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Article ; Online: Risk assessment of new sequencing information for genetically modified sugar beet H7-1.

Lenzi, Paolo / Papadopoulou, Nikoletta / Raffaello, Tommaso

EFSA journal. European Food Safety Authority

2022 Volume 20, Issue 6, Page(s) e07354

Abstract: The EFSA Panel on genetically modified organisms (GMO Panel) has previously assessed genetically modified (GM) sugar beet H7-1. This sugar beet was found to be as safe and nutritious as its conventional counterpart and commercial sugar beet varieties ... ...

Abstract	The EFSA Panel on genetically modified organisms (GMO Panel) has previously assessed genetically modified (GM) sugar beet H7-1. This sugar beet was found to be as safe and nutritious as its conventional counterpart and commercial sugar beet varieties with respect to potential effects on human and animal health and the environment in the context of its intended uses. On 19 February 2021, European Commission requested EFSA to analyse new nucleic acid sequencing data and updated bioinformatics data for GM sugar beet H7-1 and to indicate whether the previous conclusions of the GMO Panel on safety of GM sugar beet H7-1 remain valid. The new sequencing data indicated seven nucleotide differences as compared to the sequence originally provided in applications EFSA-GMO-UK-2004-08 and EFSA-GMO-RX-006: five nucleotides in the 5' genomic flanking region and two nucleotides in the T-DNA region of the insert. Two mismatches between the originally submitted H7-1 event sequence and the plasmid sequence were confirmed by the newly obtained H7-1 sequence. Based on the analysis of the provided data, EFSA considers that the newly reported sequence differences are most likely attributed to sequencing errors in the originally reported sugar beet H7-1 event sequence. The new sequencing data and the bioinformatic analyses performed on the new sequence did not give rise to safety issues. Therefore, EFSA concludes that the original risk assessment of sugar beet H7-1 remains valid.
Language	English
Publishing date	2022-06-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2540248-1
ISSN	1831-4732 ; 1831-4732
ISSN (online)	1831-4732
ISSN	1831-4732
DOI	10.2903/j.efsa.2022.7354
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Article ; Online: Combined light and electron microscopy (CLEM) to quantify methamphetamine-induced alpha-synuclein-related pathology.

Ferrucci, Michela / Lenzi, Paola / Lazzeri, Gloria / Busceti, Carla L / Frati, Alessandro / Puglisi-Allegra, Stefano / Fornai, Francesco

Journal of neural transmission (Vienna, Austria : 1996)

2024 Volume 131, Issue 4, Page(s) 335–358

Abstract: Methamphetamine (METH) produces a cytopathology, which is rather specific within catecholamine neurons both in vitro and ex vivo, in animal models and chronic METH abusers. This led some authors to postulate a sort of parallelism between METH ... ...

Abstract	Methamphetamine (METH) produces a cytopathology, which is rather specific within catecholamine neurons both in vitro and ex vivo, in animal models and chronic METH abusers. This led some authors to postulate a sort of parallelism between METH cytopathology and cell damage in Parkinson's disease (PD). In fact, METH increases and aggregates alpha-syn proto-fibrils along with producing spreading of alpha-syn. Although alpha-syn is considered to be the major component of aggregates and inclusions developing within diseased catecholamine neurons including classic Lewy body (LB), at present, no study provided a quantitative assessment of this protein in situ, neither following METH nor in LB occurring in PD. Similarly, no study addressed the quantitative comparison between occurrence of alpha-syn and other key proteins and no investigation measured the protein compared with non-protein structure within catecholamine cytopathology. Therefore, the present study addresses these issues using an oversimplified model consisting of a catecholamine cell line where the novel approach of combined light and electron microscopy (CLEM) was used measuring the amount of alpha-syn, which is lower compared with p62 or poly-ubiquitin within pathological cell domains. The scenario provided by electron microscopy reveals unexpected findings, which are similar to those recently described in the pathology of PD featuring packing of autophagosome-like vesicles and key proteins shuttling autophagy substrates. Remarkably, small seed-like areas, densely packed with p62 molecules attached to poly-ubiquitin within wide vesicular domains occurred. The present data shed new light about quantitative morphometry of catecholamine cell damage in PD and within the addicted brain.
MeSH term(s)	Animals ; Methamphetamine/pharmacology ; alpha-Synuclein/metabolism ; Parkinson Disease/metabolism ; Microscopy, Electron ; Catecholamines ; Ubiquitins
Chemical Substances	Methamphetamine (44RAL3456C) ; alpha-Synuclein ; Catecholamines ; Ubiquitins
Language	English
Publishing date	2024-02-17
Publishing country	Austria
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184163-4
ISSN	1435-1463 ; 0300-9564
ISSN (online)	1435-1463
ISSN	0300-9564
DOI	10.1007/s00702-024-02741-x
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Article ; Online: Is There a Place for Lewy Bodies before and beyond Alpha-Synuclein Accumulation? Provocative Issues in Need of Solid Explanations.

Lenzi, Paola / Lazzeri, Gloria / Ferrucci, Michela / Scotto, Marco / Frati, Alessandro / Puglisi-Allegra, Stefano / Busceti, Carla Letizia / Fornai, Francesco

International journal of molecular sciences

2024 Volume 25, Issue 7

Abstract: In the last two decades, alpha-synuclein (alpha-syn) assumed a prominent role as a major component and seeding structure of Lewy bodies (LBs). This concept is driving ongoing research on the pathophysiology of Parkinson's disease (PD). In line with this, ...

Abstract	In the last two decades, alpha-synuclein (alpha-syn) assumed a prominent role as a major component and seeding structure of Lewy bodies (LBs). This concept is driving ongoing research on the pathophysiology of Parkinson's disease (PD). In line with this, alpha-syn is considered to be the guilty protein in the disease process, and it may be targeted through precision medicine to modify disease progression. Therefore, designing specific tools to block the aggregation and spreading of alpha-syn represents a major effort in the development of disease-modifying therapies in PD. The present article analyzes concrete evidence about the significance of alpha-syn within LBs. In this effort, some dogmas are challenged. This concerns the question of whether alpha-syn is more abundant compared with other proteins within LBs. Again, the occurrence of alpha-syn compared with non-protein constituents is scrutinized. Finally, the prominent role of alpha-syn in seeding LBs as the guilty structure causing PD is questioned. These revisited concepts may be helpful in the process of validating which proteins, organelles, and pathways are likely to be involved in the damage to meso-striatal dopamine neurons and other brain regions involved in PD.
MeSH term(s)	Humans ; alpha-Synuclein ; Lewy Bodies ; Parkinson Disease ; Corpus Striatum ; Disease Progression
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2024-04-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25073929
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Article ; Online: Assessment of the 2020 post-market environmental monitoring report on the cultivation of genetically modified maize MON 810 in the EU.

Álvarez, Fernando / Martín Camargo, Ana / Messéan, Antoine / Lenzi, Paolo / Streissl, Franz

EFSA journal. European Food Safety Authority

2022 Volume 20, Issue 7, Page(s) e07406

Abstract: Following a request from the European Commission; the European Food Safety Authority (EFSA) assessed the 2020 post-market environmental monitoring (PMEM) report on the cultivation of Cry1Ab-expressing maize event MON 810. Like previous years, there was ... ...

Abstract	Following a request from the European Commission; the European Food Safety Authority (EFSA) assessed the 2020 post-market environmental monitoring (PMEM) report on the cultivation of Cry1Ab-expressing maize event MON 810. Like previous years, there was full compliance with refuge requirement in Portugal and partial compliance with refuge requirements by Spanish farmers growing MON 810 varieties. European and Mediterranean corn borer populations collected from north-eastern Spain during the 2020 maize growing season and tested for Cry1Ab susceptibility show no symptoms of resistance to maize MON 810. The assessment of farmer questionnaires and relevant scientific publications does not indicate any unanticipated adverse effects on human and animal health or the environment arising from the cultivation of maize MON 810. Overall, EFSA concludes that the evidence reported in the 2020 PMEM report does not invalidate previous EFSA evaluations on the safety of maize MON 810. However, as in previous years, EFSA identifies shortcomings on resistance monitoring that need revision in future reports. In particular, the monitoring plan, as implemented in 2020, is not sufficiently sensitive to detect the recommended 3% resistance allele frequency. Consequently, EFSA strongly recommends the consent holder to achieve full compliance with refuge obligations in areas where adoption of maize MON 810 is high and increase the sensitivity of the monitoring plan by performing periodic F
Language	English
Publishing date	2022-07-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2540248-1
ISSN	1831-4732 ; 1831-4732
ISSN (online)	1831-4732
ISSN	1831-4732
DOI	10.2903/j.efsa.2022.7406
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Article ; Online: The Relevance of Autophagy within Inner Ear in Baseline Conditions and Tinnitus-Related Syndromes.

Lazzeri, Gloria / Biagioni, Francesca / Ferrucci, Michela / Puglisi-Allegra, Stefano / Lenzi, Paola / Busceti, Carla Letizia / Giannessi, Francesco / Fornai, Francesco

International journal of molecular sciences

2023 Volume 24, Issue 23

Abstract: Tinnitus is the perception of noise in the absence of acoustic stimulation (phantom noise). In most patients suffering from chronic peripheral tinnitus, an alteration of outer hair cells (OHC) starting from the stereocilia (SC) occurs. This is common ... ...

Abstract	Tinnitus is the perception of noise in the absence of acoustic stimulation (phantom noise). In most patients suffering from chronic peripheral tinnitus, an alteration of outer hair cells (OHC) starting from the stereocilia (SC) occurs. This is common following ototoxic drugs, sound-induced ototoxicity, and acoustic degeneration. In all these conditions, altered coupling between the tectorial membrane (TM) and OHC SC is described. The present review analyzes the complex interactions involving OHC and TM. These need to be clarified to understand which mechanisms may underlie the onset of tinnitus and why the neuropathology of chronic degenerative tinnitus is similar, independent of early triggers. In fact, the fine neuropathology of tinnitus features altered mechanisms of mechanic-electrical transduction (MET) at the level of OHC SC. The appropriate coupling between OHC SC and TM strongly depends on autophagy. The involvement of autophagy may encompass degenerative and genetic tinnitus, as well as ototoxic drugs and acoustic trauma. Defective autophagy explains mitochondrial alterations and altered protein handling within OHC and TM. This is relevant for developing novel treatments that stimulate autophagy without carrying the burden of severe side effects. Specific phytochemicals, such as curcumin and berberin, acting as autophagy activators, may mitigate the neuropathology of tinnitus.
MeSH term(s)	Humans ; Tinnitus ; Hair Cells, Auditory, Outer ; Stereocilia ; Sound ; Acoustic Stimulation
Language	English
Publishing date	2023-11-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242316664
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Article ; Online: Treatment with the Glycosphingolipid Modulator THI Rescues Myelin Integrity in the Striatum of R6/2 HD Mice.

Pepe, Giuseppe / Lenzi, Paola / Capocci, Luca / Marracino, Federico / Pizzati, Ludovica / Scarselli, Pamela / Di Pardo, Alba / Fornai, Francesco / Maglione, Vittorio

International journal of molecular sciences

2023 Volume 24, Issue 6

Abstract: Huntington's disease is one of the most common dominantly inherited neurodegenerative disorders caused by an expansion of a polyglutamine (polyQ) stretch in the N-terminal region of huntingtin (Htt). Among all the molecular mechanisms, affected by the ... ...

Abstract	Huntington's disease is one of the most common dominantly inherited neurodegenerative disorders caused by an expansion of a polyglutamine (polyQ) stretch in the N-terminal region of huntingtin (Htt). Among all the molecular mechanisms, affected by the mutation, emerging evidence proposes glycosphingolipid dysfunction as one of the major determinants. High levels of sphingolipids have been found to localize in the myelin sheaths of oligodendrocytes, where they play an important role in myelination stability and functions. In this study, we investigated any potential existing link between sphingolipid modulation and myelin structure by performing both ultrastructural and biochemical analyses. Our findings demonstrated that the treatment with the glycosphingolipid modulator THI preserved myelin thickness and the overall structure and reduced both area and diameter of pathologically giant axons in the striatum of HD mice. These ultrastructural findings were associated with restoration of different myelin marker protein, such as myelin-associated glycoprotein (MAG), myelin basic protein (MBP) and 2', 3' Cyclic Nucleotide 3'-Phosphodiesterase (CNP). Interestingly, the compound modulated the expression of glycosphingolipid biosynthetic enzymes and increased levels of GM1, whose elevation has been extensively reported to be associated with reduced toxicity of mutant Htt in different HD pre-clinical models. Our study further supports the evidence that the metabolism of glycosphingolipids may represent an effective therapeutic target for the disease.
MeSH term(s)	Mice ; Animals ; Myelin Sheath/metabolism ; Glycosphingolipids/metabolism ; Corpus Striatum/metabolism ; Neostriatum/metabolism ; Huntington Disease/drug therapy ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Huntingtin Protein/genetics ; Disease Models, Animal ; Mice, Transgenic
Chemical Substances	Glycosphingolipids ; Huntingtin Protein
Language	English
Publishing date	2023-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24065956
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Article: mTOR Modulates Intercellular Signals for Enlargement and Infiltration in Glioblastoma Multiforme.

Ryskalin, Larisa / Biagioni, Francesca / Lenzi, Paola / Frati, Alessandro / Fornai, Francesco

Cancers

2020 Volume 12, Issue 9

Abstract: Recently, exosomal release has been related to the acquisition of a malignant phenotype in glioblastoma cancer stem cells (GSCs). Remarkably, intriguing reports demonstrate that GSC-derived extracellular vesicles (EVs) contribute to glioblastoma ... ...

Abstract	Recently, exosomal release has been related to the acquisition of a malignant phenotype in glioblastoma cancer stem cells (GSCs). Remarkably, intriguing reports demonstrate that GSC-derived extracellular vesicles (EVs) contribute to glioblastoma multiforme (GBM) tumorigenesis via multiple pathways by regulating tumor growth, infiltration, and immune invasion. In fact, GSCs release tumor-promoting macrovesicles that can disseminate as paracrine factors to induce phenotypic alterations in glioma-associated parenchymal cells. In this way, GBM can actively recruit different stromal cells, which, in turn, may participate in tumor microenvironment (TME) remodeling and, thus, alter tumor progression. Vice versa, parenchymal cells can transfer their protein and genetic contents to GSCs by EVs; thus, promoting GSCs tumorigenicity. Moreover, GBM was shown to hijack EV-mediated cell-to-cell communication for self-maintenance. The present review examines the role of the mammalian Target of Rapamycin (mTOR) pathway in altering EVs/exosome-based cell-to-cell communication, thus modulating GBM infiltration and volume growth. In fact, exosomes have been implicated in GSC niche maintenance trough the modulation of GSCs stem cell-like properties, thus, affecting GBM infiltration and relapse. The present manuscript will focus on how EVs, and mostly exosomes, may act on GSCs and neighbor non tumorigenic stromal cells to modify their expression and translational profile, while making the TME surrounding the GSC niche more favorable for GBM growth and infiltration. Novel insights into the mTOR-dependent mechanisms regulating EV-mediated intercellular communication within GBM TME hold promising directions for future therapeutic applications.
Language	English
Publishing date	2020-09-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12092486
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Article ; Online: Morphology, clearing efficacy, and mTOR dependency of the organelle autophagoproteasome.

Limanaqi, Fiona / Biagioni, Francesca / Salvetti, Alessandra / Puglisi-Allegra, Stefano / Lenzi, Paola / Fornai, Francesco

European journal of histochemistry : EJH

2021 Volume 65, Issue s1

Abstract: The interplay between autophagy (ATG) and ubiquitin proteasome (UP) cell-clearing systems was recently evidenced at biochemical and morphological levels, where subunits belonging to both pathways co-localize within a novel organelle named ... ...

Abstract	The interplay between autophagy (ATG) and ubiquitin proteasome (UP) cell-clearing systems was recently evidenced at biochemical and morphological levels, where subunits belonging to both pathways co-localize within a novel organelle named autophagoproteasome (APP). We previously documented that APP occurs at baseline conditions, while it is hindered by neurotoxicant administration. This is bound to the activity of the mechanistic target of rapamycin (mTOR), since APP is stimulated by mTOR inhibition, which in turn, is correlated with cell protection. In this brief report, we provide novel, morphological and biochemical evidence on APP, suggesting the presence of active UP subunits within ATG vacuoles. Although a stream of interpretation considers such a merging as a catabolic pathway to clear inactive UP subunits, our data further indicate that UP-ATG merging may rather provide an empowered catalytic organelle.
MeSH term(s)	Animals ; Autophagosomes/physiology ; Autophagosomes/ultrastructure ; Autophagy ; Organelles/physiology ; Organelles/ultrastructure ; PC12 Cells ; Proteasome Endopeptidase Complex/metabolism ; Rats ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Ubiquitin/metabolism
Chemical Substances	Ubiquitin ; mTOR protein, rat (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2021-06-01
Publishing country	Italy
Document type	Journal Article
ZDB-ID	1109511-8
ISSN	2038-8306 ; 0391-7258 ; 1121-4201 ; 1121-760X
ISSN (online)	2038-8306
ISSN	0391-7258 ; 1121-4201 ; 1121-760X
DOI	10.4081/ejh.2021.3220
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Article ; Online: Within the Ischemic Penumbra, Sub-Cellular Compartmentalization of Heat Shock Protein 70 Overlaps with Autophagy Proteins and Fails to Merge with Lysosomes.

Mastroiacovo, Federica / Biagioni, Francesca / Lenzi, Paola / Lazzeri, Gloria / Ferrucci, Michela / Puglisi-Allegra, Stefano / Frati, Alessandro / Nicoletti, Ferdinando / Fornai, Francesco

Molecules (Basel, Switzerland)

2022 Volume 27, Issue 10

Abstract: The brain area which surrounds the frankly ischemic region is named ... ...

Abstract	The brain area which surrounds the frankly ischemic region is named the
MeSH term(s)	Animals ; Autophagosomes/metabolism ; Autophagy/physiology ; HSP70 Heat-Shock Proteins/metabolism ; Ischemia/metabolism ; Lysosomes/metabolism ; Mice
Chemical Substances	HSP70 Heat-Shock Proteins
Language	English
Publishing date	2022-05-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules27103122
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Article: Occurrence of Total and Proteinase K-Resistant Alpha-Synuclein in Glioblastoma Cells Depends on mTOR Activity.

Ryskalin, Larisa / Ferese, Rosangela / Morucci, Gabriele / Biagioni, Francesca / Busceti, Carla L / Michetti, Fabrizio / Lenzi, Paola / Frati, Alessandro / Fornai, Francesco

Cancers

2022 Volume 14, Issue 6

Abstract: Alpha-synuclein (α-syn) is a protein considered to be detrimental in a number of degenerative disorders (synucleinopathies) of which α-syn aggregates are considered a pathological hallmark. The clearance of α-syn strongly depends on autophagy, which can ... ...

Abstract	Alpha-synuclein (α-syn) is a protein considered to be detrimental in a number of degenerative disorders (synucleinopathies) of which α-syn aggregates are considered a pathological hallmark. The clearance of α-syn strongly depends on autophagy, which can be stimulated by inhibiting the mechanistic target of rapamycin (mTOR). Thus, the overexpression of mTOR and severe autophagy suppression may produce α-syn accumulation, including the proteinase K-resistant protein isoform. Glioblastoma multiforme (GBM) is a lethal brain tumor that features mTOR overexpression and severe autophagy inhibition. Cell pathology in GBM is reminiscent of a fast, progressive degenerative disorder. Therefore, the present work questions whether, as is analogous to neurons during degenerative disorders, an overexpression of α-syn occurs within GBM cells. A high amount of α-syn was documented in GBM cells via real-time PCR (RT-PCR), Western blotting, immunohistochemistry, immuno-fluorescence, and ultrastructural stoichiometry, compared with the amount of β- and γ-synucleins and compared with the amount of α-syn counted within astrocytes. The present study indicates that (i) α-syn is overexpressed in GBM cells, (ii) α-syn expression includes a proteinase-K resistant isoform, (iii) α-syn is dispersed from autophagy-like vacuoles to the cytosol, (iv) α-syn overexpression and cytosol dispersion are mitigated by rapamycin, and (v) the α-syn-related GBM-like phenotype is mitigated by silencing the SNCA gene.
Language	English
Publishing date	2022-03-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14061382
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