You are here: Home / Research / Upcoming Seminars / Angelo Reggiani, Ph.D. - "Glycogen synthase kinase 3β (GSK-3β): More on its role in neuropsychiatric and neurodevelopmental disorders"

Angelo Reggiani, Ph.D. - "Glycogen synthase kinase 3β (GSK-3β): More on its role in neuropsychiatric and neurodevelopmental disorders"

Department of Drug Discovery, Italian Institute of Technology (IIT), Genova, Italy
When Feb 20, 2018
from 12:00 PM to 01:30 PM
Where tigem, Auditorium "Vesuvius"
Contact Name
Contact Phone 08119230659
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Abstract
Glycogen synthase kinase 3β (GSK-3β) is a serine/threonine protein kinase mediating phosphorylation onto serine and threonine amino acid residues of several target molecules. The enzyme is part of the so called canonical Wnt signaling pathway, is highly conserved across species  and is involved in the regulation of many cellular processes such as cellular proliferation, migration, glucose regulation, and apoptosis. Because of this widespread role aberrant GSK-3β activity has been linked to several disease conditions such as inflammation, neurodegeneration, alteration of circadian clock, neurodevelopmental and psychiatric disorders.
In my talk I will initially focus on how dysregulation of GSK-3β activity can affect mood disorders and I will discuss the potential therapeutic benefit of specific GSK-3 β inhibitors.
Then I will move to discuss the role of GSK-3β in Fragile X syndrome (FXS) also known as Martin-Bell disease, one of the most common genetic causes of autism, due to an expansion of the CGG triplet repeat within the Fragile X mental retardation 1 (FMR1) gene on the X chromosome, resulting in loss of fragile X mental retardation protein (FMRP) expression.
There is now growing evidence of an increased GSK-3β activity in FXS. For example, in FXS animal models a GSK3b overactivation  has been found,  as also confirmed by us in cultured fibroblasts from FXS patients.  Furthermore, we and others have found that in FMR-1 mice the chronic administration of selective inhibitors fully normalizes typical FXS behavioral deficits such as hyperactivity, cognitive disruption and reduced social interaction. Taken together, these findings strongly indicate that GSK3b  is dysregulated in FXS and that  selective inhibitors should ultimately provide benefit to patients. 

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