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Book ; Audio / Video ; Online ; E-Book: Drug repositioning

Dudley, Joel T. / Berliocchi, Laura

approaches and applications for neurotherapeutics

(Frontiers in neurotherapeutics series)

2017

Author's details	edited by Joel Dudley, Laura Berliocchi
Series title	Frontiers in neurotherapeutics series
Keywords	Drug development ; Neuropharmacology
Subject code	615.1
Language	English
Size	1 Online-Ressource (xvi, 314 Seiten), Illustrationen
Publisher	CRC Press
Publishing place	Boca Raton
Publishing country	United States
Document type	Book ; Audio / Video ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019425580
ISBN	978-1-4822-2084-1 ; 9781482220834 ; 1-4822-2084-9 ; 1482220830
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Interactions between mitochondrial dysfunction and other hallmarks of aging: Paving a path toward interventions that promote healthy old age.

Li, Yuan / Berliocchi, Laura / Li, Zhiquan / Rasmussen, Lene Juel

Aging cell

2023 Volume 23, Issue 1, Page(s) e13942

Abstract: Current research on human aging has largely been guided by the milestone paper "hallmarks of aging," which were first proposed in the seminal 2013 paper by Lopez-Otin et al. Most studies have focused on one aging hallmark at a time, asking whether the ... ...

Abstract	Current research on human aging has largely been guided by the milestone paper "hallmarks of aging," which were first proposed in the seminal 2013 paper by Lopez-Otin et al. Most studies have focused on one aging hallmark at a time, asking whether the underlying molecular perturbations are sufficient to drive the aging process and its associated phenotypes. More recently, researchers have begun to investigate whether aging phenotypes are driven by concurrent perturbations in molecular pathways linked to not one but to multiple hallmarks of aging and whether they present different patterns in organs and systems over time. Indeed, preliminary results suggest that more complex interactions between aging hallmarks must be considered and addressed, if we are to develop interventions that successfully promote healthy aging and/or delay aging-associated dysfunction and diseases. Here, we summarize some of the latest work and views on the interplay between hallmarks of aging, with a specific focus on mitochondrial dysfunction. Indeed, this represents a significant example of the complex crosstalk between hallmarks of aging and of the effects that an intervention targeted to a specific hallmark may have on the others. A better knowledge of these interconnections, of their cause-effect relationships, of their spatial and temporal sequence, will be very beneficial for the whole aging research field and for the identification of effective interventions in promoting healthy old age.
MeSH term(s)	Humans ; Aging/genetics ; Phenotype ; Mitochondrial Diseases
Language	English
Publishing date	2023-07-27
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13942
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Article: Pooled analysis of frontal lobe transcriptomic data identifies key mitophagy gene changes in Alzheimer's disease brain.

Mei, Taoyu / Li, Yuan / Orduña Dolado, Anna / Li, Zhiquan / Andersson, Robin / Berliocchi, Laura / Rasmussen, Lene Juel

Frontiers in aging neuroscience

2023 Volume 15, Page(s) 1101216

Abstract: Background: The growing prevalence of Alzheimer's disease (AD) is becoming a global health challenge without effective treatments. Defective mitochondrial function and mitophagy have recently been suggested as etiological factors in AD, in association ... ...

Abstract	Background: The growing prevalence of Alzheimer's disease (AD) is becoming a global health challenge without effective treatments. Defective mitochondrial function and mitophagy have recently been suggested as etiological factors in AD, in association with abnormalities in components of the autophagic machinery like lysosomes and phagosomes. Several large transcriptomic studies have been performed on different brain regions from AD and healthy patients, and their data represent a vast source of important information that can be utilized to understand this condition. However, large integration analyses of these publicly available data, such as AD RNA-Seq data, are still missing. In addition, large-scale focused analysis on mitophagy, which seems to be relevant for the aetiology of the disease, has not yet been performed. Methods: In this study, publicly available raw RNA-Seq data generated from healthy control and sporadic AD post-mortem human samples of the brain frontal lobe were collected and integrated. Sex-specific differential expression analysis was performed on the combined data set after batch effect correction. From the resulting set of differentially expressed genes, candidate mitophagy-related genes were identified based on their known functional roles in mitophagy, the lysosome, or the phagosome, followed by Protein-Protein Interaction (PPI) and microRNA-mRNA network analysis. The expression changes of candidate genes were further validated in human skin fibroblast and induced pluripotent stem cells (iPSCs)-derived cortical neurons from AD patients and matching healthy controls. Results: From a large dataset (AD: 589; control: 246) based on three different datasets (i.e., ROSMAP, MSBB, & GSE110731), we identified 299 candidate mitophagy-related differentially expressed genes (DEG) in sporadic AD patients (male: 195, female: 188). Among these, the AAA ATPase VCP, the GTPase ARF1, the autophagic vesicle forming protein GABARAPL1 and the cytoskeleton protein actin beta ACTB were selected based on network degrees and existing literature. Changes in their expression were further validated in AD-relevant human Conclusion: Through the joint analysis of multiple publicly available data sets, we identify four differentially expressed key mitophagy-related genes potentially relevant for the pathogenesis of sporadic AD. Changes in expression of these four genes were validated using two AD-relevant human
Language	English
Publishing date	2023-06-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2023.1101216
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Article: Effects of the autophagy modulators d-limonene and chloroquine on vimentin levels in SH-SY5Y cells

Gentile, Debora / Berliocchi, Laura / Russo, Rossella / Bagetta, Giacinto / Corasaniti, Maria Tiziana

Biochemical and biophysical research communications. 2020 Dec. 17, v. 533, no. 4

2020

Abstract: The molecular target and mechanism by which d-limonene induces LC3 lipidation and autophagosome formation remain elusive. Here, we report that this monoterpene rapidly enhances Ca²⁺ levels in SH-SY5Y cells; yet this effect does not lead to calpain- or ... ...

Abstract	The molecular target and mechanism by which d-limonene induces LC3 lipidation and autophagosome formation remain elusive. Here, we report that this monoterpene rapidly enhances Ca²⁺ levels in SH-SY5Y cells; yet this effect does not lead to calpain- or caspase-mediated proteolysis of α-spectrin, nor calpain activity is required for the established enhancement of LC3-II levels by d-limonene. However, d-limonene rapidly reduced vimentin levels, an unexpected effect also induced by the autophagy inhibitor chloroquine (CQ). The magnitude of vimentin reduction parallels accumulation of LC3-II caused by a brief incubation with d-limonene or CQ. For longer exposure (48 h), d-limonene does not reduce vimentin, nor it increases LC3-II levels; conversely, a clear reduction of vimentin along with a massive accumulation of LC3-II is evident in cells treated with CQ. Vimentin participates in organelle positioning and in other cellular processes that have linked this intermediate filament protein to various diseases, including cancer, inflammatory and autoimmune disorders, and to virus replication and internalization. Our findings suggest an inverse relationship between vimentin reduction and LC3-II accumulation, whose causal link needs to be examined. Further experiments are needed to dissect the role of vimentin reduction in the mechanisms through which CQ impairs fusion of autophagosome with lysosomes as well as in other effects of this drug.
Keywords	autophagosomes ; autophagy ; calpain ; chloroquine ; limonene ; lysosomes ; proteolysis ; research ; vimentin ; virus replication
Language	English
Dates of publication	2020-1217
Size	p. 764-769.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.09.073
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Effects of the autophagy modulators d-limonene and chloroquine on vimentin levels in SH-SY5Y cells.

Gentile, Debora / Berliocchi, Laura / Russo, Rossella / Bagetta, Giacinto / Corasaniti, Maria Tiziana

Biochemical and biophysical research communications

2020 Volume 533, Issue 4, Page(s) 764–769

Abstract: The molecular target and mechanism by which d-limonene induces LC3 lipidation and autophagosome formation remain elusive. Here, we report that this monoterpene rapidly enhances ... ...

Abstract	The molecular target and mechanism by which d-limonene induces LC3 lipidation and autophagosome formation remain elusive. Here, we report that this monoterpene rapidly enhances Ca
MeSH term(s)	Antineoplastic Agents/pharmacology ; Autophagy/drug effects ; Calcium/metabolism ; Calpain/metabolism ; Cell Line, Tumor ; Chloroquine/pharmacology ; Humans ; Limonene/pharmacology ; Microtubule-Associated Proteins/metabolism ; Neuroprotective Agents/pharmacology ; Vimentin/metabolism
Chemical Substances	Antineoplastic Agents ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Neuroprotective Agents ; Vimentin ; Chloroquine (886U3H6UFF) ; Limonene (9MC3I34447) ; Calpain (EC 3.4.22.-) ; Calcium (SY7Q814VUP)
Keywords	covid19
Language	English
Publishing date	2020-09-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.09.073
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Article: Effects of Aging on Formalin-Induced Pain Behavior and Analgesic Activity of Gabapentin in C57BL/6 Mice.

Scuteri, Damiana / Berliocchi, Laura / Rombolà, Laura / Morrone, Luigi Antonio / Tonin, Paolo / Bagetta, Giacinto / Corasaniti, Maria Tiziana

Frontiers in pharmacology

2020 Volume 11, Page(s) 663

Abstract: Improved living conditions have induced an increase of lifespan often accompanied by comorbidities, responsible for pain, and by cognitive impairment and dementia, impairing communication capabilities. In most cases, the elderly do not receive pain ... ...

Abstract	Improved living conditions have induced an increase of lifespan often accompanied by comorbidities, responsible for pain, and by cognitive impairment and dementia, impairing communication capabilities. In most cases, the elderly do not receive pain relief because of underdiagnosis and of aging-induced changes of systems affecting nociceptive response. Unrelieved pain is involved in the development of behavioral symptoms, as agitation, representing a difficult challenge in this fragile population. Aged C57BL/6 mice and amyloid precursor protein (APP) mice display behavioral disturbances that mimic behavioral and psychological symptoms of dementia (BPSD). Therefore, this original study focuses on the influence of aging on nociception to provide insight into the occurrence of BPSD. We have investigated how aging can affect nociception after formalin administration and gabapentin effect in C57BL/6 mice, since it represents one of the treatments of choice for chronic neuropathic pain. Based on our results, changes of nociceptive behavior in response to an algogen stimulus occur during aging. Formalin-induced behavioral pattern in older C57BL/6 mice presents a temporal shift and an increase in the peak amplitudes. Our data show that the effectiveness of gabapentin is influenced by the age of the animal; though preliminary, the latter provide evidence upon which formalin test induced long-lasting mechanical allodynia might be a reliable as rapid and viable persistent pain model. The disclosed differences in effectiveness of gabapentin according to age can form the rational basis to deepen the study of pain treatment in the elderly.
Language	English
Publishing date	2020-05-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.00663
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Book ; Online ; Thesis: Neurodegeneration induced by clostridial neurotoxins in cerebellar granule neurons

Berliocchi, Laura

a novel in vitro model for neurodegenerative disease

2000

Author's details	vorgelegt von Laura Berliocchi
Language	English
Size	Online-Ressource
Edition	[Elektronische Ressource]
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Univ., Diss--Konstanz, 2000
Database	Former special subject collection: coastal and deep sea fishing

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Article: Early LC3 lipidation induced by d-limonene does not rely on mTOR inhibition, ERK activation and ROS production and it is associated with reduced clonogenic capacity of SH-SY5Y neuroblastoma cells

Berliocchi, Laura / Carlotta Chiappini / Annagrazia Adornetto / Debora Gentile / Silvia Cerri / Rossella Russo / Giacinto Bagetta / Maria Tiziana Corasaniti

Phytomedicine. 2018 Feb. 01, v. 40

2018

Abstract: d-Limonene is a natural monoterpene abundant in Citrus essential oils. It is endowed with several biological activities, including inhibition of carcinogenesis and promotion of tumour regression. Recently, d-limonene has been shown to modulate autophagic ...

Abstract	d-Limonene is a natural monoterpene abundant in Citrus essential oils. It is endowed with several biological activities, including inhibition of carcinogenesis and promotion of tumour regression. Recently, d-limonene has been shown to modulate autophagic markers in vitro at concentrations found in vivo, in clinical pharmacokinetic studies. Autophagy is an intracellular catabolic process serving as both an adaptive metabolic response and a quality control mechanism. Because autophagy defects have been linked to a wide range of human pathologies, including neurodegeneration and cancer, there is a need for new pharmacological tools to control deregulated autophagy.To better understand the effects of d-limonene on autophagy, to identify the molecular mechanisms through which this monoterpene rapidly triggers LC3 lipidation and to evaluate the role for autophagy in long-term effects of d-limonene.Human SH-SY5Y neuroblastoma, HepG2 hepatocellular carcinoma and MCF7 breast cancer cells were used. Endogenous LC3-II levels were evaluated by western blotting. Autophagic flux assay was performed using bafilomycin A1 and chloroquine. Intracellular distribution of LC3 protein was studied by confocal microscopy analysis of LC3B-GFP transduced cells. Expression of lysosomal-membrane protein LAMP-1 was assessed by immunofluorescence analysis. Phosphorylated levels of downstream substrates of mTOR kinase (p70S6 kinase, 4E-BP1, and ULK1) and ERK were analyzed by western blotting. Production of reactive oxygen species (ROS) was assessed by live confocal microscopy of cells loaded with CellROX® Green Reagent. Clonogenic assay was used to evaluate the ability of treated cells to proliferate and form colonies.LC3 lipidation promoted by d-limonene correlates with autophagosome formation and stimulation of basal autophagy. LC3 lipidation does not rely on inhibition of mTOR kinase, which instead appears to be transiently activated. In addition, d-limonene rapidly activates ERK and stimulates ROS generation, yet none of these events is implicated in lipidation of LC3, which was only partly reduced by chelation of intracellular calcium. The early LC3 lipidation induced by d-limonene is associated with inhibition of clonogenic capacity which is reverted by the autophagy inhibitor chloroquine.d-Limonene rapidly stimulates the autophagic flux in cultured cancer cells, which could be usefully exploited for therapeutic purposes.
Keywords	Citrus ; Western blotting ; autophagy ; biochemical pathways ; breast neoplasms ; calcium ; carcinogenesis ; chelation ; chloroquine ; confocal microscopy ; essential oils ; fluorescent antibody technique ; hepatoma ; humans ; limonene ; long term effects ; mitogen-activated protein kinase ; neoplasm cells ; neurodegenerative diseases ; pharmacokinetics ; quality control ; remission ; target of rapamycin proteins
Language	English
Dates of publication	2018-0201
Size	p. 98-105.
Publishing place	Elsevier GmbH
Document type	Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2018.01.005
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Inhibition of monoacylglycerol lipase: Another signalling pathway for potential therapeutic targets in migraine?

Greco, Rosaria / Demartini, Chiara / Zanaboni, Anna Maria / Berliocchi, Laura / Piomelli, Daniele / Tassorelli, Cristina

Cephalalgia : an international journal of headache

2017 Volume 38, Issue 6, Page(s) 1138–1147

Abstract: Background Drugs that modulate endocannabinoid signalling are effective in reducing nociception in animal models of pain and may be of value in the treatment of migraine. Methods We investigated the anti-nociceptive effects of inhibition of ... ...

Abstract	Background Drugs that modulate endocannabinoid signalling are effective in reducing nociception in animal models of pain and may be of value in the treatment of migraine. Methods We investigated the anti-nociceptive effects of inhibition of monoacylglycerol lipase (MGL), a key enzyme in the hydrolysis of the 2-arachidonoylglycerol, in a rat model of migraine based on nitroglycerin (NTG) administration. We evaluated c-fos expression in specific brain areas and nociceptive behavior in trigeminal and extra-trigeminal body areas. Results URB602, a reversible MGL inhibitor, did not show any analgesic effect in the tail flick test, but it inhibited NTG-induced hyperalgesia in both the tail flick test and the formalin test applied to the hind paw or to the orofacial area. Quite unexpectedly, URB602 potentiated formalin-induced hyperalgesia in the trigeminal area when used alone. The latter result was also confirmed using a structurally distinct, irreversible MGL inhibitor, JZL184. URB602 did not induce neuronal activation in the area of interest, but significantly reduced the NTG-induced neuronal activation in the ventrolateral column of the periaqueductal grey and the nucleus trigeminalis caudalis. Conclusions These findings support the hypothesis that modulation of the endocannabinoid system may be a valuable approach for the treatment of migraine. The topographically segregated effect of MGL inhibition in trigeminal/extra-trigeminal areas calls for further mechanistic research.
MeSH term(s)	Animals ; Biphenyl Compounds/pharmacology ; Enzyme Inhibitors/pharmacology ; Hyperalgesia/enzymology ; Migraine Disorders/enzymology ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Signal Transduction/physiology
Chemical Substances	Biphenyl Compounds ; Enzyme Inhibitors ; URB602 ; Phosphotransferases (Alcohol Group Acceptor) (EC 2.7.1.-) ; acylglycerol kinase (EC 2.7.1.94)
Language	English
Publishing date	2017-08-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604567-4
ISSN	1468-2982 ; 0333-1024
ISSN (online)	1468-2982
ISSN	0333-1024
DOI	10.1177/0333102417727537
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Article ; Online: Early LC3 lipidation induced by d-limonene does not rely on mTOR inhibition, ERK activation and ROS production and it is associated with reduced clonogenic capacity of SH-SY5Y neuroblastoma cells.

Berliocchi, Laura / Chiappini, Carlotta / Adornetto, Annagrazia / Gentile, Debora / Cerri, Silvia / Russo, Rossella / Bagetta, Giacinto / Corasaniti, Maria Tiziana

Phytomedicine : international journal of phytotherapy and phytopharmacology

2018 Volume 40, Page(s) 98–105

Abstract: Background: d-Limonene is a natural monoterpene abundant in Citrus essential oils. It is endowed with several biological activities, including inhibition of carcinogenesis and promotion of tumour regression. Recently, d-limonene has been shown to ... ...

Abstract	Background: d-Limonene is a natural monoterpene abundant in Citrus essential oils. It is endowed with several biological activities, including inhibition of carcinogenesis and promotion of tumour regression. Recently, d-limonene has been shown to modulate autophagic markers in vitro at concentrations found in vivo, in clinical pharmacokinetic studies. Autophagy is an intracellular catabolic process serving as both an adaptive metabolic response and a quality control mechanism. Because autophagy defects have been linked to a wide range of human pathologies, including neurodegeneration and cancer, there is a need for new pharmacological tools to control deregulated autophagy. Purpose: To better understand the effects of d-limonene on autophagy, to identify the molecular mechanisms through which this monoterpene rapidly triggers LC3 lipidation and to evaluate the role for autophagy in long-term effects of d-limonene. Methods: Human SH-SY5Y neuroblastoma, HepG2 hepatocellular carcinoma and MCF7 breast cancer cells were used. Endogenous LC3-II levels were evaluated by western blotting. Autophagic flux assay was performed using bafilomycin A1 and chloroquine. Intracellular distribution of LC3 protein was studied by confocal microscopy analysis of LC3B-GFP transduced cells. Expression of lysosomal-membrane protein LAMP-1 was assessed by immunofluorescence analysis. Phosphorylated levels of downstream substrates of mTOR kinase (p70S6 kinase, 4E-BP1, and ULK1) and ERK were analyzed by western blotting. Production of reactive oxygen species (ROS) was assessed by live confocal microscopy of cells loaded with CellROX Results: LC3 lipidation promoted by d-limonene correlates with autophagosome formation and stimulation of basal autophagy. LC3 lipidation does not rely on inhibition of mTOR kinase, which instead appears to be transiently activated. In addition, d-limonene rapidly activates ERK and stimulates ROS generation, yet none of these events is implicated in lipidation of LC3, which was only partly reduced by chelation of intracellular calcium. The early LC3 lipidation induced by d-limonene is associated with inhibition of clonogenic capacity which is reverted by the autophagy inhibitor chloroquine. Conclusions: d-Limonene rapidly stimulates the autophagic flux in cultured cancer cells, which could be usefully exploited for therapeutic purposes.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Autophagy/drug effects ; Autophagy/physiology ; Cell Cycle Proteins ; Cell Line, Tumor ; Cyclohexenes/pharmacology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Hep G2 Cells ; Humans ; Limonene ; MCF-7 Cells ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Neuroblastoma/drug therapy ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Phosphoproteins/metabolism ; Reactive Oxygen Species/metabolism ; TOR Serine-Threonine Kinases/antagonists & inhibitors ; TOR Serine-Threonine Kinases/metabolism ; Terpenes/pharmacology
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cell Cycle Proteins ; Cyclohexenes ; EIF4EBP1 protein, human ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Phosphoproteins ; Reactive Oxygen Species ; Terpenes ; Limonene (9MC3I34447) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
Language	English
Publishing date	2018-02-26
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2018.01.005
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