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Article: Estrogens still represent an attractive therapeutic approach for Alzheimer's disease.

Tamagno, Elena / Guglielmotto, Michela

2021 Volume 17, Issue 1, Page(s) 93–94

Language	English
Publishing date	2021-06-07
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.314295
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Oxidative Stress and Beta Amyloid in Alzheimer’s Disease. Which Comes First: The Chicken or the Egg?

Tamagno, Elena / Guglielmotto, Michela / Vasciaveo, Valeria / Tabaton, Massimo

Antioxidants. 2021 Sept. 16, v. 10, no. 9

2021

Abstract: The pathogenesis of Alzheimer’s disease involves β amyloid (Aβ) accumulation known to induce synaptic dysfunction and neurodegeneration. The brain’s vulnerability to oxidative stress (OS) is considered a crucial detrimental factor in Alzheimer’s disease. ...

Abstract	The pathogenesis of Alzheimer’s disease involves β amyloid (Aβ) accumulation known to induce synaptic dysfunction and neurodegeneration. The brain’s vulnerability to oxidative stress (OS) is considered a crucial detrimental factor in Alzheimer’s disease. OS and Aβ are linked to each other because Aβ induces OS, and OS increases the Aβ deposition. Thus, the answer to the question “which comes first: the chicken or the egg?” remains extremely difficult. In any case, the evidence for the primary occurrence of oxidative stress in AD is attractive. Thus, evidence indicates that a long period of gradual oxidative damage accumulation precedes and results in the appearance of clinical and pathological AD symptoms, including Aβ deposition, neurofibrillary tangle formation, metabolic dysfunction, and cognitive decline. Moreover, oxidative stress plays a crucial role in the pathogenesis of many risk factors for AD. Alzheimer’s disease begins many years before its symptoms, and antioxidant treatment can be an important therapeutic target for attacking the disease.
Keywords	amyloid ; antioxidants ; brain ; cognitive disorders ; neurodegenerative diseases ; oxidative stress ; pathogenesis ; therapeutics
Language	English
Dates of publication	2021-0916
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091479
Database	NAL-Catalogue (AGRICOLA)

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Article: Oxidative Stress and Beta Amyloid in Alzheimer's Disease. Which Comes First: The Chicken or the Egg?

Tamagno, Elena / Guglielmotto, Michela / Vasciaveo, Valeria / Tabaton, Massimo

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 9

Abstract: The pathogenesis of Alzheimer's disease involves β amyloid (Aβ) accumulation known to induce synaptic dysfunction and neurodegeneration. The brain's vulnerability to oxidative stress (OS) is considered a crucial detrimental factor in Alzheimer's disease. ...

Abstract	The pathogenesis of Alzheimer's disease involves β amyloid (Aβ) accumulation known to induce synaptic dysfunction and neurodegeneration. The brain's vulnerability to oxidative stress (OS) is considered a crucial detrimental factor in Alzheimer's disease. OS and Aβ are linked to each other because Aβ induces OS, and OS increases the Aβ deposition. Thus, the answer to the question "which comes first: the chicken or the egg?" remains extremely difficult. In any case, the evidence for the primary occurrence of oxidative stress in AD is attractive. Thus, evidence indicates that a long period of gradual oxidative damage accumulation precedes and results in the appearance of clinical and pathological AD symptoms, including Aβ deposition, neurofibrillary tangle formation, metabolic dysfunction, and cognitive decline. Moreover, oxidative stress plays a crucial role in the pathogenesis of many risk factors for AD. Alzheimer's disease begins many years before its symptoms, and antioxidant treatment can be an important therapeutic target for attacking the disease.
Language	English
Publishing date	2021-09-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10091479
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Article: Extracellular Fragmented Self-DNA Is Involved in Plant Responses to Biotic Stress.

Barbero, Francesca / Guglielmotto, Michela / Islam, Monirul / Maffei, Massimo E

Frontiers in plant science

2021 Volume 12, Page(s) 686121

Abstract: A growing body of evidence indicates that extracellular fragmented self-DNA (eDNA), by acting as a signaling molecule, triggers inhibitory effects on conspecific plants and functions as a damage-associated molecular pattern (DAMP). To evaluate early and ... ...

Abstract	A growing body of evidence indicates that extracellular fragmented self-DNA (eDNA), by acting as a signaling molecule, triggers inhibitory effects on conspecific plants and functions as a damage-associated molecular pattern (DAMP). To evaluate early and late events in DAMP-dependent responses to eDNA, we extracted, fragmented, and applied the tomato (
Language	English
Publishing date	2021-07-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2613694-6
ISSN	1664-462X
ISSN	1664-462X
DOI	10.3389/fpls.2021.686121
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Article ; Online: Sleep fragmentation affects glymphatic system through the different expression of AQP4 in wild type and 5xFAD mouse models.

Vasciaveo, Valeria / Iadarola, Antonella / Casile, Antonino / Dante, Davide / Morello, Giulia / Minotta, Lorenzo / Tamagno, Elena / Cicolin, Alessandro / Guglielmotto, Michela

Acta neuropathologica communications

2023 Volume 11, Issue 1, Page(s) 16

Abstract: Alzheimer's disease (AD) is characterized by genetic and multifactorial risk factors. Many studies correlate AD to sleep disorders. In this study, we performed and validated a mouse model of AD and sleep fragmentation, which properly mimics a real ... ...

Abstract	Alzheimer's disease (AD) is characterized by genetic and multifactorial risk factors. Many studies correlate AD to sleep disorders. In this study, we performed and validated a mouse model of AD and sleep fragmentation, which properly mimics a real condition of intermittent awakening. We noticed that sleep fragmentation induces a general acceleration of AD progression in 5xFAD mice, while in wild type mice it affects cognitive behaviors in particular learning and memory. Both these events may be correlated to aquaporin-4 (AQP4) modulation, a crucial player of the glymphatic system activity. In particular, sleep fragmentation differentially affects aquaporin-4 channel (AQP4) expression according to the stage of the disease, with an up-regulation in younger animals, while such change cannot be detected in older ones. Moreover, in wild type mice sleep fragmentation affects cognitive behaviors, in particular learning and memory, by compromising the glymphatic system through the decrease of AQP4. Nevertheless, an in-depth study is needed to better understand the mechanism by which AQP4 is modulated and whether it could be considered a risk factor for the disease development in wild type mice. If our hypotheses are going to be confirmed, AQP4 modulation may represent the convergence point between AD and sleep disorder pathogenic mechanisms.
MeSH term(s)	Animals ; Mice ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Aquaporin 4/genetics ; Aquaporin 4/metabolism ; Brain/pathology ; Disease Models, Animal ; Glymphatic System/pathology ; Mice, Transgenic ; Sleep Deprivation/metabolism ; Sleep Wake Disorders/genetics
Chemical Substances	Amyloid beta-Peptides ; Aquaporin 4 ; Aqp4 protein, mouse
Language	English
Publishing date	2023-01-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-022-01498-2
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Article ; Online: Estrogens Inhibit Amyloid-β-Mediated Paired Helical Filament-Like Conformation of Tau Through Antioxidant Activity and miRNA 218 Regulation in hTau Mice.

Guglielmotto, Michela / Manassero, Giusi / Vasciaveo, Valeria / Venezia, Marika / Tabaton, Massimo / Tamagno, Elena

Journal of Alzheimer's disease : JAD

2020 Volume 77, Issue 3, Page(s) 1339–1351

Abstract: Background: The risk of developing Alzheimer's disease as well as its progression and severity are known to be different in men and women, and cognitive decline is greater in women than in men at the same stage of disease and could be correlated at ... ...

Abstract	Background: The risk of developing Alzheimer's disease as well as its progression and severity are known to be different in men and women, and cognitive decline is greater in women than in men at the same stage of disease and could be correlated at least in part on estradiol levels. Objective: In our work we found that biological sex influences the effect of amyloid-β42 (Aβ42) monomers on pathological tau conformational change. Methods: In this study we used transgenic mice expressing the wild-type human tau (hTau) which were subjected to intraventricular (ICV) injections of Aβ peptides in nanomolar concentration. Results: We found that Aβ42 produces pathological conformational changes and hyperphosphorylation of tau protein in male or ovariectomized female mice but not in control females. The treatment of ovariectomized females with estradiol replacement protects against the pathological conformation of tau and seems to be mediated by antioxidant activity as well as the ability to modulate the expression of miRNA 218 linked to tau phosphorylation. Conclusion: Our study indicates that factors as age, reproductive stage, hormone levels, and the interplay with other risk factors should be considered in women, in order to identify the best appropriate therapeutic approach in prevention of cognitive impairment.
MeSH term(s)	Amyloid beta-Peptides/toxicity ; Animals ; Antioxidants/administration & dosage ; Estradiol/administration & dosage ; Estrogens/deficiency ; Female ; Humans ; Injections, Intraventricular ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; MicroRNAs/biosynthesis ; Ovariectomy ; Peptide Fragments/toxicity ; Protein Conformation ; tau Proteins/biosynthesis ; tau Proteins/chemistry
Chemical Substances	Amyloid beta-Peptides ; Antioxidants ; Estrogens ; MIRN218 microRNA, mouse ; Mapt protein, mouse ; MicroRNAs ; Peptide Fragments ; amyloid beta-protein (1-42) ; tau Proteins ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2020-08-07
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-200707
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Article ; Online: Extracellular Self-DNA (esDNA), but Not Heterologous Plant or Insect DNA (etDNA), Induces Plasma Membrane Depolarization and Calcium Signaling in Lima Bean (Phaseolus lunatus) and Maize (Zea mays).

Barbero, Francesca / Guglielmotto, Michela / Capuzzo, Andrea / Maffei, Massimo E

International journal of molecular sciences

2016 Volume 17, Issue 10

Abstract: Extracellular self-DNA (esDNA) is produced during cell and tissue damage or degradation and has been shown to induce significant responses in several organisms, including plants. While the inhibitory effects of esDNA have been shown in conspecific ... ...

Abstract	Extracellular self-DNA (esDNA) is produced during cell and tissue damage or degradation and has been shown to induce significant responses in several organisms, including plants. While the inhibitory effects of esDNA have been shown in conspecific individuals, little is known on the early events involved upon plant esDNA perception. We used electrophysiology and confocal laser scanning microscopy calcium localization to evaluate the plasma membrane potential (Vm) variations and the intracellular calcium fluxes, respectively, in Lima bean (
Language	English
Publishing date	2016-09-29
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/ijms17101659
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Article ; Online: Untargeted Metabolomics in Forensic Toxicology: A New Approach for the Detection of Fentanyl Intake in Urine Samples.

Amante, Eleonora / Alladio, Eugenio / Rizzo, Rebecca / Di Corcia, Daniele / Negri, Pierre / Visintin, Lia / Guglielmotto, Michela / Tamagno, Elena / Vincenti, Marco / Salomone, Alberto

Molecules (Basel, Switzerland)

2021 Volume 26, Issue 16

Abstract: The misuse of fentanyl, and novel synthetic opioids (NSO) in general, has become a public health emergency, especially in the United States. The detection of NSO is often challenged by the limited diagnostic time frame allowed by urine sampling and the ... ...

Abstract	The misuse of fentanyl, and novel synthetic opioids (NSO) in general, has become a public health emergency, especially in the United States. The detection of NSO is often challenged by the limited diagnostic time frame allowed by urine sampling and the wide range of chemically modified analogues, continuously introduced to the recreational drug market. In this study, an untargeted metabolomics approach was developed to obtain a comprehensive "fingerprint" of any anomalous and specific metabolic pattern potentially related to fentanyl exposure. In recent years, in vitro models of drug metabolism have emerged as important tools to overcome the limited access to positive urine samples and uncertainties related to the substances actually taken, the possible combined drug intake, and the ingested dose. In this study, an in vivo experiment was designed by incubating HepG2 cell lines with either fentanyl or common drugs of abuse, creating a cohort of 96 samples. These samples, together with 81 urine samples including negative controls and positive samples obtained from recent users of either fentanyl or "traditional" drugs, were subjected to untargeted analysis using both UHPLC reverse phase and HILIC chromatography combined with QTOF mass spectrometry. Data independent acquisition was performed by SWATH in order to obtain a comprehensive profile of the urinary metabolome. After extensive processing, the resulting datasets were initially subjected to unsupervised exploration by principal component analysis (PCA), yielding clear separation of the fentanyl positive samples with respect to both controls and samples positive to other drugs. The urine datasets were then systematically investigated by supervised classification models based on soft independent modeling by class analogy (SIMCA) algorithms, with the end goal of identifying fentanyl users. A final single-class SIMCA model based on an RP dataset and five PCs yielded 96% sensitivity and 74% specificity. The distinguishable metabolic patterns produced by fentanyl in comparison to other opioids opens up new perspectives in the interpretation of the biological activity of fentanyl.
MeSH term(s)	Chromatography, Liquid ; Fentanyl/metabolism ; Fentanyl/urine ; Forensic Toxicology ; Hep G2 Cells ; Humans ; Limit of Detection ; Metabolomics ; Urinalysis/methods
Chemical Substances	Fentanyl (UF599785JZ)
Language	English
Publishing date	2021-08-18
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/molecules26164990
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Article ; Online: Stroke and Amyloid-β Downregulate TREM-2 and Uch-L1 Expression that Synergistically Promote the Inflammatory Response.

Guglielmotto, Michela / Repetto, Ivan Enrico / Monteleone, Debora / Vasciaveo, Valeria / Franchino, Claudio / Rinaldi, Sara / Tabaton, Massimo / Tamagno, Elena

Journal of Alzheimer's disease : JAD

2019 Volume 71, Issue 3, Page(s) 907–920

Abstract: Neuroinflammation is involved in the pathogenesis of Alzheimer's disease, and the transcription factor NF-κB is a player in this event. We found here that the ischemic damage alone or in association with Aβ1-42 activates the NF-κB pathway, induces an ... ...

Abstract	Neuroinflammation is involved in the pathogenesis of Alzheimer's disease, and the transcription factor NF-κB is a player in this event. We found here that the ischemic damage alone or in association with Aβ1-42 activates the NF-κB pathway, induces an increase of BACE1 and a parallel inhibition of Uch-L1 and TREM2, both in vitro and in vivo, in Tg 5XFAD and in human brains of sporadic AD. This mechanism creates a synergistic loop that fosters inflammation. We also demonstrated a significant protection exerted by the restoration of Uch-L1 activity. The rescue of the enzyme is able to abolish the decrease of TREM2 and the parameters of neuroinflammation.
MeSH term(s)	Aged ; Aged, 80 and over ; Amyloid Precursor Protein Secretases/biosynthesis ; Amyloid Precursor Protein Secretases/genetics ; Amyloid beta-Peptides/metabolism ; Animals ; Aspartic Acid Endopeptidases/biosynthesis ; Aspartic Acid Endopeptidases/genetics ; Brain Ischemia/complications ; Brain Ischemia/genetics ; Brain Ischemia/metabolism ; Cells, Cultured ; Cytokines/biosynthesis ; Down-Regulation ; Female ; Humans ; Inflammation/etiology ; Inflammation/metabolism ; Male ; Membrane Glycoproteins/metabolism ; Mice ; NF-kappa B/metabolism ; Neurons/metabolism ; Peptide Fragments/metabolism ; Receptors, Immunologic/metabolism ; Stroke/complications ; Stroke/genetics ; Stroke/metabolism ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	Amyloid beta-Peptides ; Cytokines ; Membrane Glycoproteins ; NF-kappa B ; Peptide Fragments ; Receptors, Immunologic ; Trem2 protein, mouse ; Ubiquitin carboxyl-Terminal Hydrolase L-1, mouse ; amyloid beta-protein (1-42) ; Amyloid Precursor Protein Secretases (EC 3.4.-) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; Aspartic Acid Endopeptidases (EC 3.4.23.-) ; Bace1 protein, mouse (EC 3.4.23.46)
Language	English
Publishing date	2019-08-27
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-190494
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Article ; Online: The Unexpected Role of Aβ1-42 Monomers in the Pathogenesis of Alzheimer's Disease.

Tamagno, Elena / Guglielmotto, Michela / Monteleone, Debora / Manassero, Giusi / Vasciaveo, Valeria / Tabaton, Massimo

Journal of Alzheimer's disease : JAD

2017 Volume 62, Issue 3, Page(s) 1241–1245

Abstract: Amyloid-β (Aβ) has been proposed as a biomarker and a drug target for the therapy of Alzheimer's disease (AD). The neurotoxic entity and relevance of each conformational form of Aβ to AD pathology is still under debate; Aβ oligomers are considered the ... ...

Abstract	Amyloid-β (Aβ) has been proposed as a biomarker and a drug target for the therapy of Alzheimer's disease (AD). The neurotoxic entity and relevance of each conformational form of Aβ to AD pathology is still under debate; Aβ oligomers are considered the major killer form of the peptide whereas monomers have been proposed to be involved in physiological process. Here we reviewed some different effects mediated by monomers and oligomers on mechanisms involved in AD pathogenesis such as autophagy and tau aggregation. Data reported in this review demonstrate that Aβ monomers could have a major role in sustaining the pathogenesis of AD and that AD therapy should be focused not only in the removal of oligomers but also of monomers.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Animals ; Humans ; Peptide Fragments/metabolism
Chemical Substances	Amyloid beta-Peptides ; Peptide Fragments ; amyloid beta-protein (1-42)
Language	English
Publishing date	2017-10-12
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-170581
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