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IEMbase 0700: NDUFA12-related NADH dehydrogenase alpha subcomplex subunit 12 deficiency

Scope

Field Value
IEMbase ID 700
Nosology 7.1.14.01
Nosology code IEM0426
Gene NDUFA12
External IDs OMIM:618244; ORPHA:255241
Generated mapping CANDIDATE to COX11-Related_COX_Deficiency.yaml
Candidate DisMech targets Broad complex I/Leigh context only; no exact NDUFA12 target
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents autosomal recessive NDUFA12-related NADH dehydrogenase alpha subcomplex subunit 12 deficiency, also labeled mitochondrial complex I deficiency, nuclear type 23.

The biochemical row shows decreased fibroblast complex I activity through childhood. Clinical rows include growth retardation, Leigh syndrome, psychomotor retardation, dystonia, and hypotonia.

DisMech phenotype coverage

No exact NDUFA12 or MC1DN23 local target was identified.

Leigh_Syndrome.yaml covers the broad syndrome-level features: Leigh syndrome, complex I deficiency context, dystonia/movement disorder, hypotonia, and developmental impairment. It does not include NDUFA12 as a modeled causal gene.

The generated COX11-Related_COX_Deficiency.yaml candidate is a complex IV copper-delivery disorder. It shares the nuclear-type number 23 but belongs to MC4DN23 rather than MC1DN23.

Concordance and completeness

Judgement: true local gap with broad Leigh overlap only.

The IEMbase record is a sparse but specific NDUFA12 complex I disease. Generic Leigh syndrome can provide context, but the COX11 candidate is a wrong-complex number collision and should not be accepted as disease-level coverage.

Curation actions

  • Add a dedicated NDUFA12/MC1DN23 target if curated.
  • Reject COX11-related complex IV deficiency as exact coverage.
  • Preserve decreased fibroblast complex I activity, growth retardation, Leigh syndrome, psychomotor retardation, dystonia, and hypotonia.