International Journal For Multidisciplinary Research
E-ISSN: 2582-2160
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Impact Factor: 9.24
A Widely Indexed Open Access Peer Reviewed Multidisciplinary Bi-monthly Scholarly International Journal
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Volume 8 Issue 2
March-April 2026
Indexing Partners
Ataxia as Symptom or Disease: A Review of Mechanisms of Primary Ataxia and Acquired Ataxia.
| Author(s) | Ms. Katherina Tereshchenkov |
|---|---|
| Country | United States |
| Abstract | This review examines the mechanisms underlying acquired and primary ataxias, emphasizing both their shared features and distinctions. In both primary and acquired forms, cerebellar dysfunction develops through damage to Purkinje neurons and disruptions in calcium signaling pathways that regulate excitability and motor coordination. Acquired ataxias most often result from external factors such as toxins, immune reactions, or neurodegenerative processes. Because these causes can sometimes be identified and treated, acquired ataxias may stabilize or even improve when addressed early. Primary ataxias, in contrast, arise from genetic mutations that drive progressive and irreversible cerebellar degeneration. Current treatments are largely supportive, though new research is investigating gene modulation, calcium channel regulation, and mitochondrial protection as potential therapeutic strategies. Recent advances in genetic testing and neuroimaging have improved classification and diagnostic accuracy. However, reliable biomarkers that clearly separate primary and acquired ataxias remain limited. By comparing overlapping and distinct mechanisms, this review emphasizes the importance of early diagnosis and ongoing research into calcium signaling and Purkinje neuron biology to guide future therapies for movement disorders. |
| Keywords | ataxia, purkinje neurons, calcium signaling, acquired ataxia, primary ataxia |
| Field | Biology > Medical / Physiology |
| Published In | Volume 7, Issue 5, September-October 2025 |
| Published On | 2025-10-21 |
| DOI | https://doi.org/10.36948/ijfmr.2025.v07i05.57036 |
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E-ISSN 2582-2160
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IJFMR DOI prefix is
10.36948/ijfmr
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