Academic literature on the topic 'Α-Synuclein (SNCA)'
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Journal articles on the topic "Α-Synuclein (SNCA)"
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Zhang, Xue-Ming, Sabina Anwar, Yongsoo Kim, Jennifer Brown, Isabelle Comte, Huan Cai, Ning-Ning Cai, Richard Wade-Martins, and Francis G. Szele. "The A30P α-synuclein mutation decreases subventricular zone proliferation." Human Molecular Genetics 28, no. 14 (March 19, 2019): 2283–94. http://dx.doi.org/10.1093/hmg/ddz057.
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Abstract Parkinson's disease (PD) is associated with olfactory defects in addition to dopaminergic degeneration. Dopaminergic signalling is necessary for subventricular zone (SVZ) proliferation and olfactory bulb (OB) neurogenesis. Alpha-synuclein (α-syn or Snca) modulates dopaminergic neurotransmission, and SNCA mutations cause familial PD, but how α-syn and its mutations affect adult neurogenesis is unclear. To address this, we studied a bacterial artificial chromosome transgenic mouse expressing the A30P SNCA familial PD point mutation on an Snca−/− background. We confirmed that the SNCA-A30P transgene recapitulates endogenous α-syn expression patterns and levels by immunohistochemical detection of endogenous α-syn in a wild-type mouse and transgenic SNCA-A30P α-syn protein in the forebrain. The number of SVZ stem cells (BrdU+GFAP+) was decreased in SNCA-A30P mice, whereas proliferating (phospho-histone 3+) cells were decreased in Snca−/− and even more so in SNCA-A30P mice. Similarly, SNCA-A30P mice had fewer Mash1+ transit-amplifying SVZ progenitor cells but Snca−/− mice did not. These data suggest the A30P mutation aggravates the effect of Snca loss in the SVZ. Interestingly, calbindin+ and calretinin (CalR)+ periglomerular neurons were decreased in both Snca−/−, and SNCA-A30P mice but tyrosine hydroxylase+ periglomerular OB neurons were only decreased in Snca−/− mice. Cell death decreased in the OB granule layer of Snca−/− and SNCA-A30P mice. In the same region, CalR+ numbers increased in Snca−/− and SNCA-A30P mice. Thus, α-syn loss and human A30P SNCA decrease SVZ proliferation, cell death in the OB and differentially alter interneuron numbers. Similar disruptions in human neurogenesis may contribute to the olfactory deficits, which are observed in PD.
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Di Leva, Francesca Di, Michele Filosi, Lisa Oyston, Erica Silvestri, Anne Picard, Alexandros A. Lavdas, Evy Lobbestael, et al. "Increased Levels of the Parkinson’s Disease-Associated Gene ITPKB Correlate with Higher Expression Levels of α-Synuclein, Independent of Mutation Status." International Journal of Molecular Sciences 24, no. 3 (January 19, 2023): 1984. http://dx.doi.org/10.3390/ijms24031984.
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Autosomal dominant mutations in the gene encoding α-synuclein (SNCA) were the first to be linked with hereditary Parkinson’s disease (PD). Duplication and triplication of SNCA has been observed in PD patients, together with mutations at the N-terminal of the protein, among which A30P and A53T influence the formation of fibrils. By overexpressing human α-synuclein in the neuronal system of Drosophila, we functionally validated the ability of IP3K2, an ortholog of the GWAS identified risk gene, Inositol-trisphosphate 3-kinase B (ITPKB), to modulate α-synuclein toxicity in vivo. ITPKB mRNA and protein levels were also increased in SK-N-SH cells overexpressing wild-type α-synuclein, A53T or A30P mutants. Kinase overexpression was detected in the cytoplasmatic and in the nuclear compartments in all α-synuclein cell types. By quantifying mRNAs in the cortex of PD patients, we observed higher levels of ITPKB mRNA when SNCA was expressed more (p < 0.05), compared to controls. A positive correlation was also observed between SNCA and ITPKB expression in the cortex of patients, which was not seen in the controls. We replicated this observation in a public dataset. Our data, generated in SK-N-SH cells and in cortex from PD patients, show that the expression of α-synuclein and ITPKB is correlated in pathological situations.
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Zhang, Peiyuan, Hye-Jin Park, Jie Zhang, Eunsung Junn, Ryan J. Andrews, Sai Pradeep Velagapudi, Daniel Abegg, et al. "Translation of the intrinsically disordered protein α-synuclein is inhibited by a small molecule targeting its structured mRNA." Proceedings of the National Academy of Sciences 117, no. 3 (January 3, 2020): 1457–67. http://dx.doi.org/10.1073/pnas.1905057117.
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Many proteins are refractory to targeting because they lack small-molecule binding pockets. An alternative to drugging these proteins directly is to target the messenger (m)RNA that encodes them, thereby reducing protein levels. We describe such an approach for the difficult-to-target protein α-synuclein encoded by the SNCA gene. Multiplication of the SNCA gene locus causes dominantly inherited Parkinson’s disease (PD), and α-synuclein protein aggregates in Lewy bodies and Lewy neurites in sporadic PD. Thus, reducing the expression of α-synuclein protein is expected to have therapeutic value. Fortuitously, the SNCA mRNA has a structured iron-responsive element (IRE) in its 5′ untranslated region (5′ UTR) that controls its translation. Using sequence-based design, we discovered small molecules that target the IRE structure and inhibit SNCA translation in cells, the most potent of which is named Synucleozid. Both in vitro and cellular profiling studies showed Synucleozid directly targets the α-synuclein mRNA 5′ UTR at the designed site. Mechanistic studies revealed that Synucleozid reduces α-synuclein protein levels by decreasing the amount of SNCA mRNA loaded into polysomes, mechanistically providing a cytoprotective effect in cells. Proteome- and transcriptome-wide studies showed that the compound’s selectivity makes Synucleozid suitable for further development. Importantly, transcriptome-wide analysis of mRNAs that encode intrinsically disordered proteins revealed that each has structured regions that could be targeted with small molecules. These findings demonstrate the potential for targeting undruggable proteins at the level of their coding mRNAs. This approach, as applied to SNCA, is a promising disease-modifying therapeutic strategy for PD and other α-synucleinopathies.
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Martínez-Rodríguez, Tania Yadira, and Mauricio Rey-Buitrago. "Physiological, molecular and genetic aspects of alpha-synuclein and its correlation with high alcohol consumption." Revista de la Facultad de Medicina 67, no. 3 (July 1, 2019): 315–22. http://dx.doi.org/10.15446/revfacmed.v67n3.69962.
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Introduction: Significant changes in the expression of α-synuclein (SNCA) can be seen in subjects with high alcohol consumption, altering neuroprotection and causing changes in the reward system.Objective: To present state-of-the-art studies on the physiological, molecular and genetic aspects of SNCA related to high alcohol consumption.Materials and methods: A search of records published from 2007 to 2017 was carried out in PUBMED, ScienceDirect and Cochrane with the terms alpha-synuclein, alcoholism, genetic polymorphism, gene expression, DNA methylation and molecular biology.Results: The search yielded 1 331 references, of which 51 full-texts were selected. The results describe the current evidence of the physiological and pathological aspects of α-synuclein (SNCA) and the genetic and epigenetic changes related to its expression in people with high alcohol consumption.Conclusions: The evidence suggests that a differential expression of α-synuclein (SNCA) is found in subjects with high alcohol consumption, as a result of modifications in the genetic and epigenetic mechanisms, leading to physipathological neuroadaptations. SNCA is a promising marker in the field of alcoholism research; therefore, more studies are required in this regard, taking into account the genetic heterogeneity of each population.
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Aloy, Nirjhar M., Michael W. Graner, Christina Coughlan, Sergey V. Slepenkov, Sahar Shekoohi, and Stephan N. Witt. "Abstract 1575: Knocking out alpha synuclein causes decreased release of extracellular vesicles in melanoma cells." Cancer Research 82, no. 12_Supplement (June 15, 2022): 1575. http://dx.doi.org/10.1158/1538-7445.am2022-1575.
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Abstract The purpose of this study is to understand the role of α-synuclein in the regulation of the trafficking and release of modulators of metastasis in melanoma. Metastasis causes melanoma-induced death and 5-year survival rates, subsequent to metastasis to regional lymph nodes or distal organs, of 9% and 4%, respectively, hence novel therapeutic targets are required to control metastasis. Emerging evidence suggests that α-synuclein, a 14.4 KDa protein, which is a key player in Parkinson’s disease, is significantly correlated with melanoma progression. Our hypothesis is that α-synuclein positively regulates the release of extracellular vesicles. Extracellular vesicles (EVs) have been shown to be important in tumor metastasis, immune modulation and chemoresistance. The rationale for this hypothesis is that α-synuclein is a unique membrane-associated catalyst of endocytosis and exocytosis, and, specifically, synuclein regulates neurotransmitter release through SNARE complex assembly and the dilation of the fusion pore. The objective of the study is to measure the concentration of extracellular vesicles in the conditioned media from wild type SK-MEL-28 melanoma cells, SNCA knock out cells, and rescued SNCA-KO cells (where α-synuclein is re-expressed in KO cells via lentivirus) using Nanoparticle Tracking Analysis. The expected result was that knocking out SNCA would decrease the number of EVs released per cell relative to wild type control cells. To this end, we grew wild type, SNCA-KO and rescued SNCA-KO cells for 48 hours at 37°C and collected conditioned media. EVs were extracted from each conditioned medium using the ExoQuick-TC kit (Systems Bioscience) and stored at -80°C. EVs were characterized by PAGE followed by western blotting for common EV-markers and EV samples were shipped to the University of Colorado for Nanoparticle Tracking. Here we report a significant reduction in the concentration of EVs in SNCA-KO cell lines compared to control cells (P=0.0123), an effect that was rescued upon re-expression of α-synuclein in knock-out cells (P<0.01). Unpublished data from our lab suggests that invasion and migration are significantly reduced in SNCA-KO melanoma compared to control cells, a pathological outcome that returns in rescued SNCA-KO cells. These observations point to considering α-synuclein as a therapeutic target for regulating the release of pro-metastatic factors in extracellular vesicles, an intervention that would have important health implications as a novel therapeutic approach in melanoma. Work is ongoing in our lab to elucidate the mechanistic details of how α-synuclein promotes EV release. Citation Format: Nirjhar M. Aloy, Michael W. Graner, Christina Coughlan, Sergey V. Slepenkov, Sahar Shekoohi, Stephan N. Witt. Knocking out alpha synuclein causes decreased release of extracellular vesicles in melanoma cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1575.
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Kawahata, Ichiro, David I. Finkelstein, and Kohji Fukunaga. "Pathogenic Impact of α-Synuclein Phosphorylation and Its Kinases in α-Synucleinopathies." International Journal of Molecular Sciences 23, no. 11 (June 1, 2022): 6216. http://dx.doi.org/10.3390/ijms23116216.
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α-Synuclein is a protein with a molecular weight of 14.5 kDa and consists of 140 amino acids encoded by the SNCA gene. Missense mutations and gene duplications in the SNCA gene cause hereditary Parkinson’s disease. Highly phosphorylated and abnormally aggregated α-synuclein is a major component of Lewy bodies found in neuronal cells of patients with sporadic Parkinson’s disease, dementia with Lewy bodies, and glial cytoplasmic inclusion bodies in oligodendrocytes with multiple system atrophy. Aggregated α-synuclein is cytotoxic and plays a central role in the pathogenesis of the above-mentioned synucleinopathies. In a healthy brain, most α-synuclein is unphosphorylated; however, more than 90% of abnormally aggregated α-synuclein in Lewy bodies of patients with Parkinson’s disease is phosphorylated at Ser129, which is presumed to be of pathological significance. Several kinases catalyze Ser129 phosphorylation, but the role of phosphorylation enzymes in disease pathogenesis and their relationship to cellular toxicity from phosphorylation are not fully understood in α-synucleinopathy. Consequently, this review focuses on the pathogenic impact of α-synuclein phosphorylation and its kinases during the neurodegeneration process in α-synucleinopathy.
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Reiszadeh Jahromi, Samaneh, S. R. Ramesh, David I. Finkelstein, and Mohammad Haddadi. "α-Synuclein E46K Mutation and Involvement of Oxidative Stress in a Drosophila Model of Parkinson’s Disease." Parkinson's Disease 2021 (July 3, 2021): 1–12. http://dx.doi.org/10.1155/2021/6621507.
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Parkinson’s disease (PD) is an age-associated neurodegenerative condition in which some genetic variants are known to increase disease susceptibility on interaction with environmental factors inducing oxidative stress. Different mutations in the SNCA gene are reported as the major genetic contributors to PD. E46K mutation pathogenicity has not been investigated as intensive as other SNCA gene mutations including A30P and A53T. In this study, based on the GAL4-UAS binary genetic tool, transgenic Drosophila melanogaster flies expressing wild-type and E46K-mutated copies of the human SNCA gene were constructed. Western blotting, immunohistochemical analysis, and light and confocal microscopy of flies’ brains were undertaken along with the survival rate measurement, locomotor function assay, and ethanol and paraquat (PQ) tolerance to study α-synuclein neurotoxicity. Biochemical bioassays were carried out to investigate the activity of antioxidant enzymes and alterations in levels of oxidative markers following damages induced by human α-synuclein to the neurons of the transgenic flies. Overexpression of human α-synuclein in the central nervous system of these transgenic flies led to disorganized ommatidia structures and loss of dopaminergic neurons. E46K α-synuclein caused remarkable climbing defects, reduced survivorship, higher ethanol sensitivity, and increased PQ-mediated mortality. A noticeable decline in activity of catalase and superoxide dismutase enzymes besides considerable increase in the levels of lipid peroxidation and reactive oxygen species was observed in head capsule homogenates of α-synuclein-expressing flies, which indicates obvious involvement of oxidative stress as a causal factor in SNCAE46K neurotoxicity. In all the investigations, E46K copy of the SNCA gene was found to impose more severe defects when compared to wild-type SNCA. It can be concluded that the constructed Drosophila models developed PD-like symptoms that facilitate comparative studies of molecular and cellular pathways implicated in the pathogenicity of different α-synuclein mutations.
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Zhang, Jing-Xing, Wei-Fang Tong, Ming Jiang, Kai-Ge Zhou, Xue-rui Xiang, Yi-jing He, Zhuo-yu Zhang, Qiang Guan, and Ling-Jing Jin. "MANF Inhibits α-Synuclein Accumulation through Activation of Autophagic Pathways." Oxidative Medicine and Cellular Longevity 2022 (July 8, 2022): 1–19. http://dx.doi.org/10.1155/2022/7925686.
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Progressive accumulation of misfolded SNCA/α-synuclein is key to the pathology of Parkinson’s disease (PD). Drugs aiming at degrading SNCA may be an efficient therapeutic strategy for PD. Our previous study showed that mesencephalic astrocyte-derived neurotrophic factor (MANF) facilitated the removal of misfolded SNCA and rescued dopaminergic (DA) neurons, but the underlying mechanisms remain unknown. In this study, we showed that AAV8-MANF relieved Parkinsonian behavior in rotenone-induced PD model and reduced SNCA accumulation in the substantia nigra. By establishing wildtype (WT) SNCA overexpression cellular model, we found that chaperone-mediated-autophagy (CMA) and macroautophagy were both participated in MANF-mediated degradation of SNCAWT. Nuclear factor erythroid 2-related factor (Nrf2) was activated to stimulating macroautophagy activity when CMA pathway was impaired. Using A53T mutant SNCA overexpression cellular model to mimic CMA dysfunction situation, we concluded that macroautophagy rather than CMA was responsible to the degradation of SNCAA53T, and this degradation was mediated by Nrf2 activation. Hence, our findings suggested that MANF has potential therapeutic value for PD. Nrf2 and its role in MANF-mediated degradation may provide new sights that target degradation pathways to counteract SNCA pathology in PD.
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Taguchi, Tomoyuki, Masashi Ikuno, Mari Hondo, Laxmi Kumar Parajuli, Katsutoshi Taguchi, Jun Ueda, Masanori Sawamura, et al. "α-Synuclein BAC transgenic mice exhibit RBD-like behaviour and hyposmia: a prodromal Parkinson’s disease model." Brain 143, no. 1 (December 9, 2019): 249–65. http://dx.doi.org/10.1093/brain/awz380.
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Abstract Parkinson’s disease is one of the most common movement disorders and is characterized by dopaminergic cell loss and the accumulation of pathological α-synuclein, but its precise pathogenetic mechanisms remain elusive. To develop disease-modifying therapies for Parkinson’s disease, an animal model that recapitulates the pathology and symptoms of the disease, especially in the prodromal stage, is indispensable. As subjects with α-synuclein gene (SNCA) multiplication as well as point mutations develop familial Parkinson’s disease and a genome-wide association study in Parkinson’s disease has identified SNCA as a risk gene for Parkinson’s disease, the increased expression of α-synuclein is closely associated with the aetiology of Parkinson’s disease. In this study we generated bacterial artificial chromosome transgenic mice harbouring SNCA and its gene expression regulatory regions in order to maintain the native expression pattern of α-synuclein. Furthermore, to enhance the pathological properties of α-synuclein, we inserted into SNCA an A53T mutation, two single-nucleotide polymorphisms identified in a genome-wide association study in Parkinson’s disease and a Rep1 polymorphism, all of which are causal of familial Parkinson’s disease or increase the risk of sporadic Parkinson’s disease. These A53T SNCA bacterial artificial chromosome transgenic mice showed an expression pattern of human α-synuclein very similar to that of endogenous mouse α-synuclein. They expressed truncated, oligomeric and proteinase K-resistant phosphorylated forms of α-synuclein in the regions that are specifically affected in Parkinson’s disease and/or dementia with Lewy bodies, including the olfactory bulb, cerebral cortex, striatum and substantia nigra. Surprisingly, these mice exhibited rapid eye movement (REM) sleep without atonia, which is a key feature of REM sleep behaviour disorder, at as early as 5 months of age. Consistent with this observation, the REM sleep-regulating neuronal populations in the lower brainstem, including the sublaterodorsal tegmental nucleus, nuclei in the ventromedial medullary reticular formation and the pedunculopontine nuclei, expressed phosphorylated α-synuclein. In addition, they also showed hyposmia at 9 months of age, which is consistent with the significant accumulation of phosphorylated α-synuclein in the olfactory bulb. The dopaminergic neurons in the substantia nigra pars compacta degenerated, and their number was decreased in an age-dependent manner by up to 17.1% at 18 months of age compared to wild-type, although the mice did not show any related locomotor dysfunction. In conclusion, we created a novel mouse model of prodromal Parkinson’s disease that showed RBD-like behaviour and hyposmia without motor symptoms.
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Patrakhanov, E. A., V. M. Pokrovsky, A. Yu Karagodina, A. M. Krayushkina, N. S. Zhunusov, A. V. Deykin, M. V. Korokin, M. V. Pokrovsky, and O. B. Altukhova. "DEVELOPMENT OF MURINE STEM CELLS WITH CONDITIONAL KNOCKOUT OF HUMANIZED SNCA GENE." Pharmacy & Pharmacology 10, no. 6 (February 12, 2023): 525–35. http://dx.doi.org/10.19163/2307-9266-2022-10-6-525-535.
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α-synuclein is one of the key molecular links in the pathogenesis of Parkinson’s disease. The accumulated data indicate that pathogenic mutations in the Snca gene are associated with the development of neurodegenerative brain damage, indicating the relevance of studying the synuclein neurobiological role.The aim of the study was to create a genetically modified clone of mouse stem cells with a conditional knockout of humanized α-synuclein, which can be used for the reinjection into mouse blastocysts, as well as for basic and applied in vitro research in the field of pathophysiology and neuropharmacology.Materials and methods. To create mouse stem cells with a conditional knockout of the humanized Snca gene, a previously obtained clone with the first Snca exon flanked by LoxP sites, was used. The CRISPR/Cas9-mediated homologous recombination system with donor DNA oligonucleotides of the human sites of the corresponding gene sites was used to humanize the fourth and fifth exons. Cas9 nuclease, single guide RNA, and donor DNA were transfected into mouse cells.Results. An approach to obtaining clones of mouse genetically modified stem cells expressing pathological humanized α-synuclein, has been proposed and implemented. The resulting clones were plated on Petri dishes for propagation and a further genetic analysis. Clone 126-2F4 was found out carrying the necessary genetic modifications. The results obtained are fundamentally important not only for understanding the development of the pathological process in α-synucleinopathies, but which is more important, for the development of new therapeutic approaches that will stop the extension of the human α-synuclein aggregation pathology throughout the nervous system, and the validation of these approaches in preclinical trials.Conclusion. As a result of the study, a strategy for CRISPR/Cas9-assisted homologous recombination in the genome of mouse embryonic stem cells has been developed to create a fully humanized Snca gene encoding α-synuclein, and the clone genome of mouse embryonic stem cells has been edited using a CRISPR technology. The RNA and DNA oligonucleotides necessary for the creation of RNP complexes that carry out a directed homologous recombination in the Snca locus of the mouse genome have been synthesized. The developed cell clone can serve to create a line of genetically modified mice that serve as a test system for pathophysiological and neuropharmacological studies associated with synucleinopathies. Herewith, before the induction of the Cre-dependent recombination, this line is a representative model for studying a biological role of mutant Snca. At the same time, after a Cre-dependent knockout activation, it is possible to imitate the pharmacological inhibition of α-synuclein, which is of particular interest for applied research in neuropharmacology.
Dissertations / Theses on the topic "Α-Synuclein (SNCA)"
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Janeczek, Paulina. "Mechanisms of Gene Regulation in Alcoholism: Role of α-Synuclein in the Pathophysiology of Alcohol Misuse." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367052.
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The pathophysiology of alcohol addiction is still unknown. Current research is focusing on understanding the mechanisms involved in the neurotoxic effects of ethanol on the brain and the genetic risk factors associated with alcohol misuse. The prefrontal cortex is particularly susceptible to neurotoxic damage, and neuronal loss in this region has been associated with long-term alcohol misuse. As the prefrontal cortex is involved in the development and persistence of alcohol addiction, ethanol induced neurotoxic damage in this region is likely to amplify the reinforcing effects of alcohol. α-Synuclein (SNCA), a protein abundantly expressed in neurons and involved in the dopaminergic reward pathway, has a well-established role in neurodegenerative and neuropsychological disorders, and is a candidate gene for alcohol misuse. Changes to α- synuclein expression may therefore have severe consequences on these key pathways and may increase susceptibility to alcohol addiction. This thesis investigated the regulation of α-synuclein expression and its potential role in the pathophysiology of chronic alcohol misuse.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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Conference papers on the topic "Α-Synuclein (SNCA)"
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Pitta, Marina Galdino da Rocha, Jordy Silva de Carvalho, Luzilene Pereira de Lima, and Ivan da Rocha Pitta. "iPSC therapies applied to rehabilitation in parkinson’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.022.
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Background: Parkinson’s disease (PD) is a neurological disorder that affects movement, mainly due to damage and degeneration of the nigrostriatal dopaminergic pathway. The diagnosis is made through a clinical neurological analysis where motor characteristics are considered. There is still no cure, and treatment strategies are focused on symptoms control. Cell replacement therapies emerge as an alternative. Objective: This review focused on current techniques of induced pluripotent stem cells (iPSCs). Methods: The search terms used were: “Parkinson’s Disease”, “Stem cells” and “iPSC”. Open articles written in English, from 2016-21 were selected in the Pubmed database, 10 publications were identified. Results: With the modernization of iPSC, it was possible to reprogram pluripotent human somatic cells and generate dopaminergic neurons and individual-specific glial cells. To understand the molecular basis, cell and animal models of neurons and organelles are currently being employed. Organoids are derived from stem cells in a three-dimensional matrix, such as matrigel or hydrogels derived from animals. The neuronal models are: α-synuclein (SNCA), leucine-rich repeat kinase2 (LRRK2), PARK2, putative kinase1 induced by phosphatase and tensin homolog (PINK1), DJ-1. Both models offer opportunities to investigate pathogenic mechanisms of PD and test compounds on human neurons. Conclusions: Cell replacement therapy is promising and has great capacity for the treatment of neurodegenerative diseases. Studies using iPSC neuron and PD organoid modeling is highly valuable in elucidating relevants neuronal pathways and therapeutic targets, moreover providing important models for testing future therapies.