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Maternal 15q duplication syndrome (Dup15q)

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A 4-year-old with autism spectrum disorder and refractory epilepsy has hypotonia and moderate intellectual disability. CMA reveals a maternally inherited 15q11.2-q13.1 duplication.

  • Duplication of maternal 15q11.2-q13.1 (the Prader-Willi/Angelman region)
  • Two main forms:
    • Interstitial duplication (int dup(15)): 3 copies of 15q11-q13; milder
    • Isodicentric 15 (idic(15)): supernumerary marker chromosome → 4 copies (tetrasomy); more severe
  • Parent of origin matters: maternal duplications are symptomatic because extra copies of maternally expressed UBE3A (active in brain) drive the phenotype. Paternal duplications are typically milder or asymptomatic.
  • The most common copy-number variant identified in autism spectrum disorder (~1-3% of ASD cases).
  • Autism spectrum disorder (core feature)
  • Intellectual disability (mild to severe; idic(15) more severe than interstitial)
  • Epilepsy (often refractory; multiple seizure types including infantile spasms, atypical absence, tonic, atonic, myoclonic)
  • Hypotonia in infancy
  • Motor and language delays
  • Behavioral: anxiety, sensory processing differences
  • CMA is first-line: detects the duplication and distinguishes interstitial from idic(15)
  • Parental testing / methylation analysis to confirm maternal origin (essential for prognosis and recurrence counseling)
  • EEG often shows characteristic high-amplitude beta activity (~12-17 Hz), prominent in sleep; supportive but not diagnostic
  • FISH for chromosome 15 if a marker chromosome is seen on karyotype
  • Angelman syndrome (same region, opposite mechanism: loss of maternal UBE3A)
  • Prader-Willi syndrome (same region, loss of paternal contribution)
  • Idiopathic autism, other syndromic ASDs (PTEN, MECP2 duplication, fragile X)
  • Antiepileptic management; many patients need multi-drug regimens
  • Behavioral and developmental therapies (ABA, speech, OT, PT)
  • Annual neurology follow-up; EEG as indicated by seizure activity
  • Psychiatric support for anxiety
  • Recurrence counseling based on mechanism: most are de novo (low sibling recurrence), but maternal carriers of an interstitial duplication face up to 50% recurrence

Same neighborhood, opposite directions: 15q11-q13 is the imprinted "PWS/Angelman/Dup15q corner." Dup15q is the maternal-origin overdose counterpart to Angelman's maternal-origin loss: extra UBE3A → autism + epilepsy; absent UBE3A → Angelman.

Maternal matters: in a duplication report, the first thing to ask is parent of origin. Maternal duplication = symptomatic; paternal duplication = often silent.

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