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Book: Inborn errors of metabolism

Lee, Brendan H. / Scaglia, Fernando

from neonatal screening to metabolic pathways

(Oxford monograpohs on medical genetics ; 64)

2015

Author's details	ed. by Brendan H. Lee and Fernando Scaglia
Series title	Oxford monograpohs on medical genetics ; 64 Oxford monographs on medical genetics
Collection	Oxford monographs on medical genetics
Keywords	Metabolism, Inborn Errors
Language	English
Size	X, 366 S. : Ill., graph. Darst.
Publisher	Oxford Univ. Press
Publishing place	Oxford
Publishing country	Great Britain
Document type	Book
Note	Includes bibliographical references ; Newborn screening for inborn errors of metabolism : introduction and approaches for confirmation / V. Reid Sutton and Brett H. Graham -- Human glycosylation disorders : many faces, many pathways / Hudson H. Freeze, Erik A. Eklund and Donna M. Krasnewich -- Gluconeogenesis / Erin M. Coffee and Dean R. Tolan -- Branched chain amino acid metabolism / I. Manoli and Charles Venditti -- Glycolysis / Areeg El-Gharbawy and Dwight Koeberl -- Urea cycle : ureagenesis and non-ureagenic functions / Oleg A. Shchelochkov, Sandesh CS Nagamani, Philippe M. Campeau, Ayelet Erez, Brendan H. Lee -- Fatty acid metabolism and defects / Marwan S. Shinawi and Lutfi A. Abu-Elheiga -- Mitochondrial disorders / Ayman W El-Hattab and Fernando Scaglia -- Cholesterol, sterols, and isoprenoids / Yasemen Eroglu, Jean-Baptiste Roullet, and Robert D. Steiner -- Disorders of one carbon metabolism / Luis Umana and William J. Craigen -- Neurotransmission and neurotoxicity (PKU and dopamine) / Uta Lichter-Konecki -- Cell and organ transplantation / Alberto Burlina, Andrea Bordugo, Georg F. Hoffmann, and Jochen Meyburg -- Gene replacement therapy / Nicola Brunetti-Pierri -- Protein replacement therapy / Christine Eng & Gregory Pastores -- Chaperone therapy / Marc Patterson -- Substrate deprivation theory / Ellen Sidransky
HBZ-ID	HT018476574
ISBN	978-0-19-979758-5 ; 0-19-979758-7
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Intracranial calcifications simulating Aicardi-Goutières syndrome in PARS2-related mitochondrial disease.

Gerard, Amanda / Mizerik, Elizabeth / Mohila, Carrie A / AlAwami, Sarah / Hunter, Jill V / Kearney, Debra L / Lalani, Seema R / Scaglia, Fernando

American journal of medical genetics. Part A

2024 , Page(s) e63589

Abstract: PARS2 encodes an aminoacyl-tRNA synthetase that catalyzes the ligation of proline to mitochondrial prolyl-tRNA molecules. Diseases associated with PARS2 primarily affect the central nervous system, causing early infantile developmental epileptic ... ...

Abstract	PARS2 encodes an aminoacyl-tRNA synthetase that catalyzes the ligation of proline to mitochondrial prolyl-tRNA molecules. Diseases associated with PARS2 primarily affect the central nervous system, causing early infantile developmental epileptic encephalopathies (EIDEE; DEE75; MIM #618437) with infantile-onset neurodegeneration. Dilated cardiomyopathy has also been reported in the affected individuals. About 10 individuals to date have been described with pathogenic biallelic variants in PARS2. While many of the reported individuals succumbed to the disease in the first two decades of life, autopsy findings have not yet been reported. Here, we describe neuropathological findings in a deceased male with evidence of intracranial calcifications in the basal ganglia, thalamus, cerebellum, and white matter, similar to Aicardi-Goutières syndrome. This report describes detailed autopsy findings in a child with PARS2-related mitochondrial disease and provides plausible evidence that intracranial calcifications may be a previously unrecognized feature of this disorder.
Language	English
Publishing date	2024-03-12
Publishing country	United States
Document type	Case Reports
ZDB-ID	2108614-X
ISSN	1552-4833 ; 0148-7299 ; 1552-4825
ISSN (online)	1552-4833
ISSN	0148-7299 ; 1552-4825
DOI	10.1002/ajmg.a.63589
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Article ; Online: Novel phenotype of aortic root dilatation and late-onset metabolic decompensation in a patient with TMEM70 deficiency.

Mackay, Laura / Gijavanekar, Charul / Streff, Haley / Price, Jack F / Elsea, Sarah H / Scaglia, Fernando

American journal of medical genetics. Part A

2023 Volume 191, Issue 5, Page(s) 1366–1372

Abstract: TMEM70 deficiency causing mitochondrial complex V deficiency, nuclear type 2 (MIM: 614052) is the most common nuclear encoded defect affecting ATP synthase and has been well described in the literature as being characterized by neonatal or infantile ... ...

Abstract	TMEM70 deficiency causing mitochondrial complex V deficiency, nuclear type 2 (MIM: 614052) is the most common nuclear encoded defect affecting ATP synthase and has been well described in the literature as being characterized by neonatal or infantile onset of poor feeding, hypotonia, lethargy, respiratory compromise, heart failure, lactic acidosis, hyperammonemia, and 3-methylglutaconic aciduria progressing to a phenotype of developmental delay, failure to thrive, short stature, nonprogressive cardiomyopathy, microcephaly, facial dysmorphisms, hypospadias, persistent pulmonary hypertension of the newborn, and Wolff-Parkinson-White syndrome, as well as metabolic crises followed by developmental regression. The patient with TMEM70 deficiency herein reported has the unique presentation of aortic root dilatation, differing facial dysmorphisms, and no history of neonatal metabolic decompensation or developmental delay, as well as a plasma metabolomics signature, including elevated 3-methylglutaconic acid, 3-methylglutarylcarnitine, alanine, and lactate, in addition to the commonly described increased 3-methylglutaconic acid on urine organic acid analysis that helped aid in the diagnostic interpretation of variants of uncertain significance in TMEM70.
MeSH term(s)	Male ; Humans ; Aorta, Thoracic ; Dilatation ; Cardiomyopathies ; Phenotype ; Membrane Proteins/genetics ; Mitochondrial Proteins/genetics
Chemical Substances	3-methylglutaconic acid (5746-90-7) ; TMEM70 protein, human ; Membrane Proteins ; Mitochondrial Proteins
Language	English
Publishing date	2023-02-07
Publishing country	United States
Document type	Case Reports
ZDB-ID	2108614-X
ISSN	1552-4833 ; 0148-7299 ; 1552-4825
ISSN (online)	1552-4833
ISSN	0148-7299 ; 1552-4825
DOI	10.1002/ajmg.a.63131
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Article ; Online: δ

Bononi, Monica / Tateo, Fernando / Scaglia, Barbara / Quaglia, Giancarlo

Food chemistry

2020 Volume 315, Page(s) 126292

Abstract: Using isotopic ratio mass spectrometry (IRMS) measurements, this study analyzed samples of saffron originating from two distinct geographical regions. We then used the results to distinguish saffron of the two considered origins. ... ...

Abstract	Using isotopic ratio mass spectrometry (IRMS) measurements, this study analyzed samples of saffron originating from two distinct geographical regions. We then used the results to distinguish saffron of the two considered origins. δ
MeSH term(s)	Carbon Isotopes ; Carotenoids/chemistry ; Crocus/chemistry ; Gas Chromatography-Mass Spectrometry ; Greece ; Iran ; Mass Spectrometry ; Plant Extracts/chemistry ; Triglycerides/chemistry ; Water/chemistry
Chemical Substances	Carbon Isotopes ; Plant Extracts ; Triglycerides ; Water (059QF0KO0R) ; Carotenoids (36-88-4) ; crocin (877GWI46C2)
Language	English
Publishing date	2020-02-05
Publishing country	England
Document type	Journal Article
ZDB-ID	243123-3
ISSN	1873-7072 ; 0308-8146
ISSN (online)	1873-7072
ISSN	0308-8146
DOI	10.1016/j.foodchem.2020.126292
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Article ; Online: Nuclear gene defects in mitochondrial disorders.

Scaglia, Fernando

Methods in molecular biology (Clifton, N.J.)

2012 Volume 837, Page(s) 17–34

Abstract: Most mitochondrial cytopathies in infants are caused by mutations in nuclear genes encoding proteins targeted to the mitochondria rather than by primary mutations in the mitochondrial DNA. Over the past few years, the awareness of the number of disease- ... ...

Abstract	Most mitochondrial cytopathies in infants are caused by mutations in nuclear genes encoding proteins targeted to the mitochondria rather than by primary mutations in the mitochondrial DNA. Over the past few years, the awareness of the number of disease-causing mutations in different nuclear genes has grown exponentially. These genes encode the various subunits of each respiratory chain complex, the ancillary proteins involved in the assembly of these subunits, proteins involved in mitochondrial DNA replication and maintenance, proteins involved in mitochondrial protein synthesis, and proteins involved in mitochondrial dynamics. This increased awareness has added a challenging dimension to the current diagnostic workup of mitochondrial cytopathies. The advent of new technologies such as next-generation sequencing should facilitate the resolution of this dilemma.
MeSH term(s)	Cell Nucleus/genetics ; DNA, Mitochondrial/chemistry ; DNA, Mitochondrial/genetics ; Electron Transport/genetics ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Diseases/genetics ; Mitochondrial Diseases/metabolism ; Mitochondrial Diseases/pathology ; Mitochondrial Proteins/biosynthesis
Chemical Substances	DNA, Mitochondrial ; Mitochondrial Proteins
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-61779-504-6_2
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Article ; Online: Petrography descriptions and U-Pb zircon datasets from the Archean Pavas Block, Precambrian of Uruguay.

Masquelin, Henri / Aïfa, Tahar / Scaglia, Fernando / Basei, Miguel A S

Data in brief

2021 Volume 37, Page(s) 107179

Abstract: This database is a geological and geochronological compilation made to study a small Archean/Paleoproterozoic block located in the centre of the Precambrian rock exposition of Uruguay. Petrographic and field outcrops data supporting the samples from ... ...

Abstract	This database is a geological and geochronological compilation made to study a small Archean/Paleoproterozoic block located in the centre of the Precambrian rock exposition of Uruguay. Petrographic and field outcrops data supporting the samples from which the zircons for textural analysis and U-Pb dating (LA-ICP-MS) come are presented at first with their descriptions. The first table (1) contains the new U-Pb isotopic data. The second table (2) presents a correlation of textures from different zircon samples. The last table (3) contains an inventory of different U-Pb ages found in antecedents. All these data are associated with the paper entitled: "The Archean Pavas Block in Uruguay: extension and tectonic evolution based on LA-ICP-MS U-Pb ages and airborne geophysics".
Language	English
Publishing date	2021-05-29
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2786545-9
ISSN	2352-3409 ; 2352-3409
ISSN (online)	2352-3409
ISSN	2352-3409
DOI	10.1016/j.dib.2021.107179
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Article ; Online: Mitochondrial DNA maintenance defects: potential therapeutic strategies.

Almannai, Mohammed / El-Hattab, Ayman W / Azamian, Mahshid S / Ali, May / Scaglia, Fernando

Molecular genetics and metabolism

2022 Volume 137, Issue 1-2, Page(s) 40–48

Abstract: Mitochondrial DNA (mtDNA) replication depends on the mitochondrial import of hundreds of nuclear encoded proteins that control the mitochondrial genome maintenance and integrity. Defects in these processes result in an expanding group of disorders called ...

Abstract	Mitochondrial DNA (mtDNA) replication depends on the mitochondrial import of hundreds of nuclear encoded proteins that control the mitochondrial genome maintenance and integrity. Defects in these processes result in an expanding group of disorders called mtDNA maintenance defects that are characterized by mtDNA depletion and/or multiple mtDNA deletions with variable phenotypic manifestations. As it applies for mitochondrial disorders in general, current treatment options for mtDNA maintenance defects are limited. Lately, with the development of model organisms, improved understanding of the pathophysiology of these disorders, and a better knowledge of their natural history, the number of preclinical studies and existing and planned clinical trials has been increasing. In this review, we discuss recent preclinical studies and current and future clinical trials concerning potential therapeutic options for the different mtDNA maintenance defects.
MeSH term(s)	Humans ; DNA, Mitochondrial/genetics ; DNA, Mitochondrial/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Diseases/genetics ; Mitochondrial Diseases/therapy ; Mitochondrial Diseases/metabolism
Chemical Substances	DNA, Mitochondrial
Language	English
Publishing date	2022-07-06
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1418518-0
ISSN	1096-7206 ; 1096-7192
ISSN (online)	1096-7206
ISSN	1096-7192
DOI	10.1016/j.ymgme.2022.07.003
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Article ; Online: Heteroplasmic pathogenic m.12315G>A variant in MT-TL2 presenting with MELAS syndrome and depletion of nitric oxide donors.

Snyder, Matthew T / Manor, Joshua / Gijavanekar, Charul / Mizerik, Elizabeth / Kralik, Stephen F / Elsea, Sarah H / Machol, Keren / Emrick, Lisa / Scaglia, Fernando

American journal of medical genetics. Part A

2023 Volume 194, Issue 3, Page(s) e63461

Abstract: The MT-TL2 m.12315G>A pathogenic variant has previously been reported in five individuals with mild clinical phenotypes. Herein we report the case of a 5-year-old child with heteroplasmy for this variant who developed neurological regression and stroke- ... ...

Abstract	The MT-TL2 m.12315G>A pathogenic variant has previously been reported in five individuals with mild clinical phenotypes. Herein we report the case of a 5-year-old child with heteroplasmy for this variant who developed neurological regression and stroke-like episodes similar to those observed in mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Biochemical evaluation revealed depletion of arginine on plasma amino acid analysis and low z-scores for citrulline on untargeted plasma metabolomics analysis. These findings suggested that decreased availability of nitric oxide may have contributed to the stroke-like episodes. The use of intravenous arginine during stroke-like episodes and daily enteral L-citrulline supplementation normalized her biochemical values of arginine and citrulline. Untargeted plasma metabolomics showed the absence of nicotinamide and 1-methylnicotinamide, and plasma total glutathione levels were low; thus, nicotinamide riboside and N-acetylcysteine therapies were initiated. This report expands the phenotype associated with the rare mitochondrial variant MT-TL2 m.12315G>A to include neurological regression and a MELAS-like phenotype. Individuals with this variant should undergo in-depth biochemical analysis to include untargeted plasma metabolomics, plasma amino acids, and glutathione levels to help guide a targeted approach to treatment.
MeSH term(s)	Child, Preschool ; Female ; Humans ; Acidosis, Lactic ; Arginine/genetics ; Citrulline ; Glutathione/metabolism ; MELAS Syndrome/diagnosis ; MELAS Syndrome/genetics ; MELAS Syndrome/complications ; Mitochondrial Encephalomyopathies ; Nitric Oxide Donors/metabolism ; Stroke/complications ; Stroke/drug therapy
Chemical Substances	Arginine (94ZLA3W45F) ; Citrulline (29VT07BGDA) ; Glutathione (GAN16C9B8O) ; Nitric Oxide Donors
Language	English
Publishing date	2023-11-12
Publishing country	United States
Document type	Case Reports
ZDB-ID	2108614-X
ISSN	1552-4833 ; 0148-7299 ; 1552-4825
ISSN (online)	1552-4833
ISSN	0148-7299 ; 1552-4825
DOI	10.1002/ajmg.a.63461
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Article ; Online: Hyperkinetic Movement Disorder Caused by the Recurrent c.892C>T NACC1 Variant.

Komulainen-Ebrahim, Jonna / Kangas, Salla M / López-Martín, Estrella / Feyma, Timothy / Scaglia, Fernando / Martínez-Delgado, Beatriz / Kuismin, Outi / Suo-Palosaari, Maria / Carr, Lucinda / Hinttala, Reetta / Kurian, Manju A / Uusimaa, Johanna

Movement disorders clinical practice

2024

Abstract: Background: Genetic syndromes of hyperkinetic movement disorders associated with epileptic encephalopathy and intellectual disability are becoming increasingly recognized. Recently, a de novo heterozygous NACC1 (nucleus accumbens-associated 1) missense ... ...

Abstract	Background: Genetic syndromes of hyperkinetic movement disorders associated with epileptic encephalopathy and intellectual disability are becoming increasingly recognized. Recently, a de novo heterozygous NACC1 (nucleus accumbens-associated 1) missense variant was described in a patient cohort including one patient with a combined mitochondrial oxidative phosphorylation (OXPHOS) deficiency. Objectives: The objective is to characterize the movement disorder in affected patients with the recurrent c.892C>T NACC1 variant and study the NACC1 protein and mitochondrial function at the cellular level. Methods: The movement disorder was analyzed on four patients with the NACC1 c.892C>T (p.Arg298Trp) variant. Studies on NACC1 protein and mitochondrial function were performed on patient-derived fibroblasts. Results: All patients had a generalized hyperkinetic movement disorder with chorea and dystonia, which occurred cyclically and during sleep. Complex I was found altered, whereas the other OXPHOS enzymes and the mitochondria network seemed intact in one patient. Conclusions: The movement disorder is a prominent feature of NACC1-related disease.
Language	English
Publishing date	2024-05-02
Publishing country	United States
Document type	Journal Article
ISSN	2330-1619
ISSN (online)	2330-1619
DOI	10.1002/mdc3.14051
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Article ; Online: Expanded clinical phenotype and untargeted metabolomics analysis in RARS2-related mitochondrial disorder: a case report.

Walimbe, Ameya S / Machol, Keren / Kralik, Stephen F / Mizerik, Elizabeth A / Gofin, Yoel / Bekheirnia, Mir Reza / Gijavanekar, Charul / Elsea, Sarah H / Emrick, Lisa T / Scaglia, Fernando

BMC neurology

2024 Volume 24, Issue 1, Page(s) 87

Abstract: Background: RARS2-related mitochondrial disorder is an autosomal recessive mitochondrial encephalopathy caused by biallelic pathogenic variants in the gene encoding the mitochondrial arginyl-transfer RNA synthetase 2 (RARS2, MIM *611524, NM_020320.5). ... ...

Abstract	Background: RARS2-related mitochondrial disorder is an autosomal recessive mitochondrial encephalopathy caused by biallelic pathogenic variants in the gene encoding the mitochondrial arginyl-transfer RNA synthetase 2 (RARS2, MIM 611524, NM_020320.5). RARS2 catalyzes the transfer of L-arginine to its cognate tRNA during the translation of mitochondrially-encoded proteins. The classical presentation of RARS2-related mitochondrial disorder includes pontocerebellar hypoplasia (PCH), progressive microcephaly, profound developmental delay, feeding difficulties, and hypotonia. Most patients also develop severe epilepsy by three months of age, which consists of focal or generalized seizures that frequently become pharmacoresistant and lead to developmental and epileptic encephalopathy (DEE). Case presentation:* Here, we describe a six-year-old boy with developmental delay, hypotonia, and failure to thrive who developed an early-onset DEE consistent with Lennox-Gastaut Syndrome (LGS), which has not previously been observed in this disorder. He had dysmorphic features including bilateral macrotia, overriding second toes, a depressed nasal bridge, retrognathia, and downslanting palpebral fissures, and he did not demonstrate progressive microcephaly. Whole genome sequencing identified two variants in RARS2, c.36 + 1G > T, a previously unpublished variant that is predicted to affect splicing and is, therefore, likely pathogenic and c.419 T > G (p.Phe140Cys), a known pathogenic variant. He exhibited significant, progressive generalized brain atrophy and ex vacuo dilation of the supratentorial ventricular system on brain MRI and did not demonstrate PCH. Treatment with a ketogenic diet (KD) reduced seizure frequency and enabled him to make developmental progress. Plasma untargeted metabolomics analysis showed increased levels of lysophospholipid and sphingomyelin-related metabolites. Conclusions: Our work expands the clinical spectrum of RARS2-related mitochondrial disorder, demonstrating that patients can present with dysmorphic features and an absence of progressive microcephaly, which can help guide the diagnosis of this condition. Our case highlights the importance of appropriate seizure phenotyping in this condition and indicates that patients can develop LGS, for which a KD may be a viable therapeutic option. Our work further suggests that analytes of phospholipid metabolism may serve as biomarkers of mitochondrial dysfunction.
MeSH term(s)	Humans ; Male ; Child ; Microcephaly/genetics ; Muscle Hypotonia ; Phenotype ; Mitochondrial Diseases/genetics ; Seizures ; Arginine-tRNA Ligase/genetics
Chemical Substances	RARS2 protein, human (EC 6.1.1.19) ; Arginine-tRNA Ligase (EC 6.1.1.19)
Language	English
Publishing date	2024-03-04
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	2041347-6
ISSN	1471-2377 ; 1471-2377
ISSN (online)	1471-2377
ISSN	1471-2377
DOI	10.1186/s12883-024-03571-w
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