 2016; Poewe et al. 2017; Simon, Tanner, and Brundin 2020). Consequently dopamine deficiency within the basal ganglia leads to a movement disorder termed classical parkinsonism (Liu, Yamada, and Osawa 2014; Wichmann 2019). In addition, PD also presents non-motor symptoms that commonly appear prior to motor impairment, such as autonomous dysfunction, anxiety, anosmia, cognitive and sleep disturbances (Zis et al. 2015). These symptoms arising from PD progression were shown to affect other extra-nigral dopaminergic, serotoninergic, and cholinergic tracts (Surmeier, Obeso, and Halliday 2017).
Effects of mild running on substantia nigra during early neurodegeneration
Published in Journal of Sports Sciences, 2018
Michael F. Almeida, Carolliny M. Silva, Rodrigo S. Chaves, Nathan C. R. Lima, Renato S. Almeida, Karla P. Melo, Marilene Demasi, Tiago Fernandes, Edilamar M. Oliveira, Luis E. S. Netto, Sandra M. Cardoso, Merari F. R. Ferrari
PD is the second most common age-related neurodegenerative disease, characterized by motor and non-motor symptoms, which decrease quality of life and increase mortality. PD is characterized by progressive degeneration of dopaminergic neurons of the substantia nigra pars compacta as well as the presence of intracellular insoluble inclusions, called Lewy Bodies, consisting primarily of aggregated α-synuclein protein. Although the cause of PD is unknown, aging is considered the major risk factor; nevertheless, genetic and environmental factors contribute to neurodegeneration (Collier, Kanaan, & Kordower, 2011; Dawson & Dawson, 2003).