Congress: Movement Disorder Society (MDS) International Congress 2026
Dates: October 4-8, 2026
Location: Seoul, Korea — COEX Convention and Exhibition Center
The MDS 2026 congress will feature dedicated sessions on ataxias and cerebellar disorders, covering both inherited genetic ataxias and acquired cerebellar conditions. These sessions will address the latest advances in diagnosis, genotype-phenotype correlations, disease-modifying therapies, and symptomatic management approaches["@mds"].
Spinocerebellar Ataxias (SCAs)
Overview
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Congress: Movement Disorder Society (MDS) International Congress 2026
Dates: October 4-8, 2026
Location: Seoul, Korea — COEX Convention and Exhibition Center
Overview
Mermaid diagram (expand to render)
The MDS 2026 congress will feature dedicated sessions on ataxias and cerebellar disorders, covering both inherited genetic ataxias and acquired cerebellar conditions. These sessions will address the latest advances in diagnosis, genotype-phenotype correlations, disease-modifying therapies, and symptomatic management approaches["@mds"].
Spinocerebellar Ataxias (SCAs)
Overview
The spinocerebellar ataxias are a heterogeneous group of autosomal dominant neurodegenerative disorders characterized by progressive cerebellar ataxia, often accompanied by other neurological features including oculomotor abnormalities, peripheral neuropathy, and cognitive impairment[@klockgether2018].
Major SCA Subtypes
SCA1 (ATXN1)
Gene: ATXN1 (CAG repeat expansion)
Features: Ataxia, spasticity, slow saccades
Therapeutic status: ASO clinical trials ongoing
SCA2 (ATXN2)
Gene: ATXN2 (CAG repeat expansion)
Features: Ataxia, slow saccades, myoclonus
SCA3 (ATXN3) — Machado-Joseph Disease
Gene: ATXN3 (CAG repeat expansion)
Features: Ataxia, spasticity, ophthalmoplegia
Most common SCA worldwide
SCA6 (CACNA1A)
Gene: CACNA1A (channelopathy)
Features: Pure cerebellar ataxia, episodic ataxia
Therapeutic: Calcium channel modulators under investigation
SCA7
Gene: ATXN7 (CAG repeat expansion)
Features: Ataxia with retinal degeneration
Emerging Therapies
Antisense Oligonucleotides (ASOs)
SCA1: ASOs targeting ATXN1 — preclinical and early clinical stages
SCA3: ASOs targeting ATXN3 — multiple preclinical studies
SCA2: ASOs targeting ATXN2 — proof-of-concept in models
Gene Therapy Approaches
AAV-vector delivery: Gene silencing and replacement strategies
CRISPR-based editing: Precise genetic correction in development
Symptomatic Management
CoQ10 supplementation: For mitochondrial function support
Physical therapy: Balance and gait training
Speech therapy: For dysarthria management[@ashida2021]
Friedreich's Ataxia
Overview
Friedreich's ataxia (FA) is an autosomal recessive disorder caused by GAA repeat expansions in the FXN gene, leading to frataxin deficiency and mitochondrial dysfunction. It is the most common inherited ataxia with onset typically in adolescence[@martindale2022].
Clinical Features
Progressive gait and limb ataxia
Dysarthria
Loss of deep tendon reflexes
Cardiomyopathy (in >50% of patients)
Diabetes mellitus (in ~30% of patients)
Scoliosis
Disease-Modifying Therapies
Frataxin Restoration
Gene therapy: AAV-based FXN replacement in preclinical development
Protein replacement: Frataxin analogs in early-stage trials
Mitochondrial Function
CoQ10 + vitamin E: Combination therapy trials
Idebenone: Antioxidant therapy (approved in some regions)
EPI-743 (vatiquinone): Phase 2/3 trials ongoing
Clinical Trials at MDS 2026
Novel antioxidant compounds
Gene therapy updates
Cardiac outcome measures in FA trials
Episodic Ataxias
Overview
The episodic ataxias are channelopathies characterized by recurrent ataxic episodes with complete or partial recovery between episodes.
Major Types
EA1 (KCNA1)
Gene: KCNA1 (potassium channel)
Features: Brief episodes (seconds to minutes), myokymia
Treatment: Acetazolamide, carbamazepine
EA2 (CACNA1A)
Gene: CACNA1A (calcium channel)
Features: Longer episodes (hours to days), ataxia, dysarthria
Treatment: Acetazolamide, 4-aminopyridine
Novel Therapies
Channel blockers: Targeted small molecules
Gene therapy: For severe EA2 cases
Cerebellar Degeneration: Non-Genetic Causes
Paraneoplastic Cerebellar Degeneration
Anti-Yo, anti-Hu, anti-Tr antibodies
Underlying oncology identification
Immunotherapy approaches
Alcohol-Related Cerebellar Degeneration
Chronic alcohol consumption as risk factor
Thiamine supplementation strategies
Autoimmune Ataxias
Gluten ataxia
Opsoclonus-myoclonus syndrome
Gait Ataxia
Clinical Assessment
Tandem walking evaluation
Dynamic gait index
Computerized gait analysis
Therapeutic Approaches
Rehabilitation
Intensive balance training
Gait-specific physical therapy
Assistive devices (canes, walkers)
Pharmacologic
Amantadine (controversial benefit)
4-Aminopyridine for cerebellar ataxia
Buspirone (serotonergic modulation)
Surgical
Deep brain stimulation for select cases
Cerebellar stimulation trials ongoing
Pediatric Ataxias
Ataxia-Telangiectasia
ATM gene mutations
Immunodeficiency and cancer risk
Novel therapeutic targets
Ataxia with Oculomotor Apraxia (AOA)
AOA1 (APT1 gene)
AOA2 (SETX gene)
Typical onset in childhood
Research Priorities at MDS 2026
Biomarkers
Serum neurofilament light chain (NfL) for disease progression
Imaging biomarkers (MRI volumetric measures)
Genetic testing standardization
Clinical Trial Design
Natural history study harmonization
Endpoint standardization (SARA, ICARS scales)
Biomarker-guided patient selection
Emerging Modalities
RNA therapeutics: ASOs and siRNA for genetic ataxias
[MDS Congress 2026](https://www.mdscongress.org) — Movement Disorder Society International Congress. October 4-8, 2026; Seoul, Korea.
[Klockgether T, et al., Ataxias: autosomal dominant and sporadic. Lancet Neurol. 2018](https://doi.org/10.1016/S1474-4422(18)30162-5)
[Ashida R, et al., Gene therapy for inherited ataxias. J Neurol. 2021](https://pubmed.ncbi.nlm.nih.gov/34569732/)
[Martindale J, et al., Spinocerebellar ataxia: current treatments and emerging therapies. Nat Rev Neurol. 2022](https://pubmed.ncbi.nlm.nih.gov/35654919/)