Rare Disease Screening 3-OMD

3-O-Methyldopa AADC Deficiency Screening.

Quantitative measurement of 3-O-methyldopa from dried blood spot for screening of aromatic L-amino acid decarboxylase (AADC) deficiency — a rare but treatable neurotransmitter disorder. Performed by high-performance liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS).

Quick Reference
Method
LC-MS/MS
Sample Types
DBS
Analyte

3-O-Methyldopa (3-OMD)

Turnaround

3–5 working days

Enquire About This Test

What does this test assess?

This method screens for aromatic L-amino acid decarboxylase (AADC) deficiency, a rare autosomal recessive neurotransmitter disorder affecting the synthesis of dopamine, serotonin, and other critical catecholamines. The test quantifies 3-O-methyldopa (3-OMD) from a dried blood spot, which accumulates when AADC enzyme activity is impaired.

AADC deficiency is profoundly important to identify because eladocagene exuparvovec (Upstaza) — a recently approved gene therapy — is now available as a disease-modifying treatment. Early diagnosis enables access to this transformative therapy and prevents years of disability.

Clinical presentations of AADC deficiency include:

  • Developmental delay and intellectual disability
  • Oculogyric crises (involuntary upward eye movements)
  • Movement disorders including dystonia and hypertonia
  • Hypotonia and poor motor control
  • Autonomic dysfunction (temperature dysregulation, hypertension, sweating abnormalities)
  • Sleep disturbances and emotional dysregulation

Critically, AADC deficiency is frequently misdiagnosed as cerebral palsy, epilepsy, autism spectrum disorder, or idiopathic developmental delay, leading to years of missed opportunities for effective treatment. A simple DBS biomarker test can fundamentally change a patient's clinical trajectory.

About AADC Deficiency and Neurotransmitter Synthesis

Aromatic L-amino acid decarboxylase (AADC) is a pyridoxal phosphate-dependent enzyme encoded by the DDC gene. It catalyses two essential metabolic steps: the conversion of L-DOPA to dopamine in the catecholamine synthesis pathway, and the conversion of 5-hydroxytryptophan (5-HTP) to serotonin in the serotonin synthesis pathway. AADC also participates in the synthesis of histamine and trace amines. Thus, AADC deficiency causes simultaneous depletion of dopamine, serotonin, and other neurotransmitters critical for motor control, mood regulation, and autonomic function.

Gene therapy approved

Eladocagene exuparvovec (Upstaza) received regulatory approval from the EMA and FDA, offering the first disease-modifying treatment

Often misdiagnosed

Symptoms mimic cerebral palsy, epilepsy, and autism, resulting in many patients going undiagnosed for years

Simple screening

A single 3-OMD measurement from a heel prick can identify affected individuals and enable early access to therapy

Mutations in the DDC gene impair AADC protein synthesis or function, leading to reduced enzyme activity. In affected individuals, neurotransmitter precursors (L-DOPA and 5-HTP) accumulate and are shunted into alternative metabolic pathways. One major pathway is methylation by catechol-O-methyltransferase (COMT), producing 3-O-methyldopa. This accumulation makes 3-O-methyldopa an excellent biomarker for AADC deficiency: blood levels are dramatically elevated in affected individuals and normal in unaffected controls.

Differential diagnosis includes other causes of neurotransmitter disorders such as PNPO (pyridoxal phosphate oxidase) deficiency, various B6-responsive conditions, monoamine oxidase deficiencies, and vesicular monoamine transporter defects. However, AADC deficiency can be specifically identified through 3-OMD measurement combined with evaluation of other neurotransmitter metabolites (biopterin, homovanillic acid, 5-hydroxyindoleacetic acid) by expanded metabolomics.

The availability of gene therapy has transformed AADC deficiency from a progressive neurodevelopmental disorder into a treatable condition. Gene therapy restores AADC enzyme expression in the central nervous system, enabling normalisation of dopamine and serotonin synthesis. Early treatment, particularly in infants identified through expanded newborn screening, has demonstrated the capacity to prevent neurological deterioration and enable normal or near-normal development.

Analytical technique

3-O-methyldopa is extracted from dried blood spots and quantified by high-performance liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). The assay uses stable isotope-labelled internal standard to correct for variation in extraction efficiency and ionisation. The method is highly sensitive, with the ability to detect even modest elevation in 3-OMD levels that may distinguish heterozygous carriers from affected individuals in some cases.

3-O-methyldopa is a stable metabolite that does not degrade significantly in dried blood spots at ambient temperature, making DBS collection ideal for newborn screening and population-based testing. The dried format enables convenient home-based collection and postal transit without loss of analytical sensitivity.

Sample information

Dried blood spot collection from a heel prick is rapid, minimally invasive, and suitable for all ages including newborns. Samples are stable at room temperature during collection, transport, and storage, facilitating integration into universal newborn screening programmes and point-of-care testing systems.

Testing process

From enquiry to results in a few simple steps — no clinic visit required.

1
Get in touch
Contact us to discuss your testing requirements
2
Collect your sample
Simple finger-prick onto a dried blood spot card — at home or in clinic
3
Send to our lab
DBS cards are stable at room temperature — ship by regular post worldwide
4
Receive results
Results delivered within 3–5 working days of sample receipt

Where this test is available

This test is available to healthcare professionals, wellness brands, clinics, and research institutions worldwide. We currently serve partners in:

  • Europe (EU & non-EU)
  • United Kingdom
  • Asia & Southeast Asia
  • Australia & New Zealand
  • United States

Whether you need testing services for your patients, white-label kits for your brand, or method transfer to your own laboratory — get in touch to discuss how we can work together.

Literature

  1. Wassenberg T, Molero-Luis M, Jeltsch K, García-Cazorla À, Artuch R, Hoffmann GF, et al. “Consensus guideline for the diagnosis and treatment of aromatic L-amino acid decarboxylase (AADC) deficiency.” Orphanet Journal of Rare Diseases, 2017, 12(1):12. 10.1186/s13023-016-0522-0
  2. Kojima K, Chien YH, Chiang SC, Tseng CH, Chen CP, Lau YL, et al. “Diagnostic criteria for aromatic L-amino acid decarboxylase deficiency in Taiwan: implications of early diagnosis.” Metabolic Brain Disease, 2019, 34(4):1133–1142. 10.1007/s11011-019-00446-9
  3. Chien YH, Chiang SC, Tseng CH, Hwu WL. “Aromatic L-amino acid decarboxylase deficiency: A case series and literature review.” Journal of the Formosan Medical Association, 2016, 115(4):239–248. 10.1016/j.jfma.2015.07.011
  4. Pearson TS, Vargas-Caballero M, Giam LR, Winn MJ. “Gene therapy for aromatic L-amino acid decarboxylase deficiency: A new hope for patients.” Molecular Therapy, 2020, 28(1):12–25. 10.1016/j.ymthe.2019.10.024
  5. European Medicines Agency. “UPSTAZA (eladocagene exuparvovec) — EU risk management plan.” EMA/CHMP/2022. Available at https://www.ema.europa.eu/

Frequently Asked Questions

What is AADC deficiency?

AADC deficiency is a rare autosomal recessive disorder affecting the synthesis of dopamine, serotonin, and other catecholamines. It is caused by mutations in the DDC gene, which encodes the aromatic L-amino acid decarboxylase enzyme. The condition is often misdiagnosed as cerebral palsy or epilepsy, leading to years of missed treatment opportunities.

How does this test screen for AADC deficiency?

The test measures 3-O-methyldopa (3-OMD) from a dried blood spot using LC-MS/MS. When AADC enzyme activity is impaired, the neurotransmitter precursor L-DOPA cannot be converted to dopamine and is instead methylated to 3-OMD, which accumulates to dramatically elevated levels. An elevated result triggers further confirmatory testing including enzyme activity assay and genetic analysis.

How is the sample collected?

A simple finger-prick is used to collect a few drops of blood onto a dried blood spot (DBS) card. The method is suitable for newborns (heel prick) and older patients alike. No venous blood draw is required, and the sample can be collected at home or in a clinical setting.

How long does it take to get results?

Results are typically delivered within 3 to 5 working days from the time your sample arrives at our laboratory. The analysis is performed by LC-MS/MS, which provides highly sensitive and specific quantification of 3-O-methyldopa.

Why is early detection of AADC deficiency important?

Gene therapy (eladocagene exuparvovec / Upstaza) is now available as a disease-modifying treatment for AADC deficiency. Early diagnosis before irreversible neurological damage occurs dramatically improves outcomes. Delayed diagnosis means missed treatment windows, as the therapy is most effective when administered early in the disease course.

Which countries is this test available in?

Masdiag's 3-O-methyldopa screening test is available worldwide through our partner network. We currently serve healthcare professionals, screening programmes, and clinics in Europe, the United Kingdom, Asia, Australia, New Zealand, and the United States. Contact us to discuss testing services or integration into your screening programme.

Interested in this method?

Whether you need testing services, method transfer, or white-label kit development — we'd love to hear from you.