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Hallervorden-Spatz disease; pantothenate kinase associated neurodegeneration (PKAN); neurodegeneration with brain iron accumulation type 1 (NBIA1); pigmentary pallidal degeneration

Epidemiology: 1) often presents in infancy 2) onset can occur as adult Pathology: - iron deposition & axonal spheroids seen in globus pallidus, substantia nigra & medulla - Lewy body (LB)-like intraneuronal inclusions - glial inclusions - neurofibrillary tangles - SNCA is found in LB-like inclusions, glial inclusions & spheroids - SNCB & SNCG are found in axonal spheroids, but not in inclusions Genetics: 1) autosomal recessive disorder 2) associated with mutations in pantothenate kinase 2 gene Clinical manifestations: - delayed motor & language development - deterioration of gait & hand skills ~3 - 6 yrs - dysarthria - aphasia - spasticity - bilateral retinopathy - optic atrophy - seizures - acanthocytosis Management: - prognosis: death usually occurs ~ 10 yrs after onset

Interactions

disease interactions

Related

alpha-synuclein; non-A beta component of AD amyloid; non-A4 component of amyloid; NACP (SNCA, NACP, PARK1) neurodegeneration with brain iron accumulation 2A; infantile neuroaxonal dystrophy; Seitelberger disease pantothenate kinase

General

basal ganglia disease neurodegeneration with brain iron accumulation synucleinopathy (includes alpha-synucleinopathy)

Database Correlations

OMIM correlations MORBIDMAP 606157

References

  1. OMIM #234200
  2. Giasson BI et al Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions. Science 290:985-9, 2000 PMID: 11062131
  3. Neurodegeneration with Brain Iron Accumulation Information Page https://www.ninds.nih.gov/Disorders/All-Disorders/Neurodegeneration-Brain-Iron-Accumulation-Information-Page