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Article ; Online: A form of inherited hyperferritinemia associated with bi-allelic pathogenic variants of STAB1.

Monfrini, Edoardo / Pelucchi, Sara / Hollmén, Maija / Viitala, Miro / Mariani, Raffaella / Bertola, Francesca / Majore, Silvia / Di Fonzo, Alessio / Piperno, Alberto

American journal of human genetics

2023 Volume 110, Issue 8, Page(s) 1436–1443

Abstract: Hyperferritinemia is a frequent finding in several conditions, both genetic and acquired. We previously studied eleven healthy subjects from eight different families presenting with unexplained hyperferritinemia. Their findings suggested the existence of ...

Abstract	Hyperferritinemia is a frequent finding in several conditions, both genetic and acquired. We previously studied eleven healthy subjects from eight different families presenting with unexplained hyperferritinemia. Their findings suggested the existence of an autosomal-recessive disorder. We carried out whole-exome sequencing to detect the genetic cause of hyperferritinemia. Immunohistochemistry and flow cytometry assays were performed on liver biopsies and monocyte-macrophages to confirm the pathogenic role of the identified candidate variants. Through a combined approach of whole-exome sequencing and homozygosity mapping, we found bi-allelic STAB1 variants in ten subjects from seven families. STAB1 encodes the multifunctional scavenger receptor stabilin-1. Immunohistochemistry and flow cytometry analyses showed absent or markedly reduced stabilin-1 in liver samples, monocytes, and monocyte-derived macrophages. Our findings show a strong association between otherwise unexplained hyperferritinemia and bi-allelic STAB1 mutations suggesting the existence of another genetic cause of hyperferritinemia without iron overload and an unexpected function of stabilin-1 in ferritin metabolism.
MeSH term(s)	Humans ; Hyperferritinemia ; Iron Overload/genetics ; Iron Overload/diagnosis ; Ferritins/genetics ; Macrophages ; Alleles
Chemical Substances	Ferritins (9007-73-2)
Language	English
Publishing date	2023-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	219384-x
ISSN	1537-6605 ; 0002-9297
ISSN (online)	1537-6605
ISSN	0002-9297
DOI	10.1016/j.ajhg.2023.07.004
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Article ; Online: Clinical and neuroimaging characterization of the first frontotemporal dementia family carrying the MAPT p.K298E mutation.

Pozzi, Federico Emanuele / Aprea, Vittoria / Giovannelli, Ginevra / Lattuada, Francesca / Crivellaro, Cinzia / Bertola, Francesca / Castelnovo, Veronica / Canu, Elisa / Filippi, Massimo / Appollonio, Ildebrando / Ferrarese, Carlo / Agosta, Federica / Tremolizzo, Lucio

Neurogenetics

2024

Abstract: We present an in-depth clinical and neuroimaging analysis of a family carrying the MAPT K298E mutation associated with frontotemporal dementia (FTD). Initial identification of this mutation in a single clinical case led to a comprehensive investigation ... ...

Abstract	We present an in-depth clinical and neuroimaging analysis of a family carrying the MAPT K298E mutation associated with frontotemporal dementia (FTD). Initial identification of this mutation in a single clinical case led to a comprehensive investigation involving four affected siblings allowing to elucidate the mutation's phenotypic expression.A 60-year-old male presented with significant behavioral changes and progressed rapidly, exhibiting speech difficulties and cognitive decline. Neuroimaging via FDG-PET revealed asymmetrical frontotemporal hypometabolism. Three siblings subsequently showed varied but consistent clinical manifestations, including abnormal behavior, speech impairments, memory deficits, and motor symptoms correlating with asymmetric frontotemporal atrophy observed in MRI scans.Based on the genotype-phenotype correlation, we propose that the p.K298E mutation results in early-onset behavioral variant FTD, accompanied by a various constellation of speech and motor impairment.This detailed characterization expands the understanding of the p.K298E mutation's clinical and neuroimaging features, underlining its role in the pathogenesis of FTD. Further research is crucial to comprehensively delineate the clinical and epidemiological implications of the MAPT p.K298E mutation.
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	1339887-8
ISSN	1364-6753 ; 1364-6745
ISSN (online)	1364-6753
ISSN	1364-6745
DOI	10.1007/s10048-024-00756-w
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Article: Identification of Novel Mutations by Targeted NGS Panel in Patients with Hyperferritinemia

Ravasi, Giulia / Pelucchi, Sara / Bertola, Francesca / Capelletti, Martina Maria / Mariani, Raffaella / Piperno, Alberto

Genes. 2021 Nov. 09, v. 12, no. 11

2021

Abstract: Background. Several inherited diseases cause hyperferritinemia with or without iron overload. Differential diagnosis is complex and requires an extensive work-up. Currently, a clinical-guided approach to genetic tests is performed based on gene-by-gene ... ...

Abstract	Background. Several inherited diseases cause hyperferritinemia with or without iron overload. Differential diagnosis is complex and requires an extensive work-up. Currently, a clinical-guided approach to genetic tests is performed based on gene-by-gene sequencing. Although reasonable, this approach is expensive and time-consuming and Next Generation Sequencing (NGS) technology may provide cheaper and quicker large-scale DNA sequencing. Methods. We analysed 36 patients with non-HFE-related hyperferritinemia. Liver iron concentration was measured in 33 by magnetic resonance. A panel of 25 iron related genes was designed using SureDesign software. Custom libraries were generated and then sequenced using Ion Torrent PGM. Results. We identified six novel mutations in SLC40A1, three novel and one known mutation in TFR2, one known mutation and a de-novo deletion in HJV, and a novel mutation in HAMP in ten patients. In silico analyses supported the pathogenic role of the mutations. Conclusions. Our results support the use of an NGS-based panel in selected patients with hyperferritinemia in a tertiary center for iron metabolism disorders. However, 26 out of 36 patients did not show genetic variants that can individually explain hyperferritinemia and/or iron overload suggesting the existence of other genetic defects or gene-gene and gene-environment interactions needing further studies.
Keywords	DNA ; computer simulation ; computer software ; iron ; iron absorption ; iron overload ; liver ; magnetism ; mutation
Language	English
Dates of publication	2021-1109
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12111778
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Article ; Online: Identification of Novel Mutations by Targeted NGS Panel in Patients with Hyperferritinemia.

Ravasi, Giulia / Pelucchi, Sara / Bertola, Francesca / Capelletti, Martina Maria / Mariani, Raffaella / Piperno, Alberto

Genes

2021 Volume 12, Issue 11

Abstract: Background: Several inherited diseases cause hyperferritinemia with or without iron overload. Differential diagnosis is complex and requires an extensive work-up. Currently, a clinical-guided approach to genetic tests is performed based on gene-by-gene ... ...

Abstract	Background: Several inherited diseases cause hyperferritinemia with or without iron overload. Differential diagnosis is complex and requires an extensive work-up. Currently, a clinical-guided approach to genetic tests is performed based on gene-by-gene sequencing. Although reasonable, this approach is expensive and time-consuming and Next Generation Sequencing (NGS) technology may provide cheaper and quicker large-scale DNA sequencing. Methods: We analysed 36 patients with non- Results: We identified six novel mutations in Conclusions: Our results support the use of an NGS-based panel in selected patients with hyperferritinemia in a tertiary center for iron metabolism disorders. However, 26 out of 36 patients did not show genetic variants that can individually explain hyperferritinemia and/or iron overload suggesting the existence of other genetic defects or gene-gene and gene-environment interactions needing further studies.
MeSH term(s)	Adult ; Cation Transport Proteins/genetics ; Child ; Female ; GPI-Linked Proteins/genetics ; Gene-Environment Interaction ; Hemochromatosis Protein/genetics ; Hepcidins/genetics ; High-Throughput Nucleotide Sequencing ; Humans ; Hyperferritinemia/genetics ; Male ; Middle Aged ; Mutation ; Receptors, Transferrin/genetics ; Sequence Analysis, DNA/methods ; Tertiary Care Centers ; Young Adult
Chemical Substances	Cation Transport Proteins ; GPI-Linked Proteins ; HAMP protein, human ; HJV protein, human ; Hemochromatosis Protein ; Hepcidins ; Receptors, Transferrin ; TFR2 protein, human ; metal transporting protein 1
Language	English
Publishing date	2021-11-09
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12111778
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Article ; Online: Biochemical and molecular analysis in mucopolysaccharidoses: what a paediatrician must know.

Filocamo, Mirella / Tomanin, Rosella / Bertola, Francesca / Morrone, Amelia

Italian journal of pediatrics

2018 Volume 44, Issue Suppl 2, Page(s) 129

Abstract: Mucopolysaccharidoses (MPS) are rare inherited disorders caused by a deficit of the lysosomal hydrolases involved in the degradation of mucopolysaccharides, also known as glycosaminoglycans (GAGs). They are all monogenic defects, transmitted in an ... ...

Abstract	Mucopolysaccharidoses (MPS) are rare inherited disorders caused by a deficit of the lysosomal hydrolases involved in the degradation of mucopolysaccharides, also known as glycosaminoglycans (GAGs). They are all monogenic defects, transmitted in an autosomal recessive way, except for MPS type II which is X-linked. The enzymatic deficit causes a pathologic accumulation of undegraded or partially degraded substrates inside lysosomes as well as in the extracellular compartment. MPS generally present with recognizable signs and symptoms to raise a clinical suspicion. However, although they have individual peculiarities, often signs and symptoms may overlap between different MPS types. Therefore, a deeper evaluation of specific disease biomarkers becomes necessary to reach an appropriate diagnosis. This paper stresses the central role of the laboratory in completing and confirming the clinical suspicion of MPS according to a standardized procedure: first, a biochemical evaluation of the patient samples, including qualitative/quantitative urinary GAG analysis and a determination of enzyme activities, and then the molecular diagnosis. We also encourage a constant and close communication between clinicians and laboratory personnel to address a correct and early MPS diagnosis.
MeSH term(s)	Child ; Glycosaminoglycans/metabolism ; Humans ; Hydrolases/genetics ; Mucopolysaccharidoses/diagnosis ; Mucopolysaccharidoses/genetics ; Mucopolysaccharidoses/metabolism
Chemical Substances	Glycosaminoglycans ; Hydrolases (EC 3.-)
Language	English
Publishing date	2018-11-16
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2088556-8
ISSN	1824-7288 ; 1720-8424
ISSN (online)	1824-7288
ISSN	1720-8424
DOI	10.1186/s13052-018-0553-2
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Article ; Online: First report of PSEN2 mutation presenting as posterior cortical atrophy.

Tremolizzo, Lucio / Susani, Emanuela / Mapelli, Cristina / Isella, Valeria / Bertola, Francesca / Ferrarese, Carlo / Appollonio, Ildebrando

Alzheimer disease and associated disorders

2015 Volume 29, Issue 3, Page(s) 249–251

MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/genetics ; Atrophy/genetics ; Genetic Predisposition to Disease ; Genetic Testing/methods ; Humans ; Male ; Middle Aged ; Mutation/genetics ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/pathology ; Pedigree ; Presenilin-2/genetics
Chemical Substances	PSEN2 protein, human ; Presenilin-2
Language	English
Publishing date	2015-07
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	1002700-2
ISSN	1546-4156 ; 0893-0341
ISSN (online)	1546-4156
ISSN	0893-0341
DOI	10.1097/WAD.0000000000000052
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Article ; Online: Molecular diagnosis of patients affected by mucopolysaccharidosis: a multicenter study.

Zanetti, Alessandra / D'Avanzo, Francesca / Rigon, Laura / Rampazzo, Angelica / Concolino, Daniela / Barone, Rita / Volpi, Nicola / Santoro, Lucia / Lualdi, Susanna / Bertola, Francesca / Scarpa, Maurizio / Tomanin, Rosella

European journal of pediatrics

2019 Volume 178, Issue 5, Page(s) 739–753

Abstract: Mucopolysaccharidoses (MPS) are a subgroup of 11 monogenic lysosomal storage disorders due to the deficit of activity of the lysosomal hydrolases deputed to the degradation of mucopolysaccharides. Although individually rare, all together they account for ...

Abstract	Mucopolysaccharidoses (MPS) are a subgroup of 11 monogenic lysosomal storage disorders due to the deficit of activity of the lysosomal hydrolases deputed to the degradation of mucopolysaccharides. Although individually rare, all together they account for at least 1:25,000 live births. In this study, we present the genetic analysis of a population of 71 MPS patients enrolled in a multicenter Italian study. We re-annotated all variants, according to the latest recommendations, and re-classified them as suggested by the American College of Medical Genetics and Genomics. Variant distribution per type was mainly represented by missense mutations. Overall, 10 patients had received no molecular diagnosis, although 6 of them had undergone either HSCT or ERT, based on clinical and enzymatic evaluations. Moreover, nine novel variants are reported.Conclusions: Our analysis underlines the need to complete the molecular diagnosis in patients previously diagnosed only on a biochemical basis, suggests a periodical re-annotation of the variants and solicits their deposition in public databases freely available to clinicians and researchers. We strongly recommend a molecular diagnosis based on the analysis of the "trio" instead of the sole proband. These recommendations will help to obtain a complete and correct diagnosis of mucopolysaccharidosis, rendering also possible genetic counseling. What is known • MPS are a group of 11 metabolic genetic disorders due to deficits of enzymes involved in the mucopolysaccharides degradation. • Molecular analysis is commonly performed to confirm enzymatic assays. What is new • Eighty-six percent of the 71 patients we collected received a molecular diagnosis; among them, 9 novel variants were reported. • We stress the importance of molecular diagnosis in biochemically diagnosed patients, encourage a periodical re-annotation of variants according to the recent nomenclature and their publication in open databases.
MeSH term(s)	Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Genetic Association Studies ; Genetic Counseling ; Genetic Markers ; Genetic Testing ; Humans ; Infant ; Italy ; Male ; Molecular Diagnostic Techniques ; Mucopolysaccharidoses/diagnosis ; Mucopolysaccharidoses/genetics ; Mutation, Missense ; Young Adult
Chemical Substances	Genetic Markers
Language	English
Publishing date	2019-02-26
Publishing country	Germany
Document type	Clinical Trial ; Journal Article ; Multicenter Study
ZDB-ID	194196-3
ISSN	1432-1076 ; 0340-6199 ; 0943-9676
ISSN (online)	1432-1076
ISSN	0340-6199 ; 0943-9676
DOI	10.1007/s00431-019-03341-8
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Article ; Online: Analysis of vesicular monoamine transporter 2 polymorphisms in Parkinson's disease.

Brighina, Laura / Riva, Chiara / Bertola, Francesca / Saracchi, Enrico / Fermi, Silvia / Goldwurm, Stefano / Ferrarese, Carlo

Neurobiology of aging

2013 Volume 34, Issue 6, Page(s) 1712.e9–13

Abstract: Generation of reactive oxygen species during dopamine (DA) oxidation could be one of the factors leading to the selective loss of nigral dopaminergic neurons in Parkinson's disease (PD). Vesicular monoamine transporter type 2 (VMAT2) proteins in nerve ... ...

Abstract	Generation of reactive oxygen species during dopamine (DA) oxidation could be one of the factors leading to the selective loss of nigral dopaminergic neurons in Parkinson's disease (PD). Vesicular monoamine transporter type 2 (VMAT2) proteins in nerve terminals uptake dopamine into synaptic vesicles, preventing its cytoplasmic accumulation and toxic damage to nigral neurons. Polymorphisms in VMAT2 gene and in its regulatory regions might therefore serve as genetic risk factors for PD. In the present study, we have analyzed 8 single-nucleotide polymorphisms (SNPs) located within/around the VMAT2 gene for association with PD in an Italian cohort composed of 704 PD patients and 678 healthy controls. Among the 8 SNPs studied, only the 2 located within the promoter region (rs363371 and rs363324) were significantly associated with PD. In the dominant model, odds ratios were 0.72 (95% confidence interval [CI]: 0.6-0.9, p < 0.005) for rs363371 and 0.76 (95% CI: 0.6-0.9, p = 0.01) for rs363324; in the additive model, odds ratios were 0.78 (95% CI: 0.65-0.94, p = 0.008) for rs363371 and 0.85 (95% CI: 0.7-20.92, p = 0.04) for rs363324. There were no significant relationships between the remaining SNPs (rs363333, rs363399, rs363387, rs363343, rs4752045, and rs363236) and the risk of sporadic PD in any genetic model. This study adds to the previous evidence suggesting that variability in VMAT2 promoter region may confer a reduced risk of developing PD, presumably via mechanisms of gene overexpression.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Cohort Studies ; Female ; Humans ; Male ; Middle Aged ; Parkinson Disease/diagnosis ; Parkinson Disease/epidemiology ; Parkinson Disease/genetics ; Polymorphism, Single Nucleotide/genetics ; Vesicular Monoamine Transport Proteins/genetics
Chemical Substances	SLC18A2 protein, human ; Vesicular Monoamine Transport Proteins
Language	English
Publishing date	2013-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2012.12.020
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Article: Possible Use of Minocycline in Adjunction to Intranasal Esketamine for the Management of Difficult to Treat Depression following Extensive Pharmacogenomic Testing: Two Case Reports.

Marcatili, Matteo / Borgonovo, Riccardo / Cimminiello, Noemi / Cornaggia, Ranieri Domenico / Casati, Giulia / Pellicioli, Cristian / Maggioni, Laura / Motta, Federico / Redaelli, Chiara / Ledda, Luisa / Pozzi, Federico Emanuele / Krivosova, Michaela / Pagano, Jessica / Nava, Roberto / Colmegna, Fabrizia / Dakanalis, Antonios / Caldiroli, Alice / Capuzzi, Enrico / Benatti, Beatrice /

Dell'Osso, Bernardo / Bertola, Francesca / Villa, Nicoletta / Piperno, Alberto / Ippolito, Silvia / Appollonio, Ildebrando / Sala, Carlo / Conti, Luciano / Clerici, Massimo

Journal of personalized medicine

2022 Volume 12, Issue 9

Abstract: The advent of intra-nasal esketamine (ESK), one of the first so ... ...

Abstract	The advent of intra-nasal esketamine (ESK), one of the first so called
Language	English
Publishing date	2022-09-16
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm12091524
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Article ; Online: Homozygous deletion of HFE: the Sardinian hemochromatosis?

Pelucchi, Sara / Mariani, Raffaella / Bertola, Francesca / Arosio, Cristina / Piperno, Alberto

Blood

2009 Volume 113, Issue 16, Page(s) 3886

MeSH term(s)	Disease Progression ; Female ; Gene Deletion ; Genotype ; Hemochromatosis Protein ; Histocompatibility Antigens Class I/genetics ; Homozygote ; Humans ; Male ; Membrane Proteins/genetics ; Mutation, Missense ; Pedigree ; Phenotype
Chemical Substances	HFE protein, human ; Hemochromatosis Protein ; Histocompatibility Antigens Class I ; Membrane Proteins
Language	English
Publishing date	2009-04-16
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2008-12-196493
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