Alberto Tozzi · Pharmacological enhancement of mGlu5 receptors rescues behavioral deficits in SHANK3 knock-out mice.

From Dr. Alberto Tozzi

Article1 min read·Published Oct 2026

Pharmacological enhancement of mGlu5 receptors rescues behavioral deficits in SHANK3 knock-out mice.

pubmed.ncbi.nlm.nih.gov

Pharmacological enhancement of mGlu5 receptors rescues behavioral deficits in SHANK3 knock-out mice.

Alberto Tozzi

SHANK3 (also called PROSAP2) genetic haploinsufficiency is thought to be the major cause of neuropsychiatric symptoms in Phelan-McDermid syndrome (PMS). PMS is a rare genetic disorder that causes a severe form of intellectual disability (ID), expressive language delays and other autistic features. Furthermore, a significant number of SHANK3 mutations have been identified in patients with autism sp…

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Article · Oct 2026 · 1 min read

In brief

In brief

This preclinical study demonstrates that pharmacological enhancement of metabotropic glutamate receptor 5 (mGlu5) can rescue behavioral and synaptic deficits in SHANK3 knockout mouse models of Phelan-McDermid syndrome. The findings suggest mGlu5 modulation as a potential therapeutic target for treating autism-related symptoms in patients with SHANK3 haploinsufficiency.

Written by the GCMD Library team from the article.

Alberto Tozzi

SHANK3 (also called PROSAP2) genetic haploinsufficiency is thought to be the major cause of neuropsychiatric symptoms in Phelan-McDermid syndrome (PMS). PMS is a rare genetic disorder that causes a severe form of intellectual disability (ID), expressive language delays and other autistic features. Furthermore, a significant number of SHANK3 mutations have been identified in patients with autism sp…

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