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Article ; Online: Circular RNAs: Emblematic Players of Neurogenesis and Neurodegeneration.

D'Anca, Marianna / Buccellato, Francesca R / Fenoglio, Chiara / Galimberti, Daniela

International journal of molecular sciences

2022 Volume 23, Issue 8

Abstract: In the fascinating landscape of non-coding RNAs (ncRNAs), circular RNAs (circRNAs) are peeping out as a new promising and appreciated class of molecules with great potential as diagnostic and prognostic biomarkers. They come from circularization of ... ...

Abstract	In the fascinating landscape of non-coding RNAs (ncRNAs), circular RNAs (circRNAs) are peeping out as a new promising and appreciated class of molecules with great potential as diagnostic and prognostic biomarkers. They come from circularization of single-stranded RNA molecules covalently closed and generated through alternative mRNA splicing. Dismissed for many years, similar to aberrant splicing by-products, nowadays, their role has been regained. They are able to regulate the expression of linear mRNA transcripts at different levels acting as miRNA sponges, interacting with ribonucleoproteins or exerting a control on gene expression. On the other hand, being extremely conserved across phyla and stable, cell and tissue specific, mostly abundant than the linear RNAs, it is not surprising that they should have critical biological functions. Curiously, circRNAs are particularly expressed in brain and they build up during aging and age-related diseases. These extraordinary peculiarities make circRNAs potentially suitable as promising molecular biomarkers, especially of aging and neurodegenerative diseases. This review aims to explore new evidence on circRNAs, emphasizing their role in aging and pathogenesis of major neurodegenerative disorders, Alzheimer's disease, frontotemporal dementia, and Parkinson's diseases with a look toward their potential usefulness in biomarker searching.
MeSH term(s)	Biomarkers ; Humans ; MicroRNAs/genetics ; Neurodegenerative Diseases/genetics ; Neurogenesis/genetics ; RNA, Circular/genetics ; RNA, Messenger
Chemical Substances	Biomarkers ; MicroRNAs ; RNA, Circular ; RNA, Messenger
Language	English
Publishing date	2022-04-08
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/ijms23084134
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Article: Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery

Buccellato, Francesca Romana / D’Anca, Marianna / Fenoglio, Chiara / Scarpini, Elio / Galimberti, Daniela

Antioxidants. 2021 Aug. 26, v. 10, no. 9

2021

Abstract: Alzheimer’s disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. The lack of effective treatments for overt AD urges the ... ...

Abstract	Alzheimer’s disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. The lack of effective treatments for overt AD urges the discovery of biomarkers for early diagnosis, i.e., in subjects with mild cognitive impairment (MCI) or prodromal AD. The brain is exposed to oxidative stress as levels of reactive oxygen species (ROS) are increased, whereas cellular antioxidant defenses are decreased. Increased ROS levels can damage cellular structures or molecules, leading to protein, lipid, DNA, or RNA oxidation. Oxidative damage is involved in the molecular mechanisms which link the accumulation of amyloid-β and neurofibrillary tangles, containing hyperphosphorylated tau, to microglia response. In this scenario, microglia are thought to play a crucial role not only in the early events of AD pathogenesis but also in the progression of the disease. This review will focus on oxidative damage products as possible peripheral biomarkers in AD and in the preclinical phases of the disease. Particular attention will be paid to biological fluids such as blood, CSF, urine, and saliva, and potential future use of molecules contained in such body fluids for early differential diagnosis and monitoring the disease course. We will also review the role of oxidative damage and microglia in the pathogenesis of AD and, more broadly, in neurodegeneration.
Keywords	DNA ; RNA ; biomarkers ; blood ; brain ; cognitive disorders ; death ; disease course ; disease progression ; early diagnosis ; lipids ; neurodegenerative diseases ; neuroglia ; oxidation ; oxidative stress ; pathogenesis ; reactive oxygen species ; saliva ; urine
Language	English
Dates of publication	2021-0826
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091353
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Extracellular Vesicles in Multiple Sclerosis: Role in the Pathogenesis and Potential Usefulness as Biomarkers and Therapeutic Tools.

D'Anca, Marianna / Fenoglio, Chiara / Buccellato, Francesca Romana / Visconte, Caterina / Galimberti, Daniela / Scarpini, Elio

Cells

2021 Volume 10, Issue 7

Abstract: Although extracellular vesicles (EVs) were initially relegated to a waste disposal role, nowadays, they have gained multiple fundamental functions working as messengers in intercellular communication as well as exerting active roles in physiological and ... ...

Abstract	Although extracellular vesicles (EVs) were initially relegated to a waste disposal role, nowadays, they have gained multiple fundamental functions working as messengers in intercellular communication as well as exerting active roles in physiological and pathological processes. Accumulating evidence proves the involvement of EVs in many diseases, including those of the central nervous system (CNS), such as multiple sclerosis (MS). Indeed, these membrane-bound particles, produced in any type of cell, carry and release a vast range of bioactive molecules (nucleic acids, proteins, and lipids), conferring genotypic and phenotypic changes to the recipient cell. This means that not only EVs per se but their content, especially, could reveal new candidate disease biomarkers and/or therapeutic agents. This review is intended to provide an overview regarding current knowledge about EVs' involvement in MS, analyzing the potential versatility of EVs as a new therapeutic tool and source of biomarkers.
MeSH term(s)	Biomarkers/metabolism ; Extracellular Vesicles/metabolism ; Humans ; Multiple Sclerosis/complications ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/therapy ; Nerve Degeneration/complications ; Nerve Degeneration/pathology ; Neuroprotection
Chemical Substances	Biomarkers
Language	English
Publishing date	2021-07-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10071733
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Article: Role of Oxidative Damage in Alzheimer's Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery.

Buccellato, Francesca Romana / D'Anca, Marianna / Fenoglio, Chiara / Scarpini, Elio / Galimberti, Daniela

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 9

Abstract: Alzheimer's disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. The lack of effective treatments for overt AD urges the ... ...

Abstract	Alzheimer's disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. The lack of effective treatments for overt AD urges the discovery of biomarkers for early diagnosis, i.e., in subjects with mild cognitive impairment (MCI) or prodromal AD. The brain is exposed to oxidative stress as levels of reactive oxygen species (ROS) are increased, whereas cellular antioxidant defenses are decreased. Increased ROS levels can damage cellular structures or molecules, leading to protein, lipid, DNA, or RNA oxidation. Oxidative damage is involved in the molecular mechanisms which link the accumulation of amyloid-β and neurofibrillary tangles, containing hyperphosphorylated tau, to microglia response. In this scenario, microglia are thought to play a crucial role not only in the early events of AD pathogenesis but also in the progression of the disease. This review will focus on oxidative damage products as possible peripheral biomarkers in AD and in the preclinical phases of the disease. Particular attention will be paid to biological fluids such as blood, CSF, urine, and saliva, and potential future use of molecules contained in such body fluids for early differential diagnosis and monitoring the disease course. We will also review the role of oxidative damage and microglia in the pathogenesis of AD and, more broadly, in neurodegeneration.
Language	English
Publishing date	2021-08-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091353
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Article ; Online: Progranulin as a therapeutic target for dementia.

Galimberti, Daniela / Fenoglio, Chiara / Scarpini, Elio

Expert opinion on therapeutic targets

2018 Volume 22, Issue 7, Page(s) 579–585

Abstract: Introduction: Progranulin (PGRN) is an acrosomal glycoprotein that is synthesized during spermatogenesis. It is overexpressed in tumors and has anti-inflammatory properties. The protein may be cleaved into granulins which display pro-inflammatory ... ...

Abstract	Introduction: Progranulin (PGRN) is an acrosomal glycoprotein that is synthesized during spermatogenesis. It is overexpressed in tumors and has anti-inflammatory properties. The protein may be cleaved into granulins which display pro-inflammatory properties. In 2006, mutations in progranulin gene (GRN) that cause haploinsufficiency were found in familial cases of frontotemporal dementia (FTD). Patients with null mutations in GRN display very low-plasma PGRN levels; this analysis is useful for identifying mutation carriers, independent of the clinical presentation, and in those before the appearance of symptoms. Areas covered: Here, we review the current knowledge of PGRN physiological functions and GRN mutations associated with FTD; we also summarize state of the art clinical trials and those compounds able to replace PGRN loss in preclinical models. Expert opinion: PGRN represents a promising therapeutic target for FTD. Cohorts suitable for treatment, ideally at the preclinical stage, where pathogenic mechanisms ongoing in the brain are targeted, are available. However, PGRN may have side effects, such as the risk of tumorigenesis, and the risk/benefit ratio of any intervention cannot be predicted. Furthermore, at present, the situation is complicated by the absence of adequate outcome measures.
MeSH term(s)	Animals ; Brain/physiopathology ; Drug Development ; Frontotemporal Dementia/drug therapy ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/physiopathology ; Haploinsufficiency/genetics ; Humans ; Loss of Function Mutation ; Progranulins/blood ; Progranulins/genetics
Chemical Substances	GRN protein, human ; Progranulins
Language	English
Publishing date	2018-06-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1080/14728222.2018.1487951
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Article ; Online: Epigenetic regulatory modifications in genetic and sporadic frontotemporal dementia.

Fenoglio, Chiara / Scarpini, Elio / Galimberti, Daniela

Expert review of neurotherapeutics

2018 Volume 18, Issue 6, Page(s) 469–475

Abstract: Introduction: Epigenetic modifications have recently been linked to neurodegenerative diseases, such as frontotemporal dementia (FTD), which represents the second most common form of dementia in adulthood after Alzheimer's disease (AD). Epigenetic ... ...

Abstract	Introduction: Epigenetic modifications have recently been linked to neurodegenerative diseases, such as frontotemporal dementia (FTD), which represents the second most common form of dementia in adulthood after Alzheimer's disease (AD). Epigenetic regulation occurs at different cellular levels and serve as a way to alter genetic information not only in aging but also following environmental signals. Thus, epigenetics mechanisms could exert their function at early stage of the disease, especially in sporadic cases. Areas covered: Herein, the available evidence supporting the concept that epigenetic-driven changes might shed the light into the pathogenic mechanisms of FTD will be summarized, with particular regard to their influence in underlying sporadic/familiar FTD onset and/or severity, and to the possibility to open a new scenario to facilitate early diagnosis and the identification of novel therapeutic targets. Bibliographic search through PubMed was used to find the studies included in this review. Expert commentary: Although epigenetic investigation in neurodegenerative disorders is in its infancy, recent advances in the technology of epigenetic change determination has led to novel, challenging findings. In particular, the knowledge and the characterization of epigenetic events could result in novel therapeutic strategies.
MeSH term(s)	Epigenesis, Genetic/genetics ; Frontotemporal Dementia/genetics ; Humans
Language	English
Publishing date	2018-06-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2112534-X
ISSN	1744-8360 ; 1473-7175
ISSN (online)	1744-8360
ISSN	1473-7175
DOI	10.1080/14737175.2018.1481389
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Article ; Online: Role of Genetics and Epigenetics in the Pathogenesis of Alzheimer's Disease and Frontotemporal Dementia.

Fenoglio, Chiara / Scarpini, Elio / Serpente, Maria / Galimberti, Daniela

Journal of Alzheimer's disease : JAD

2018 Volume 62, Issue 3, Page(s) 913–932

Abstract: Alzheimer's disease (AD) and frontotemporal dementia (FTD) represent the first cause of dementia in senile and pre-senile population, respectively. A percentage of cases have a genetic cause, inherited with an autosomal dominant pattern of transmission. ... ...

Abstract	Alzheimer's disease (AD) and frontotemporal dementia (FTD) represent the first cause of dementia in senile and pre-senile population, respectively. A percentage of cases have a genetic cause, inherited with an autosomal dominant pattern of transmission. The majority of cases, however, derive from complex interactions between a number of genetic and environmental factors. Gene variants may act as risk or protective factors. Their combination with a variety of environmental exposures may result in increased susceptibility to these diseases or may influence their course. The scenario is even more complicated considering the effect of epigenetics, which encompasses mechanisms able to alter the expression of genes without altering the DNA sequence. In this review, an overview of the current genetic and epigenetic progresses in AD and FTD will be provided, with particular focus on 1) causative genes, 2) genetic risk factors and disease modifiers, and 3) epigenetics, including methylation, non-coding RNAs and chromatin remodeling.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Animals ; Epigenesis, Genetic ; Frontotemporal Dementia/genetics ; Frontotemporal Dementia/metabolism ; Genetic Predisposition to Disease ; Humans
Language	English
Publishing date	2018-03-21
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-170702
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Article ; Online: miRNA Expression Is Increased in Serum from Patients with Semantic Variant Primary Progressive Aphasia.

Serpente, Maria / Ghezzi, Laura / Fenoglio, Chiara / Buccellato, Francesca R / Fumagalli, Giorgio G / Rotondo, Emanuela / Arcaro, Marina / Arighi, Andrea / Galimberti, Daniela

International journal of molecular sciences

2022 Volume 23, Issue 15

Abstract: Primary progressive aphasia (PPA) damages the parts of the brain that control speech and language. There are three clinical PPA variants: nonfluent/agrammatic (nfvPPA), logopenic (lvPPA) and semantic (svPPA). The pathophysiology underlying PPA variants ... ...

Abstract	Primary progressive aphasia (PPA) damages the parts of the brain that control speech and language. There are three clinical PPA variants: nonfluent/agrammatic (nfvPPA), logopenic (lvPPA) and semantic (svPPA). The pathophysiology underlying PPA variants is not fully understood, including the role of micro (mi)RNAs which were previously shown to play a role in several neurodegenerative diseases. Using a two-step analysis (array and validation through real-time PCR), we investigated the miRNA expression pattern in serum from 54 PPA patients and 18 controls. In the svPPA cohort, we observed a generalized upregulation of miRNAs with miR-106b-5p and miR-133a-3p reaching statistical significance (miR-106b-5p: 2.69 ± 0.89 mean ± SD vs. 1.18 ± 0.28, p < 0.0001; miR-133a-3p: 2.09 ± 0.10 vs. 0.74 ± 0.11 mean ± SD, p = 0.0002). Conversely, in lvPPA, the majority of miRNAs were downregulated. GO enrichment and KEGG pathway analyses revealed that target genes of both miRNAs are involved in pathways potentially relevant for the pathogenesis of neurodegenerative diseases. This is the first study that investigates the expression profile of circulating miRNAs in PPA variant patients. We identified a specific miRNA expression profile in svPPA that could differentiate this pathological condition from other PPA variants. Nevertheless, these preliminary results need to be confirmed in a larger independent cohort.
MeSH term(s)	Aphasia, Primary Progressive/genetics ; Aphasia, Primary Progressive/pathology ; Brain/pathology ; Humans ; Language ; MicroRNAs/genetics ; Semantics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2022-07-30
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/ijms23158487
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Article ; Online: CLIC1 Protein Accumulates in Circulating Monocyte Membrane during Neurodegeneration.

Carlini, Valentina / Verduci, Ivan / Cianci, Francesca / Cannavale, Gaetano / Fenoglio, Chiara / Galimberti, Daniela / Mazzanti, Michele

International journal of molecular sciences

2020 Volume 21, Issue 4

Abstract: Pathologies that lead to neurodegeneration in the central nervous system (CNS) represent a major contemporary medical challenge. Neurodegenerative processes, like those that occur in Alzheimer's disease (AD) are progressive, and at the moment, they are ... ...

Abstract	Pathologies that lead to neurodegeneration in the central nervous system (CNS) represent a major contemporary medical challenge. Neurodegenerative processes, like those that occur in Alzheimer's disease (AD) are progressive, and at the moment, they are unstoppable. Not only is an adequate therapy missing but diagnosis is also extremely complicated. The most reliable method is the measurement of beta amyloid and tau peptides concentration in the cerebrospinal fluid (CSF). However, collecting liquid samples from the CNS is an invasive procedure, thus it is not suitable for a large-scale prevention program. Ideally, blood testing is the most manageable and appropriate diagnostic procedure for a massive population screening. Recently, a few candidates, including proteins or microRNAs present in plasma/serum have been identified. The aim of the present work is to propose the chloride intracellular channel 1 (CLIC1) protein as a potential marker of neurodegenerative processes. CLIC1 protein accumulates in peripheral blood mononuclear cells (PBMCs), and increases drastically when the CNS is in a chronic inflammatory state. In AD patients, both immunolocalization and mRNA quantification are able to show the behavior of CLIC1 during a persistent inflammatory state of the CNS. In particular, confocal microscopy analysis and electrophysiological measurements highlight the significant presence of transmembrane CLIC1 (tmCLIC1) in PBMCs from AD patients. Recent investigations suggest that tmCLIC1 has a very specific role. This provides an opportunity to use blood tests and conventional technologies to discriminate between healthy individuals and patients with ongoing neurodegenerative processes.
MeSH term(s)	Aged ; Alzheimer Disease/blood ; Alzheimer Disease/pathology ; Biomarkers/blood ; Cell Membrane/metabolism ; Cell Membrane/pathology ; Chloride Channels/blood ; Female ; Humans ; Male ; Middle Aged ; Monocytes/metabolism ; Monocytes/pathology
Chemical Substances	Biomarkers ; CLIC1 protein, human ; Chloride Channels
Language	English
Publishing date	2020-02-21
Publishing country	Switzerland
Document type	Clinical Trial ; 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/ijms21041484
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Article ; Online: Altered Extracellular Vesicle miRNA Profile in Prodromal Alzheimer's Disease.

Visconte, Caterina / Fenoglio, Chiara / Serpente, Maria / Muti, Paola / Sacconi, Andrea / Rigoni, Marta / Arighi, Andrea / Borracci, Vittoria / Arcaro, Marina / Arosio, Beatrice / Ferri, Evelyn / Golia, Maria Teresa / Scarpini, Elio / Galimberti, Daniela

International journal of molecular sciences

2023 Volume 24, Issue 19

Abstract: Extracellular vesicles (EVs) are nanosized vesicles released by almost all body tissues, representing important mediators of cellular communication, and are thus promising candidate biomarkers for neurodegenerative diseases like Alzheimer's disease (AD). ...

Abstract	Extracellular vesicles (EVs) are nanosized vesicles released by almost all body tissues, representing important mediators of cellular communication, and are thus promising candidate biomarkers for neurodegenerative diseases like Alzheimer's disease (AD). The aim of the present study was to isolate total EVs from plasma and characterize their microRNA (miRNA) contents in AD patients. We isolated total EVs from the plasma of all recruited subjects using ExoQuickULTRA exosome precipitation solution (SBI). Subsequently, circulating total EVs were characterized using Nanosight nanoparticle tracking analysis (NTA), transmission electron microscopy (TEM), and Western blotting. A panel of 754 miRNAs was determined with RT-qPCR using TaqMan OpenArray technology in a QuantStudio 12K System (Thermo Fisher Scientific). The results demonstrated that plasma EVs showed widespread deregulation of specific miRNAs (miR-106a-5p, miR-16-5p, miR-17-5p, miR-195-5p, miR-19b-3p, miR-20a-5p, miR-223-3p, miR-25-3p, miR-296-5p, miR-30b-5p, miR-532-3p, miR-92a-3p, and miR-451a), some of which were already known to be associated with neurological pathologies. A further validation analysis also confirmed a significant upregulation of miR-16-5p, miR-25-3p, miR-92a-3p, and miR-451a in prodromal AD patients, suggesting these dysregulated miRNAs are involved in the early progression of AD.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; MicroRNAs/genetics ; Biomarkers ; Extracellular Vesicles/genetics ; Exosomes/genetics
Chemical Substances	MicroRNAs ; Biomarkers ; MIRN296 microRNA, human ; MIRN532 microRNA, human
Language	English
Publishing date	2023-09-29
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/ijms241914749
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