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A clinically and genetically heterogeneous group of neurodegenerative diseases characterized by a slowly progressive ataxia of gait, stance and limbs, dysarthria and/or oculomotor disorder, due to cerebellar degeneration in the absence of coexisting diseases. The degenerative process can be limited to the cerebellum (ADCA type 3) or may additionally involve the retina (ADCA type 2), optic nerve, ponto-medullary systems, basal ganglia, cerebral cortex, spinal tracts or peripheral nerves (ADCA typ
Dual chemical chaperone approach targeting IRE1α and PERK pathways to reduce unfolded protein response activation caused by mutant CACNA1A, PRKCG, and other ADCA-associated proteins accumulating in cerebellar Purkinje cell endoplasmic reticulum
Enhancing mGluR1 signaling at parallel fiber-Purkinje cell synapses to restore long-term depression and motor learning capacity compromised by ITPR1, CACNA1A, or PRKCG mutations through PKC and IP3 pathway normalization
Gastrodin from Gastrodia elata enhances GABAA receptor sensitivity and increases GAD67 expression in cerebellar Purkinje cells, counteracting the excitotoxicity and motor dysfunction characteristic of ADCA mutations in SCA1/ATXN1 and SCA6/CACNA1A
MitoQ delivery of CoQ10 specifically to cerebellar mitochondria to restore electron transport chain function and reduce ROS production in neurons affected by ANO10, SETX, and other ADCA mutations causing mitochondrial dysfunction
Bacosides from Bacopa monnieri induce HSP70 and HSP40 chaperone expression, facilitating proper folding of mutant ataxin proteins (ATXN1, ATXN2, ATXN3) and reducing polyglutamine aggregation in cerebellar neurons
Temporary blood-brain barrier opening specifically in cerebellar regions using focused ultrasound to enhance delivery of neuroprotective compounds (BDNF, small molecules) that cannot normally cross BBB to target affected Purkinje cells
Saikosaponins and other compounds in Saiko-keishi-to promote anti-inflammatory M2 microglial activation and reduce IL-1β, TNF-α production that contributes to cerebellar neurodegeneration in ADCA through NLRP3 inflammasome inhibition