TY - JOUR
T1 - Phelan McDermid Syndrome
T2 - From Genetic Discoveries to Animal Models and Treatment
AU - Harony-Nicolas, Hala
AU - De Rubeis, Silvia
AU - Kolevzon, Alexander
AU - Buxbaum, Joseph D.
N1 - Publisher Copyright:
© SAGE Publications.
PY - 2015/12/1
Y1 - 2015/12/1
N2 - Phelan-McDermid syndrome or 22q13.3 deletion syndrome is a rare neurodevelopmental disorder characterized by generalized developmental delay, intellectual disability, absent or delayed speech, seizures, autism spectrum disorder, neonatal hypotonia, physical dysmorphic features, and recurrent medical comorbidities. Individuals with Phelan-McDermid syndrome have terminal deletions of the chromosomal region 22q13.3 encompassing SHANK3, a gene encoding a structural component of excitatory synapses indispensable for proper synaptogenesis and neuronal physiology, or point mutations within the gene. Here, we review the clinical aspects of the syndrome and the genetic findings shedding light onto the underlying etiology. We also provide an overview on the evidence from genetic studies and mouse models that supports SHANK3 haploinsufficiency as a major contributor of the neurobehavioral manifestations of Phelan-McDermid syndrome. Finally, we discuss how all these discoveries are uncovering the pathophysiology of Phelan-McDermid syndrome and are being translated into clinical trials for novel therapeutics ameliorating the core symptoms of the disorder.
AB - Phelan-McDermid syndrome or 22q13.3 deletion syndrome is a rare neurodevelopmental disorder characterized by generalized developmental delay, intellectual disability, absent or delayed speech, seizures, autism spectrum disorder, neonatal hypotonia, physical dysmorphic features, and recurrent medical comorbidities. Individuals with Phelan-McDermid syndrome have terminal deletions of the chromosomal region 22q13.3 encompassing SHANK3, a gene encoding a structural component of excitatory synapses indispensable for proper synaptogenesis and neuronal physiology, or point mutations within the gene. Here, we review the clinical aspects of the syndrome and the genetic findings shedding light onto the underlying etiology. We also provide an overview on the evidence from genetic studies and mouse models that supports SHANK3 haploinsufficiency as a major contributor of the neurobehavioral manifestations of Phelan-McDermid syndrome. Finally, we discuss how all these discoveries are uncovering the pathophysiology of Phelan-McDermid syndrome and are being translated into clinical trials for novel therapeutics ameliorating the core symptoms of the disorder.
KW - Phelan McDermid syndrome
KW - SHANK3
KW - animal models
KW - autism spectrum disorder
KW - postsynaptic density
UR - http://www.scopus.com/inward/record.url?scp=84947048874&partnerID=8YFLogxK
U2 - 10.1177/0883073815600872
DO - 10.1177/0883073815600872
M3 - Review article
C2 - 26350728
AN - SCOPUS:84947048874
SN - 0883-0738
VL - 30
SP - 1861
EP - 1870
JO - Journal of Child Neurology
JF - Journal of Child Neurology
IS - 14
ER -