prikaz prve stranice dokumenta Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency
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undergraduate thesis
Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency
2023. urn:nbn:hr:193:509609
Kolarić, Marta
University of Rijeka
Faculty of Biotechnology and Drug Development

Cite this document

Kolarić, M. (2023). Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency (Undergraduate thesis). Rijeka: University of Rijeka. Retrieved from https://urn.nsk.hr/urn:nbn:hr:193:509609

Kolarić, Marta. "Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency." Undergraduate thesis, University of Rijeka, 2023. https://urn.nsk.hr/urn:nbn:hr:193:509609

Kolarić, Marta. "Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency." Undergraduate thesis, University of Rijeka, 2023. https://urn.nsk.hr/urn:nbn:hr:193:509609

Kolarić, M. (2023). 'Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency', Undergraduate thesis, University of Rijeka, accessed 02 April 2025, https://urn.nsk.hr/urn:nbn:hr:193:509609

Kolarić M. Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency [Undergraduate thesis]. Rijeka: University of Rijeka; 2023 [cited 2025 April 02] Available at: https://urn.nsk.hr/urn:nbn:hr:193:509609

M. Kolarić, "Analysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency", Undergraduate thesis, University of Rijeka, Rijeka, 2023. Available at: https://urn.nsk.hr/urn:nbn:hr:193:509609

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Metadata
TitleAnalysis of potential neuroinflammatory pathology in the spinal cords of mice with optineurin insufficiency
Title (croatian)Analiza potencijalne neuroinflamatorne patologije u leđnim moždinama miševa s insuficijencijom optineurina
AuthorMarta Kolarić
MentorIvana Munitić (mentor)
Committee memberDaniela Kalafatović (predsjednik povjerenstva)
Committee memberKatarina Kapuralin (član povjerenstva)
Committee memberIvana Munitić (član povjerenstva)
Committee memberJurica Novak (član povjerenstva)
GranterUniversity of Rijeka
(Faculty of Biotechnology and Drug Development)
Rijeka
Defense date and country2023-07-18, Croatia
Scientific / art field,
discipline and subdiscipline		BIOTECHNICAL SCIENCES
Biotechnology
Abstract
Amyotrophic lateral sclerosis (ALS) is a complex neurodegenerative disease characterised by motor neuron loss in the brain, brainstem, and spinal cord. ALS is caused by mutations in more than 50 genes, including OPTN, encoding for optineurin, a ubiquitin-binding protein that regulates inflammatory signalling. It has been hypothesized that ALS-linked optineurin mutations cause protein loss-of-function, leading to dysregulated immune response that could trigger ALS. However, the exact... More mechanism of disease pathogenesis is still unclear given that optineurin participates in various other cellular functions including autophagy, cell death and others. Since most ALS cases display spinal onset, we characterised the potential neuroinflammatory pathology in the lumbar spinal cord of young adult mice carrying ALS-like optineurin truncation (Optn470T). We assessed if this optineurin mutation is by itself sufficient to induce ALS-like neuropathology, or whether the latter could be provoked by lipopolysaccharide (LPS). We demonstrated an absence of exaggerated neuroinflammation, TDP-43 aggregation and neurodegeneration in the lumbar spinal cords of Optn470T mice for both basal and LPS-stimulated conditions. Our results indicate that optineurin truncation in mice does not induce ALS-like neuropathology in these settings, suggesting that a short-term inflammatory stimulus is insufficient to precipitate the disease. It is still an open question if chronic inflammation or mutation in other ALS-affected genes together with optineurin truncation could uncover the role of optineurin in neuropathology Less
Abstract (croatian)
Amiotrofična lateralna skleroza (ALS) je kompleksna neurodegenerativna bolest karakterizirana gubitkom motoričkih neurona u mozgu, moždanom deblu i leđnoj moždini. ALS je uzrokovan mutacijama u više od 50 gena, uključujući i OPTN, koji kodira optineurin, ubikvitin vezujući protein uključen u regulaciju upalne signalizacije. Pretpostavlja se da mutacije optineurina u ALS-u uzrokuju gubitak funkcije proteina koje mogu izazvati narušeni imunosni odgovor te dovesti do razvoja ALS-a.... More Međutim, točan mehanizam patogeneze bolesti i dalje nije poznat budući da optineurin sudjeluje u raznim drugim staničnim funkcijama kao što je autofagija, stanična smrt i drugi. S obzirom na to da ALS slučajevi pokazuju spinalni oblik bolesti, okarakterizirali smo potencijalnu neuroinflamatornu patologiju u lumbalnim dijelovima leđne moždine mladih miševa s trunkacijom optineurina nalik ALS-u (Optn470T). Ispitali smo ukoliko je mutacija optineurina sama po sebi dovoljna da izazove neuropatologiju nalik ALS-u ili ukoliko ju se može izazvati lipopolisaharidom (LPS). Demonstrirali smo odsustvo pretjerane upale, TDP-43 agregata te neurodegeneracije u lumbalnom dijelu leđne moždine Optn470T miševa pri bazalnim i LPS stimuliranim uvjetima. Naši rezultati ukazuju na to da trunkacija optineurina ne dovodi do ALS-slične neuropatologije u ovim uvjetima te sugeriraju da je kratkotrajni upalni podražaj nedovoljan kako bi uzrokovao bolest. I dalje je otvoreno pitanje mogu li kronična upala ili mutacije u drugim ALS-zahvaćenim genima zajedno s trunkacijom optineurina objasniti ulogu optineurina u neuropatologiji., Less
Keywords
Keywords (croatian)
Languageenglish
URN:NBNurn:nbn:hr:193:509609
Study programmeTitle: Biotechnology and drug research
Study programme type: university
Study level: undergraduate
Academic / professional title: sveučilišni/a prvostupnik/prvostupnica biotehnologije i istraživanja lijekova (sveučilišni/a prvostupnik/prvostupnica biotehnologije i istraživanja lijekova)
Type of resourceText
File originBorn digital
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2023-10-11 12:56:45
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