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Article ; Online: Analytical and clinical validation of a blood progranulin ELISA in frontotemporal dementias.

Meda, Francisco / Simrén, Joel / Borroni, Barbara / Cantoni, Valentina / Archetti, Silvana / Biasiotto, Giorgio / Andreasson, Ulf / Blennow, Kaj / Kvartsberg, Hlin / Zetterberg, Henrik

Clinical chemistry and laboratory medicine

2023 Volume 61, Issue 12, Page(s) 2195–2204

Abstract: Objectives: Heterozygous mutations in the granulin (: Methods: Analytical validation parameters including assay precision, selectivity, measurement range, dilution linearity, interferences and sample stability were tested according to previously ... ...

Abstract	Objectives: Heterozygous mutations in the granulin ( Methods: Analytical validation parameters including assay precision, selectivity, measurement range, dilution linearity, interferences and sample stability were tested according to previously described procedures. For clinical validation, PGRN levels were measured in plasma from 32 cognitively healthy individuals, 52 confirmed Results: Among the analytical validation parameters, assay precision and repeatability were very stable (coefficients of variation <7 %). Spike recovery was 96 %, the measurement range was 6.25-400 μg/L and dilution linearity ranged from 1:50-1:200. Hemolysis did not interfere with progranulin levels, and these were resistant to freeze/thaw cycles and storage at different temperatures. For the clinical validation, the assay was capable of distinguishing Conclusions: In this study, we demonstrate robust analytical and diagnostic performance of this commercial progranulin kit for implementation in clinical laboratory practice. This easy-to-use test allows identification of potential
MeSH term(s)	Humans ; Progranulins/genetics ; Frontotemporal Dementia/diagnosis ; Frontotemporal Dementia/genetics ; Intercellular Signaling Peptides and Proteins/genetics ; Mutation ; Enzyme-Linked Immunosorbent Assay
Chemical Substances	Progranulins ; Intercellular Signaling Peptides and Proteins
Language	English
Publishing date	2023-07-24
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1418007-8
ISSN	1437-4331 ; 1434-6621 ; 1437-8523
ISSN (online)	1437-4331
ISSN	1434-6621 ; 1437-8523
DOI	10.1515/cclm-2023-0562
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Article ; Online: Classification accuracy of blood-based and neurophysiological markers in the differential diagnosis of Alzheimer's disease and frontotemporal lobar degeneration.

Benussi, Alberto / Cantoni, Valentina / Rivolta, Jasmine / Archetti, Silvana / Micheli, Anna / Ashton, Nicholas / Zetterberg, Henrik / Blennow, Kaj / Borroni, Barbara

Alzheimer's research & therapy

2022 Volume 14, Issue 1, Page(s) 155

Abstract: Background: In the last decade, non-invasive blood-based and neurophysiological biomarkers have shown great potential for the discrimination of several neurodegenerative disorders. However, in the clinical workup of patients with cognitive impairment, ... ...

Abstract	Background: In the last decade, non-invasive blood-based and neurophysiological biomarkers have shown great potential for the discrimination of several neurodegenerative disorders. However, in the clinical workup of patients with cognitive impairment, it will be highly unlikely that any biomarker will achieve the highest potential predictive accuracy on its own, owing to the multifactorial nature of Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD). Methods: In this retrospective study, performed on 202 participants, we analysed plasma neurofilament light (NfL), glial fibrillary acidic protein (GFAP), and tau phosphorylated at amino acid 181 (p-Tau Results: We observed significant differences in plasma NfL, GFAP, and p-Tau Conclusions: The combined assessment of plasma and neurophysiological measures may greatly improve the differential diagnosis of AD and FTLD.
MeSH term(s)	Alzheimer Disease/diagnosis ; Amino Acids ; Amyloid beta-Peptides ; Biomarkers ; Diagnosis, Differential ; Frontotemporal Dementia/diagnosis ; Frontotemporal Lobar Degeneration/diagnosis ; Glial Fibrillary Acidic Protein ; Humans ; Retrospective Studies ; tau Proteins
Chemical Substances	Amino Acids ; Amyloid beta-Peptides ; Biomarkers ; Glial Fibrillary Acidic Protein ; tau Proteins
Language	English
Publishing date	2022-10-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-022-01094-5
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Article ; Online: Myeloid neoplasm occurrence during stable molecular remission of NPM1-mutated AML: are we facing secondary disease or AML relapse?

Giupponi, Carlotta / Bertoli, Diego / Borlenghi, Erika / Cattaneo, Chiara / Zollner, Tatiana / Masina, Lorenzo / Bagnasco, Samuele / Cerqui, Elisa / Federico, Francesca / Pagani, Chiara / Archetti, Silvana / Brugnoni, Duilio / Rossi, Giuseppe / Tucci, Alessandra

Blood cancer journal

2023 Volume 13, Issue 1, Page(s) 194

MeSH term(s)	Humans ; Neoplasm Recurrence, Local/genetics ; Nuclear Proteins/genetics ; Nucleophosmin ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Prognosis
Chemical Substances	Nuclear Proteins ; Nucleophosmin (117896-08-9)
Language	English
Publishing date	2023-12-21
Publishing country	United States
Document type	Letter
ZDB-ID	2600560-8
ISSN	2044-5385 ; 2044-5385
ISSN (online)	2044-5385
ISSN	2044-5385
DOI	10.1038/s41408-023-00959-8
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Article ; Online: Anti-GluA3 autoantibodies define a new sub-population of frontotemporal lobar degeneration patients with distinct neuropathological features.

Brain, behavior, and immunity

2024 Volume 118, Page(s) 380–397

Abstract: Autoantibodies directed against the GluA3 subunit (anti-GluA3 hIgGs) of AMPA receptors have been identified in 20%-25% of patients with frontotemporal lobar degeneration (FTLD). Data from patients and in vitro/ex vivo pre-clinical studies indicate that ... ...

Abstract	Autoantibodies directed against the GluA3 subunit (anti-GluA3 hIgGs) of AMPA receptors have been identified in 20%-25% of patients with frontotemporal lobar degeneration (FTLD). Data from patients and in vitro/ex vivo pre-clinical studies indicate that anti-GluA3 hIgGs negatively affect glutamatergic neurotransmission. However, whether and how the chronic presence of anti-GluA3 hIgGs triggers synaptic dysfunctions and the appearance of FTLD-related neuropathological and behavioural signature has not been clarified yet. To address this question, we developed and characterized a pre-clinical mouse model of passive immunization with anti-GluA3 hIgGs purified from patients. In parallel, we clinically compared FTLD patients who were positive for anti-GluA3 hIgGs to negative ones. Clinical data showed that the presence of anti-GluA3 hIgGs defined a subgroup of patients with distinct clinical features. In the preclinical model, anti-GluA3 hIgGs administration led to accumulation of phospho-tau in the postsynaptic fraction and dendritic spine loss in the prefrontal cortex. Remarkably, the preclinical model exhibited behavioural disturbances that mostly reflected the deficits proper of patients positive for anti-GluA3 hIgGs. Of note, anti-GluA3 hIgGs-mediated alterations were rescued in the animal model by enhancing glutamatergic neurotransmission with a positive allosteric modulator of AMPA receptors. Overall, our study clarified the contribution of anti-GluA3 autoantibodies to central nervous system symptoms and pathology and identified a specific subgroup of FTLD patients. Our findings will be instrumental in the development of a therapeutic personalised medicine strategy for patients positive for anti-GluA3 hIgGs.
MeSH term(s)	Animals ; Humans ; Mice ; Autoantibodies/metabolism ; Frontotemporal Dementia ; Frontotemporal Lobar Degeneration/metabolism ; Frontotemporal Lobar Degeneration/pathology ; Receptors, AMPA ; Synaptic Transmission ; tau Proteins/metabolism
Chemical Substances	Autoantibodies ; Receptors, AMPA ; tau Proteins ; Anti-AMPAR antibody
Language	English
Publishing date	2024-03-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2024.03.018
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Prognostic Relevance of

Borlenghi, Erika / Cattaneo, Chiara / Bertoli, Diego / Cerqui, Elisa / Archetti, Silvana / Passi, Angela / Oberti, Margherita / Zollner, Tatiana / Giupponi, Carlotta / Pagani, Chiara / Bianchetti, Nicola / Bottelli, Chiara / Bagnasco, Samuele / Sciumè, Margherita / Tucci, Alessandra / Rossi, Giuseppe

Cancers

2022 Volume 14, Issue 19

Abstract: The prognosis of acute myeloid leukemia depends on genetic aberrations, particularly NPM1 and FLT3-ITD mutations. The targeted drugs’ availability has renewed interest in FLT3 mutations, but the impact of these genetic alterations using these treatments ... ...

Abstract	The prognosis of acute myeloid leukemia depends on genetic aberrations, particularly NPM1 and FLT3-ITD mutations. The targeted drugs’ availability has renewed interest in FLT3 mutations, but the impact of these genetic alterations using these treatments is yet to be confirmed. Our objective was to evaluate the results obtained with the intensified NILG-AML 01/00 protocol (ClinicalTrials.gov Identifier: NCT 00400673) in 171 unselected patients (median age, 54.5 years, range 15−74) carrying the FLT3 (ITD or TKD) and/or NPM1 mutations. The CR rate and 5-y survival were 88.3% and 58% +/− 4, respectively, significantly higher in the NPM1-mutated (CR 93.9%, p: 0.0001; survival 71% +/− 6, p: 0.0017, respectively). In isolated ITD patients, the CR was lower (66.7%, p: 0.0009), and the 3 years-relapse-free survival worse (24%, p: <0.0002). The presence of ITD, irrespective of the allelic ratio, or TKD mutation, did not significantly affect the survival or relapse-free survival among the NPM1-co-mutated patients. Our data indicate that a high dose of ARAC plus idarubicin consolidation exerts a strong anti-leukemic effect in NPM1-mutated patients both with the FLT3 wild-type and mutated AML, while in the NPM1 wild-type and FLT3-mutated, the therapeutic effect remains unsatisfactory. New strategies incorporating target therapy with second-generation inhibitors will improve these results and their addition to this aggressive chemotherapeutic program merits testing.
Language	English
Publishing date	2022-09-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14194716
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Article ; Online: Differences Between Plasma and Cerebrospinal Fluid p-tau181 and p-tau231 in Early Alzheimer's Disease.

Pilotto, Andrea / Parigi, Marta / Bonzi, Giulio / Battaglio, Beatrice / Ferrari, Elisabetta / Mensi, Lorenza / Benussi, Alberto / Caratozzolo, Salvatore / Cosseddu, Maura / Turrone, Rosanna / Archetti, Silvana / Ashton, Nicholas J / Zetterberg, Henrik / Giliani, Silvia / Padovani, Alessandro

Journal of Alzheimer's disease : JAD

2022 Volume 87, Issue 3, Page(s) 991–997

Abstract: Plasma phosphorylated tau species have been recently proposed as peripheral markers of Alzheimer's disease (AD) pathology. In this cross-sectional study including 91 subjects, plasma and cerebrospinal fluid (CSF) p-tau181 and p-tau231 levels were ... ...

Abstract	Plasma phosphorylated tau species have been recently proposed as peripheral markers of Alzheimer's disease (AD) pathology. In this cross-sectional study including 91 subjects, plasma and cerebrospinal fluid (CSF) p-tau181 and p-tau231 levels were elevated in the early symptomatic stages of AD. Plasma p-tau231 and p-tau181 were strongly related to CSF phosphorylated tau, total tau and amyloid and exhibited a high accuracy-close to CSF p-tau231 and p-tau181-to identify AD already in the early stage of the disease. The findings might support the use as diagnostic and prognostic peripheral AD biomarkers in both research and clinical settings.
MeSH term(s)	Alzheimer Disease/cerebrospinal fluid ; Amyloid beta-Peptides/cerebrospinal fluid ; Biomarkers/cerebrospinal fluid ; Cross-Sectional Studies ; Humans ; Phosphorylation ; tau Proteins/cerebrospinal fluid
Chemical Substances	Amyloid beta-Peptides ; Biomarkers ; tau Proteins
Language	English
Publishing date	2022-04-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-215646
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Article ; Online: Iron and Neurodegeneration: Is Ferritinophagy the Link?

Biasiotto, Giorgio / Di Lorenzo, Diego / Archetti, Silvana / Zanella, Isabella

Molecular neurobiology

2016 Volume 53, Issue 8, Page(s) 5542–5574

Abstract: Mounting evidence indicates that the lysosome-autophagy pathway plays a critical role in iron release from ferritin, the main iron storage cellular protein, hence in the distribution of iron to the cells. The recent identification of nuclear receptor co- ... ...

Abstract	Mounting evidence indicates that the lysosome-autophagy pathway plays a critical role in iron release from ferritin, the main iron storage cellular protein, hence in the distribution of iron to the cells. The recent identification of nuclear receptor co-activator 4 as the receptor for ferritin delivery to selective autophagy sheds further light on the understanding of the mechanisms underlying this pathway. The emerging view is that iron release from ferritin through the lysosomes is a general mechanism in normal and tumour cells of different tissue origins, but it has not yet been investigated in brain cells. Defects in the lysosome-autophagy pathway are often involved in the pathogenesis of neurodegenerative disorders, and brain iron homeostasis disruption is a hallmark of many of these diseases. However, in most cases, it has not been established whether iron dysregulation is directly involved in the pathogenesis of the diseases or if it is a secondary effect derived from other pathogenic mechanisms. The recent evidence of the crucial involvement of autophagy in cellular iron handling offers new perspectives about the role of iron in neurodegeneration, suggesting that autophagy dysregulation could cause iron dyshomeostasis. In this review, we recapitulate our current knowledge on the routes through which iron is released from ferritin, focusing on the most recent advances. We summarise the current evidence concerning lysosome-autophagy pathway dysfunctions and those of iron metabolism and discuss their potential interconnections in several neurodegenerative disorders, such as Alzheimer's, Parkinson's and Huntington's diseases; amyotrophic lateral sclerosis; and frontotemporal lobar dementia.
Language	English
Publishing date	2016-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-015-9473-y
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Article ; Online: Serum total TDP-43 levels are decreased in frontotemporal dementia patients with C9orf72 repeat expansion or concomitant motoneuron disease phenotype.

Katisko, Kasper / Huber, Nadine / Kokkola, Tarja / Hartikainen, Päivi / Krüger, Johanna / Heikkinen, Anna-Leena / Paananen, Veera / Leinonen, Ville / Korhonen, Ville E / Helisalmi, Seppo / Herukka, Sanna-Kaisa / Cantoni, Valentina / Gadola, Yasmine / Archetti, Silvana / Remes, Anne M / Haapasalo, Annakaisa / Borroni, Barbara / Solje, Eino

Alzheimer's research & therapy

2022 Volume 14, Issue 1, Page(s) 151

Abstract: Background: Frontotemporal dementia (FTD) covers a spectrum of neurodegenerative disorders with various clinical and neuropathological subtypes. The two major pathological proteins accumulating in the brains of FTD patients, depending on their genetic ... ...

Abstract	Background: Frontotemporal dementia (FTD) covers a spectrum of neurodegenerative disorders with various clinical and neuropathological subtypes. The two major pathological proteins accumulating in the brains of FTD patients, depending on their genetic background, are TDP-43 and tau. We aimed to evaluate whether total TDP-43 levels measured from the serum associate with the genotype or clinical phenotype of the FTD patients and whether serum TDP-43 provides prognostic or diagnostic value in the FTD spectrum disorders. Methods: The study cohort included 254 participants with a clinical diagnosis of FTD (including all major genotypes and clinical phenotypes) and 105 cognitively healthy controls. Serum total TDP-43 levels measured with a single-molecule array (Simoa) were compared within the FTD group according to the genotype, clinical phenotype, and predicted neuropathological subtype of the patients. We also evaluated the associations between the TDP-43 levels and disease severity or survival in FTD. Results: Total TDP-43 levels in the serum were significantly lower in the FTD group as compared to the healthy control group (275.3 pg/mL vs. 361.8 pg/mL, B = 0.181, 95%CI = 0.014-0.348, p = 0.034). The lowest TDP-43 levels were observed in the subgroup of FTD patients harboring predicted TDP-43 brain pathology (FTD-TDP, 241.4 pg/mL). The low levels in the FTD-TDP group were especially driven by C9orf72 repeat expansion carriers (169.2 pg/mL) and FTD patients with concomitant motoneuron disease (FTD-MND, 113.3 pg/mL), whereas GRN mutation carriers did not show decreased TDP-43 levels (328.6 pg/mL). Serum TDP-43 levels showed no correlation with disease severity nor progression in FTD. Conclusions: Our results indicate that the total levels of TDP-43 in the serum are decreased especially in FTD patients with the C9orf72 repeat expansion or FTD-MND phenotype, both subtypes strongly associated with TDP-43 type B brain pathology. Serum-based measurement of TDP-43 could represent a useful tool in indicating C9orf72 repeat expansion and FTD-MND-related TDP-43 neuropathology for future diagnostics and intervention studies.
MeSH term(s)	C9orf72 Protein/genetics ; DNA Repeat Expansion ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Frontotemporal Dementia/pathology ; Humans ; Motor Neuron Disease/genetics ; Motor Neuron Disease/metabolism ; Motor Neuron Disease/pathology ; Motor Neurons/metabolism ; Motor Neurons/pathology ; Phenotype
Chemical Substances	C9orf72 Protein ; C9orf72 protein, human ; DNA-Binding Proteins ; TARDBP protein, human
Language	English
Publishing date	2022-10-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-022-01091-8
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Article ; Online: The role of clonal hematopoiesis as driver of therapy-related myeloid neoplasms after autologous stem cell transplantation.

Gramegna, Doriana / Bertoli, Diego / Cattaneo, Chiara / Almici, Camillo / Re, Alessandro / Belotti, Angelo / Borlenghi, Erika / Lanzi, Gaetana / Archetti, Silvana / Verardi, Rosanna / Brugnoni, Duilio / Sciumè, Margherita / Daffini, Rosa / Roccaro, Aldo M / Tucci, Alessandra / Rossi, Giuseppe

Annals of hematology

2022 Volume 101, Issue 6, Page(s) 1227–1237

Abstract: Therapy-related myeloid neoplasm (t-MN) is a threatening complication of autologous stem cell transplantation (ASCT). Detecting clonal hematopoiesis (CH) mutations in cryopreserved cells before ASCT has been associated with a higher risk of t-MN, but the ...

Abstract	Therapy-related myeloid neoplasm (t-MN) is a threatening complication of autologous stem cell transplantation (ASCT). Detecting clonal hematopoiesis (CH) mutations in cryopreserved cells before ASCT has been associated with a higher risk of t-MN, but the evolution of molecular abnormalities from pre-ASCT to t-MN, within the same patient, remains to be elucidated. We evaluated the mutational profile of 19 lymphoma/myeloma patients, at both pre-ASCT and t-MN diagnosis, using a targeted NGS approach; 26 non-developing t-MN control patients were also studied pre-ASCT. At ASCT, we found a higher frequency of CH in patients developing t-MN (58%) than in those who did not (23%) (P = 0.029); mutations in epigenetic (DNMT3A, TET2, and ASXL1) and DNA repair genes (PPM1D, RAD21, TP53, and STAG2) were the most represented. At t-MN, CH increased to 82% of patients. Cumulative mutational burden and variant allele frequency (VAF) also increased at t-MN. CH clones detected at ASCT were found at t-MN in eight out of 16 patients, mainly with stable VAF. Among the new driver mutations appeared at t-MN, TP53 increased from one to 13 mutations, in nine patients; being associated with complex karyotype. Mutations in transcription factor (RUNX1, CEBPA) and intracellular signaling genes (FLT3, RAS genes) also increased from three to 17 mutations in eight patients, presenting with a normal karyotype. Overall, we found that preexisting CH at ASCT rarely causes t-MN directly, but may rather facilitate the appearance of new mutations, especially those involving TP53, RUNX1, and RAS, that can drive the evolution to t-MN of at least two distinct types.
MeSH term(s)	Clonal Hematopoiesis/genetics ; Core Binding Factor Alpha 2 Subunit/genetics ; Hematopoiesis/genetics ; Hematopoietic Stem Cell Transplantation/adverse effects ; Humans ; Mutation ; Myeloproliferative Disorders/complications ; Myeloproliferative Disorders/genetics ; Myeloproliferative Disorders/therapy ; Neoplasms, Second Primary/genetics ; Transplantation, Autologous/adverse effects
Chemical Substances	Core Binding Factor Alpha 2 Subunit
Language	English
Publishing date	2022-04-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1064950-5
ISSN	1432-0584 ; 0939-5555 ; 0945-8077
ISSN (online)	1432-0584
ISSN	0939-5555 ; 0945-8077
DOI	10.1007/s00277-022-04806-x
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Article ; Online: Serum neurofilament light in professional soccer players: goal on safety.

Cornali, Claudio / Amaddeo, Paolo / Benussi, Alberto / Perrone, Federica / Manes, Marta / Zanardini, Roberta / Benussi, Luisa / Belotti, Francesco / Bellini, Gianandrea / Bruzzone, Andrea / Bruzzone, Marco / Morelli, Daniela / Archetti, Silvana / Latronico, Nicola / Padovani, Alessandro / Fontanella, Marco Maria / Ghidoni, Roberta / Borroni, Barbara

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology

2022 Volume 43, Issue 8, Page(s) 5087–5090

Abstract: Background: Sports-related concussion (SRC) is a subset of mild traumatic brain injuries occurring in contact sports. Most people recover spontaneously, but in retired professional players, the risk for neurodegenerative diseases is increased. A ... ...

Abstract	Background: Sports-related concussion (SRC) is a subset of mild traumatic brain injuries occurring in contact sports. Most people recover spontaneously, but in retired professional players, the risk for neurodegenerative diseases is increased. A biomarker, such as neurofilament light chains (NfL), would help to address this issue and demonstrate sports' safety. Assessing NfL in professional soccer players may be the best way to investigate if repetitive head-impact exposure in the typical lower and asymptomatic range is harmful. Objective: To evaluate whether the NfL in serum is a sensitive biomarker to detect mild brain injury in professional soccer players. Methods: Thirty-six soccer players belonging to a professional Italian team underwent serum NfL assessment using ultrasensitive single-molecule array technology. Sixteen healthy nonathletic controls were also enrolled. Differences between groups and changes over time, considering pre-season vs. season, were considered. Results: Serum NfL concentrations were comparable in the soccer professional players (median [interquartile range], 6.44 pg/mL [4.60-8.27] and controls (6.50 pg/mL [5.26-7.04]), with a median difference of - 0.06 pg/mL (95% CI -1.36 to 1.18), p = 0.957. No significant differences according to players' role (goalkeeper, defender, midfielder or forward) or according to timing of sampling (pre-season vs. season) were found. Conclusions: These results suggest that professional soccer, even when played at the highest level of competition, may be considered safe. Future studies assessing serum NfL levels after soccer-related concussions should be carried out, to evaluate their usefulness as a return-to-play marker avoiding second impact syndrome.
MeSH term(s)	Biomarkers ; Brain Concussion/diagnosis ; Humans ; Intermediate Filaments ; Soccer/injuries ; Sports
Chemical Substances	Biomarkers
Language	English
Publishing date	2022-05-18
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2016546-8
ISSN	1590-3478 ; 1590-1874
ISSN (online)	1590-3478
ISSN	1590-1874
DOI	10.1007/s10072-022-06109-5
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