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Article ; Online: Fragile X syndrome: from gene discovery to therapy.

Heulens, Inge / Kooy, Frank

Frontiers in bioscience (Landmark edition)

2011 Volume 16, Issue 4, Page(s) 1211–1232

Abstract: A dynamic mutation in the fragile X mental retardation 1 gene, FMR1, was found to cause fragile X syndrome almost 20 years ago. Since, a wealth of information regarding the function of the gene has been gathered. It plays a role in RNA transport and ... ...

Abstract	A dynamic mutation in the fragile X mental retardation 1 gene, FMR1, was found to cause fragile X syndrome almost 20 years ago. Since, a wealth of information regarding the function of the gene has been gathered. It plays a role in RNA transport and stability and RNA-binding influences the function of a multitude of other genes. In this review, we focus on the recent knowledge of molecular and biochemical pathways shown to be relevant in the fragile X syndrome and how these insights have led to a first series of clinical trials in fragile X patients.
MeSH term(s)	Animals ; Antipsychotic Agents/therapeutic use ; Disease Models, Animal ; Drosophila melanogaster ; Fragile X Mental Retardation Protein/genetics ; Fragile X Mental Retardation Protein/metabolism ; Fragile X Syndrome/genetics ; Fragile X Syndrome/therapy ; Humans ; Hypothalamo-Hypophyseal System/physiology ; Mice ; Pituitary-Adrenal System/physiology ; Receptors, GABA-A/drug effects ; Receptors, GABA-A/physiology ; Receptors, Metabotropic Glutamate/drug effects ; Receptors, Metabotropic Glutamate/physiology ; Zebrafish ; rho GTP-Binding Proteins/physiology
Chemical Substances	Antipsychotic Agents ; Receptors, GABA-A ; Receptors, Metabotropic Glutamate ; Fragile X Mental Retardation Protein (139135-51-6) ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2011-01-01
Publishing country	Singapore
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2704569-9
ISSN	2768-6698 ; 1093-9946
ISSN (online)	2768-6698
ISSN	1093-9946
DOI	10.2741/3785
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Article ; Online: Metabonomics adds a new dimension to fragile X syndrome.

Heulens, Inge / Braat, Sien / Kooy, R Frank

Genome medicine

2011 Volume 3, Issue 12, Page(s) 80

Abstract: Fragile X syndrome is the most common cause of inherited intellectual disability, but the underlying pathophysiology is complex and effective treatments are lacking. In a recent study of fragile X mental retardation 1 (Fmr1) knockout mice, the metabolic ... ...

Abstract	Fragile X syndrome is the most common cause of inherited intellectual disability, but the underlying pathophysiology is complex and effective treatments are lacking. In a recent study of fragile X mental retardation 1 (Fmr1) knockout mice, the metabolic profile of the fragile X brain was determined using proton high-resolution magic angle spinning nuclear magnetic resonance spectroscopy. This analysis revealed deficiencies in four metabolic categories: neurotransmission, osmoregulation, energy metabolism and oxidative stress response. Abnormalities in the metabolic phenotype were linked to the fragile X mental retardation protein using an integrated metabolome and interactome mapping approach, allowing a global picture of the disorder to emerge.
Language	English
Publishing date	2011-12-28
Publishing country	England
Document type	Journal Article
ZDB-ID	2484394-5
ISSN	1756-994X ; 1756-994X
ISSN (online)	1756-994X
ISSN	1756-994X
DOI	10.1186/gm296
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Article ; Online: Pharmacological treatment of fragile X syndrome with GABAergic drugs in a knockout mouse model.

Heulens, Inge / D'Hulst, Charlotte / Van Dam, Debby / De Deyn, Peter P / Kooy, R Frank

Behavioural brain research

2012 Volume 229, Issue 1, Page(s) 244–249

Abstract: Molecular and electrophysiological studies have provided evidence for a general downregulation of the GABAergic system in the Fmr1 knockout mouse. GABA(A) receptors are the main inhibitory receptors in the brain and the GABA(A) receptor was proposed as a ...

Abstract	Molecular and electrophysiological studies have provided evidence for a general downregulation of the GABAergic system in the Fmr1 knockout mouse. GABA(A) receptors are the main inhibitory receptors in the brain and the GABA(A) receptor was proposed as a novel target for treatment of the fragile X syndrome, the most frequent form of intellectual disability. This study examined the functionality of the GABA(A) receptor in rotarod and elevated plus maze tests with fragile X mice treated with GABA(A) receptor agonists, the benzodiazepine diazepam and the neuroactive steroid alphaxalone. In addition, the effect of GABA(A) receptor activation on the audiogenic seizure activity was determined. We proved that the GABA(A) receptor is still sensitive to GABAergic drugs as the sedative effect of diazepam resulted in a decreased latency time on the rotarod and alphaxalone had a clear anxiolytic effect in the elevated plus maze, decreasing the frequency of entries, the total time spent and the path length in the closed arms. We also observed that treatment with ganaxolone could rescue audiogenic seizures in Fmr1 knockout mice. These findings support the hypothesis that the GABA(A) receptor is a potential therapeutic target for fragile X syndrome.
MeSH term(s)	Analysis of Variance ; Anesthetics/therapeutic use ; Animals ; Diazepam/therapeutic use ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Epilepsy, Reflex/drug therapy ; Epilepsy, Reflex/genetics ; Fragile X Mental Retardation Protein/genetics ; Fragile X Syndrome/drug therapy ; Fragile X Syndrome/genetics ; Fragile X Syndrome/physiopathology ; GABA Modulators/therapeutic use ; Male ; Maze Learning/drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/drug effects ; Pregnanediones/therapeutic use ; Psychomotor Performance/drug effects ; Rotarod Performance Test
Chemical Substances	Anesthetics ; Fmr1 protein, mouse ; GABA Modulators ; Pregnanediones ; Fragile X Mental Retardation Protein (139135-51-6) ; alphaxalone (BD07M97B2A) ; Diazepam (Q3JTX2Q7TU)
Language	English
Publishing date	2012-04-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2012.01.031
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Article ; Online: Involvement and therapeutic potential of the GABAergic system in the fragile X syndrome.

Heulens, Inge / D'Hulst, Charlotte / Braat, Sien / Rooms, Liesbeth / Kooy, R Frank

TheScientificWorldJournal

2010 Volume 10, Page(s) 2198–2206

Abstract: Many drugs have been developed that are able to modulate the GABAergic system, which is involved in anxiety, depression, epilepsy, insomnia, and learning and memory. The recent observation that the GABA(A) receptor is underexpressed in the fragile X ... ...

Abstract	Many drugs have been developed that are able to modulate the GABAergic system, which is involved in anxiety, depression, epilepsy, insomnia, and learning and memory. The recent observation that the GABA(A) receptor is underexpressed in the fragile X syndrome, an inherited mental retardation disorder, therefore raised hopes for targeted therapy of the disorder. This review summarizes the lines of evidence that demonstrate a malfunction of the GABAergic system. The GABAergic system clearly emerges as an attractive target for therapy of the fragile X syndrome, and thus provides an excellent example of how genetic research can lead to unique opportunities for treatment.
MeSH term(s)	Animals ; Fragile X Syndrome/drug therapy ; Fragile X Syndrome/metabolism ; GABA Agonists/therapeutic use ; Humans ; Models, Biological ; Receptors, GABA-A/metabolism ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	GABA Agonists ; Receptors, GABA-A ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2010-11-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2075968-X
ISSN	1537-744X ; 1537-744X
ISSN (online)	1537-744X
ISSN	1537-744X
DOI	10.1100/tsw.2010.211
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Article ; Online: The GABAA receptor is an FMRP target with therapeutic potential in fragile X syndrome.

Braat, Sien / D'Hulst, Charlotte / Heulens, Inge / De Rubeis, Silvia / Mientjes, Edwin / Nelson, David L / Willemsen, Rob / Bagni, Claudia / Van Dam, Debby / De Deyn, Peter P / Kooy, R Frank

Cell cycle (Georgetown, Tex.)

2015 Volume 14, Issue 18, Page(s) 2985–2995

Abstract: Previous research indicates that the GABAAergic system is involved in the pathophysiology of the fragile X syndrome, a frequent form of inherited intellectual disability and associated with autism spectrum disorder. However, the molecular mechanism ... ...

Abstract	Previous research indicates that the GABAAergic system is involved in the pathophysiology of the fragile X syndrome, a frequent form of inherited intellectual disability and associated with autism spectrum disorder. However, the molecular mechanism underlying GABAAergic deficits has remained largely unknown. Here, we demonstrate reduced mRNA expression of GABAA receptor subunits in the cortex and cerebellum of young Fmr1 knockout mice. In addition, we show that the previously reported underexpression of specific subunits of the GABAA receptor can be corrected in YAC transgenic rescue mice, containing the full-length human FMR1 gene in an Fmr1 knockout background. Moreover, we demonstrate that FMRP directly binds several GABAA receptor mRNAs. Finally, positive allosteric modulation of GABAA receptors with the neurosteroid ganaxolone can modulate specific behaviors in Fmr1 knockout mice, emphasizing the therapeutic potential of the receptor.
MeSH term(s)	Animals ; Fragile X Mental Retardation Protein/genetics ; Fragile X Mental Retardation Protein/metabolism ; Fragile X Mental Retardation Protein/physiology ; Fragile X Syndrome/therapy ; GABA-A Receptor Antagonists/pharmacology ; Genotype ; Humans ; Male ; Mice ; Mice, Knockout ; Mice, Transgenic ; Pregnanolone/analogs & derivatives ; Pregnanolone/pharmacology ; RNA, Messenger/metabolism ; Receptors, GABA-A/genetics ; Receptors, GABA-A/metabolism
Chemical Substances	Fmr1 protein, mouse ; GABA-A Receptor Antagonists ; RNA, Messenger ; Receptors, GABA-A ; Fragile X Mental Retardation Protein (139135-51-6) ; ganaxolone (98WI44OHIQ) ; Pregnanolone (BXO86P3XXW)
Language	English
Publishing date	2015-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/15384101.2014.989114
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Article ; Online: Involvement and Therapeutic Potential of the GABAergic System in the Fragile X Syndrome

Inge Heulens / Charlotte D'Hulst / Sien Braat / Liesbeth Rooms / R. Frank Kooy

The Scientific World Journal, Vol 10, Pp 2198-

2010 Volume 2206

Abstract: Many drugs have been developed that are able to modulate the GABAergic system, which is involved in anxiety, depression, epilepsy, insomnia, and learning and memory. The recent observation that the GABAA receptor is underexpressed in the fragile X ... ...

Abstract	Many drugs have been developed that are able to modulate the GABAergic system, which is involved in anxiety, depression, epilepsy, insomnia, and learning and memory. The recent observation that the GABAA receptor is underexpressed in the fragile X syndrome, an inherited mental retardation disorder, therefore raised hopes for targeted therapy of the disorder. This review summarizes the lines of evidence that demonstrate a malfunction of the GABAergic system. The GABAergic system clearly emerges as an attractive target for therapy of the fragile X syndrome, and thus provides an excellent example of how genetic research can lead to unique opportunities for treatment.
Keywords	Technology ; T ; Medicine ; R ; Science ; Q
Language	English
Publishing date	2010-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Positron Emission Tomography (PET) Quantification of GABAA Receptors in the Brain of Fragile X Patients.

D'Hulst, Charlotte / Heulens, Inge / Van der Aa, Nathalie / Goffin, Karolien / Koole, Michel / Porke, Kathleen / Van De Velde, Marc / Rooms, Liesbeth / Van Paesschen, Wim / Van Esch, Hilde / Van Laere, Koen / Kooy, R Frank

PloS one

2015 Volume 10, Issue 7, Page(s) e0131486

Abstract: Over the last several years, evidence has accumulated that the GABAA receptor is compromised in animal models for fragile X syndrome (FXS), a common hereditary form of intellectual disability. In mouse and fly models, agonists of the GABAA receptor were ... ...

Abstract	Over the last several years, evidence has accumulated that the GABAA receptor is compromised in animal models for fragile X syndrome (FXS), a common hereditary form of intellectual disability. In mouse and fly models, agonists of the GABAA receptor were able to rescue specific consequences of the fragile X mutation. Here, we imaged and quantified GABAA receptors in vivo in brain of fragile X patients using Positron Emission Topography (PET) and [11C]flumazenil, a known high-affinity and specific ligand for the benzodiazepine site of GABAA receptors. We measured regional GABAA receptor availability in 10 fragile X patients and 10 control subjects. We found a significant reduction of on average 10% in GABAA receptor binding potential throughout the brain in fragile X patients. In the thalamus, the brain region showing the largest difference, the GABAA receptor availability was even reduced with 17%. This is one of the first reports of a PET study of human fragile X brain and directly demonstrates that the GABAA receptor availability is reduced in fragile X patients. The study reinforces previous hypotheses that the GABAA receptor is a potential target for rational pharmacological treatment of fragile X syndrome.
MeSH term(s)	Adolescent ; Adult ; Animals ; Brain/diagnostic imaging ; Brain/metabolism ; Female ; Flumazenil/administration & dosage ; Fragile X Syndrome/diagnostic imaging ; Fragile X Syndrome/metabolism ; Humans ; Male ; Mice ; Middle Aged ; Positron-Emission Tomography ; Radiography ; Receptors, GABA-A/metabolism
Chemical Substances	Receptors, GABA-A ; Flumazenil (40P7XK9392)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0131486
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Article ; Online: Craniofacial characteristics of fragile X syndrome in mouse and man.

Heulens, Inge / Suttie, Michael / Postnov, Andrei / De Clerck, Nora / Perrotta, Concetta S / Mattina, Teresa / Faravelli, Francesca / Forzano, Francesca / Kooy, R Frank / Hammond, Peter

European journal of human genetics : EJHG

2012 Volume 21, Issue 8, Page(s) 816–823

Abstract: For a disorder as common as fragile X syndrome, the most common hereditary form of cognitive impairment, the facial features are relatively ill defined. An elongated face and prominent ears are the most commonly accepted dysmorphic hallmarks. We analysed ...

Abstract	For a disorder as common as fragile X syndrome, the most common hereditary form of cognitive impairment, the facial features are relatively ill defined. An elongated face and prominent ears are the most commonly accepted dysmorphic hallmarks. We analysed 3D facial photographs of 51 males and 15 females with full FMR1 mutations and 9 females with a premutation using dense-surface modelling techniques and a new technique that forms a directed graph with normalized face shapes as nodes and edges linking those with closest dysmorphism. In addition to reconfirming known features, we confirmed the occurrence of some at an earlier age than previously recorded. We also identified as yet unrecorded facial characteristics such as reduced facial depth, hypoplasticity of the nasal bone-cartilage interface and narrow mid-facial width exaggerating ear prominence. As no consistent craniofacial abnormalities had been reported in animal models, we analysed micro-CT images of the fragile X mouse model. Results indicated altered dimensions in the mandible and both outer and inner skull, with the latter potentially reflecting differences in neuroanatomy. We extrapolated the mouse results to face shape differences of the human fragile X face.
MeSH term(s)	Adolescent ; Adult ; Animals ; Child ; Child, Preschool ; Craniofacial Abnormalities/genetics ; Disease Models, Animal ; Female ; Fragile X Mental Retardation Protein/genetics ; Fragile X Syndrome/genetics ; Fragile X Syndrome/pathology ; Humans ; Male ; Mandible/abnormalities ; Mandible/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; Models, Anatomic ; Mutation ; Skull/abnormalities ; Skull/metabolism ; X-Ray Microtomography ; Young Adult
Chemical Substances	FMR1 protein, human ; Fragile X Mental Retardation Protein (139135-51-6)
Language	English
Publishing date	2012-12-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/ejhg.2012.265
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Article ; Online: Positron Emission Tomography (PET) Quantification of GABAA Receptors in the Brain of Fragile X Patients.

Charlotte D'Hulst / Inge Heulens / Nathalie Van der Aa / Karolien Goffin / Michel Koole / Kathleen Porke / Marc Van De Velde / Liesbeth Rooms / Wim Van Paesschen / Hilde Van Esch / Koen Van Laere / R Frank Kooy

PLoS ONE, Vol 10, Iss 7, p e

2015 Volume 0131486

Abstract	Over the last several years, evidence has accumulated that the GABAA receptor is compromised in animal models for fragile X syndrome (FXS), a common hereditary form of intellectual disability. In mouse and fly models, agonists of the GABAA receptor were able to rescue specific consequences of the fragile X mutation. Here, we imaged and quantified GABAA receptors in vivo in brain of fragile X patients using Positron Emission Topography (PET) and [11C]flumazenil, a known high-affinity and specific ligand for the benzodiazepine site of GABAA receptors. We measured regional GABAA receptor availability in 10 fragile X patients and 10 control subjects. We found a significant reduction of on average 10% in GABAA receptor binding potential throughout the brain in fragile X patients. In the thalamus, the brain region showing the largest difference, the GABAA receptor availability was even reduced with 17%. This is one of the first reports of a PET study of human fragile X brain and directly demonstrates that the GABAA receptor availability is reduced in fragile X patients. The study reinforces previous hypotheses that the GABAA receptor is a potential target for rational pharmacological treatment of fragile X syndrome.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Global distribution of the most prevalent deletions causing hypotonia-cystinuria syndrome.

Martens, Kevin / Heulens, Inge / Meulemans, Sandra / Zaffanello, Marco / Tilstra, David / Hes, Frederik J / Rooman, Raoul / François, Inge / de Zegher, Francis / Jaeken, Jaak / Matthijs, Gert / Creemers, John W M

European journal of human genetics : EJHG

2007 Volume 15, Issue 10, Page(s) 1029–1033

Abstract: Hypotonia-cystinuria syndrome (HCS) is a recessive disorder caused by microdeletions of SLC3A1 and PREPL on chromosome 2p21. Patients present with generalized hypotonia at birth, failure to thrive, growth retardation and cystinuria type I. While the ... ...

Abstract	Hypotonia-cystinuria syndrome (HCS) is a recessive disorder caused by microdeletions of SLC3A1 and PREPL on chromosome 2p21. Patients present with generalized hypotonia at birth, failure to thrive, growth retardation and cystinuria type I. While the initially described HCS families live in small regions in Belgium and France, we have now identified HCS alleles in patients and carriers from the Netherlands, Italy, Canada and United States of America. Surprisingly, among the nine deletions detected in those patients, only one novel deletion was found. Furthermore, one previously described deletion was found six times, another twice. Finally, we have investigated the frequency of both deletions using a random Belgian cohort. Given the global occurrence, HCS should be considered in the differential diagnosis of neonatal hypotonia.
MeSH term(s)	Amino Acid Transport Systems, Basic/genetics ; Amino Acid Transport Systems, Neutral/genetics ; Chromosome Deletion ; Chromosomes, Human, Pair 2/genetics ; Cystinuria/genetics ; DNA Primers/genetics ; Genes, Recessive ; Genetics, Population ; Haplotypes ; Homozygote ; Humans ; Infant, Newborn ; Muscle Hypotonia/congenital ; Muscle Hypotonia/genetics ; Phenotype ; Polymerase Chain Reaction ; Serine Endopeptidases/genetics ; Syndrome
Chemical Substances	Amino Acid Transport Systems, Basic ; Amino Acid Transport Systems, Neutral ; DNA Primers ; SLC3A1 protein, human ; Serine Endopeptidases (EC 3.4.21.-) ; prolyl oligopeptidase (EC 3.4.21.26)
Language	English
Publishing date	2007-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/sj.ejhg.5201881
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