Creative Biolabs

Ataxia

Ataxia

Ataxia is a degenerative disease of the nervous system. It is a clinical manifestation indicating dysfunction of the parts of the nervous system that coordinates movement, such as the cerebellum. Ataxia can have an insidious onset with a chronic and progressive clinical course (e.g. spinocerebellar ataxias of genetic origin) or have an acute onset resulting from cerebellar infarction, hemorrhage, or infection. Ataxia usually manifests as:

  • Lack of coordination
  • Trouble eating and swallowing
  • Slurred speech
  • Difficulty in walking
  • Eye movement abnormalities
  • Deterioration of fine motor skills
  • Tremors
  • Gait abnormalities
  • Heart problems

Fig.1 Mitochondrial pathophysiology in Friedreich's Ataxia.Fig.1 Mitochondrial pathophysiology in Friedreich's Ataxia.

Ataxia can be a symptom of a multisystemic disorder, and an underlying etiology needs to be investigated. Ongoing discoveries of genetic abnormalities suggest the possible relations to mitochondrial dysfunction, related protein misfolding, abnormal mechanisms of DNA repair, oxidative stress, and abnormalities in cytoskeletal proteins.

Creative Biolabs is committed to promoting neurology disorders’ research and has developed a series of products to study those treatable and reversible etiologies of Ataxia, especially those from potentially life-threatening causes. These products portfolio includes recombinant proteins, antibodies, analytical/diagnostic kits and other small molecules.

Pathways and Genes Related to Ataxia

Super Pathways Top Affiliating Genes
A Double-Strand Break Repair XRCC1, TDP1, PNKP, LIG3, FEN1, ATM
TCR Signaling WASL, WAS, PIK3R5, CACNA1A, ATM, ACTA1
Chks in Checkpoint Regulation XRCC1, PNKP, LIG3, FEN1, ATM
G-protein Signaling RAC1 in Cellular Process WASL, WASF1, WAS, PIK3R5, ACTA1
Iron Metabolism in Placenta TFRC, ACO1
Mitochondrial Iron-sulfur Cluster Biogenesis LYRM4, FXN

For Research Use Only. Not For Clinical Use.
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