ArticleFrontiers in neurology and neuroscience research2020
GDNF Receptor Agonist Alleviates Motor Imbalance in Unilateral 6-Hydroxydopamine Model of Parkinson's Disease.
Article in Frontiers in neurology and neuroscience research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Neuroprotective Potential of a Small Molecule RET Agonist in Cultured Dopamine Neurons and Hemiparkinsonian Rats.Journal of Parkinson's disease · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is an incurable neurodegenerative disorder affecting up to 10 million people in the world. Diagnostic motor symptoms of PD appear as a result of progressive degeneration and death of nigrostriatal dopamine neurons. Current PD treatments only relieve symptoms without halting the progression of the disease, and their use is complicated by severe adverse effects emerging as the disease progresses. Therefore, there is an urgent need for new therapies for PD management. We developed a small molecule compound, BT13, targeting receptor tyrosine kinase RET. RET is the signalling receptor for a known survival factor for dopamine neurons called glial cell line-derived neurotrophic factor (GDNF). Previously we showed that BT13 prevents the death of cultured dopamine neurons, stimulates dopamine release and activates pro-survival signalling cascades in naïve rodent brain. In the present study, we evaluate the effects of BT13 on motor imbalance and nigrostriatal dopamine neurons in a unilateral 6-hydroxydopamine rat model of PD. We show that BT13 alleviates motor dysfunction in experimental animals. Further studies are needed to make a conclusion whether BT13 can protect the integrity of the nigrostriatal dopamine system since even the positive control, GDNF protein, was unable to produce a clear neuroprotective effect in the model used in the present work. In contrast to GDNF, BT13 is able to cross the blood-brain barrier, which together with the ability to reduce motor symptoms of the disease makes it a valuable lead for further development as a potential disease-modifying agent to treat PD.
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Identifiers
33479704PMC7116613W3125469330What OpenQuestion holds
Registered trials
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