Abstract
In the past decades advances in medicine have led to an extended life span of the general population, which, as a negative consequence, increased the occurrence of age-related neurodegenerative diseases. The necessity to improve the quality of life together with the urge to decrease the economic burden related to patients with neurodegenerative diseases, brings focus to the development of novel treatment strategies for these disorders as the current medical interventions are mostly symptomatic and do not slow down the progression of the diseases.
In this thesis, we study neurodegenerative diseases in a fruit fly, which is widely used for these kinds of experiments. Our hypothesis was that neurodegeneration could be treated using different approaches: either focusing on the cause of this particular disease or using a general treatment. We show that both of these therapies can be efficient in the example of two diseases, Spinocerebellar ataxia type 3 and pantothenate kinase-associated neurodegeneration. In case of a general therapy, we show how production of hydrogen sulfide inside the body positively influences neurodegeneration. In case of the specific treatment, we supplement a substance called coenzyme A to organisms that lack it and we observe a partial rescue of the disease. Further, we demonstrate how these therapies work on the molecular level and create a new fly model for a more efficient study of pantothenate kinase-associated neurodegeneration.
In this thesis, we study neurodegenerative diseases in a fruit fly, which is widely used for these kinds of experiments. Our hypothesis was that neurodegeneration could be treated using different approaches: either focusing on the cause of this particular disease or using a general treatment. We show that both of these therapies can be efficient in the example of two diseases, Spinocerebellar ataxia type 3 and pantothenate kinase-associated neurodegeneration. In case of a general therapy, we show how production of hydrogen sulfide inside the body positively influences neurodegeneration. In case of the specific treatment, we supplement a substance called coenzyme A to organisms that lack it and we observe a partial rescue of the disease. Further, we demonstrate how these therapies work on the molecular level and create a new fly model for a more efficient study of pantothenate kinase-associated neurodegeneration.
Original language | English |
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Qualification | Doctor of Philosophy |
Awarding Institution |
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Supervisors/Advisors |
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Award date | 25-Apr-2016 |
Place of Publication | [Groningen] |
Publisher | |
Print ISBNs | 978-94-6233-275-1 |
Publication status | Published - 2016 |