What is the Difference Between Prader Willi and Angelman Syndrome?
🆚 Go to Comparative Table 🆚Prader-Willi Syndrome (PWS) and Angelman Syndrome (AS) are two clinically distinct genetic disorders associated with multiple features. They share a similar genetic basis, as they involve genes located in the same region in the genome and are characterized by genomic imprinting. Genomic imprinting refers to the process where certain genes are preferentially expressed from either the maternal or paternal allele. Here are the key differences between the two syndromes:
- Chromosomal regions: Both PWS and AS are caused by abnormalities in the 15q11-q13 region on chromosome 15, but they result in the loss of either the maternal or paternal contribution, respectively.
- Causes: PWS is caused by the loss of multiple genes in the 15q11-q13 region, including the SNRPN gene, which encodes a component of mRNA splicing. AS, on the other hand, is associated with the loss of the maternal contribution in the same region. AS can also be caused by a mutation in the gene that causes it, while a comparable cause is not present in PWS.
- Symptoms: PWS patients suffer from extreme feeding problems, including hyperphagia (extreme, insatiable appetite and obsession with food) and developmental delays in motor skills due to decreased muscle tone. In contrast, AS patients exhibit symptoms such as severe intellectual disability, limited speech, seizures, and motor dysfunction.
- Molecular mechanisms: PWS and AS can result from deletions, uniparental disomy (both members of the pair come from the same parent), or imprinting mutations.
Management of both syndromes usually involves a multidisciplinary team that includes medical subspecialists and therapists.
Comparative Table: Prader Willi vs Angelman Syndrome
Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are genetic imprinting disorders that result from the absence or reduced expression of paternal or maternal genes in chromosome 15q. They are clinically distinct but share some overlapping features. Here is a table summarizing the differences between PWS and AS:
| Feature | Prader-Willi Syndrome (PWS) | Angelman Syndrome (AS) |
|---|---|---|
| Onset | Begins in early infancy | Develops in later infancy or early childhood |
| Hyperphagia | Present | Absent |
| Obesity | High risk | Low risk |
| Cognitive Impairment | Mild to moderate delays | Severe developmental delay |
| Speech | Delayed language development | Absent or minimal speech |
| Motor Milestones | Delayed | Severe developmental delay |
| Characteristic Facies | Oval face, almond-shaped eyes, high forehead, wide mouth, thin upper lip, nonpursing lips, underdeveloped jaw, and straight eyebrows | Flattened bridge of the nose, wide mouth with full lower lip, and protruding tongue |
| Genetic Cause | Deletion or uniparental disomy of paternal chromosome 15 or imprinting defect on paternal chromosome 15 | Deletion or uniparental disomy of maternal chromosome 15 or imprinting defect on maternal chromosome 15 |
The most common genetic cause of PWS is the deletion of the paternal chromosome 15q11q13 region, while the most common genetic cause of AS is the deletion of the maternal chromosome 15q11q13 region.
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