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Article ; Online: LRRK2 signaling in neurodegeneration: two decades of progress.

Iannotta, Lucia / Greggio, Elisa

2022 Volume 65, Issue 7, Page(s) 859–872

Abstract: Leucine-rich repeat kinase 2 (LRRK2) is a complex GTPase/kinase orchestrating cytoskeletal dynamics and multiple steps of the endolysosomal pathway through interaction with a host of partners and phosphorylation of a subset of Rab GTPases. Mutations in ... ...

Abstract	Leucine-rich repeat kinase 2 (LRRK2) is a complex GTPase/kinase orchestrating cytoskeletal dynamics and multiple steps of the endolysosomal pathway through interaction with a host of partners and phosphorylation of a subset of Rab GTPases. Mutations in LRRK2 cause late-onset Parkinson's disease (PD) and common variants in the locus containing LRRK2 have been associated with sporadic PD, progressive supranuclear palsy as well as a number of inflammatory diseases. This review encompasses the major discoveries in the field of LRRK2 pathobiology, from the initial gene cloning to the latest progress in LRRK2 inhibition as a promising therapeutic approach to fight neurodegeneration.
MeSH term(s)	Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/metabolism ; Lysosomes/metabolism ; Mutation ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Phosphorylation ; Signal Transduction
Chemical Substances	LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
Language	English
Publishing date	2022-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1744-1358 ; 0071-1365
ISSN (online)	1744-1358
ISSN	0071-1365
DOI	10.1042/EBC20210013
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Article: Editorial: LRRK2-Fifteen Years From Cloning to the Clinic.

Rideout, Hardy / Greggio, Elisa / Kortholt, Arjan / Nichols, R Jeremy

Frontiers in neuroscience

2022 Volume 16, Page(s) 880914

Language	English
Publishing date	2022-04-11
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2022.880914
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Article ; Online: Leucine-rich repeat kinase 2 (LRRK2): an update on the potential therapeutic target for Parkinson's disease.

Kluss, Jillian H / Lewis, Patrick A / Greggio, Elisa

Expert opinion on therapeutic targets

2022 Volume 26, Issue 6, Page(s) 537–546

Abstract: Areas covered: In this review, we will provide an update on the current status of drugs and other technologies that have emerged in recent years and provide an overview of their efficacy in ameliorating LRRK2 kinase activity and overall safety in animal ...

Abstract	Areas covered: In this review, we will provide an update on the current status of drugs and other technologies that have emerged in recent years and provide an overview of their efficacy in ameliorating LRRK2 kinase activity and overall safety in animal models and humans. Expert opinion: The growth of both target discovery and innovative drug design has sparked a lot of excitement for the future of how we treat Parkinson's disease. Given the immense focus on LRRK2 as a therapeutic target, it is expected within the next decade to determine its therapeutic properties, or lack thereof, for PD.
MeSH term(s)	Animals ; Drug Design ; Leucine/therapeutic use ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Parkinson Disease/drug therapy
Chemical Substances	Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; Leucine (GMW67QNF9C)
Language	English
Publishing date	2022-06-02
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
ZDB-ID	2055208-7
ISSN	1744-7631 ; 1472-8222
ISSN (online)	1744-7631
ISSN	1472-8222
DOI	10.1080/14728222.2022.2082937
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Zs.A 5244: Show issues

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Article ; Online: LRRK2 as a target for modulating immune system responses.

Russo, Isabella / Bubacco, Luigi / Greggio, Elisa

Neurobiology of disease

2022 Volume 169, Page(s) 105724

Abstract: Mutations in the Leucine-Rich Repeat Kinase 2 (LRRK2) gene are associated with familial and sporadic cases of Parkinson's disease (PD) but are also found in patients with immune- related disorders, such as inflammatory bowel disease (IBD) and leprosy, ... ...

Abstract	Mutations in the Leucine-Rich Repeat Kinase 2 (LRRK2) gene are associated with familial and sporadic cases of Parkinson's disease (PD) but are also found in patients with immune- related disorders, such as inflammatory bowel disease (IBD) and leprosy, linking LRRK2 to the immune system. Supporting this genetic evidence, in the last decade LRRK2 was robustly shown to modulate inflammatory responses at both systemic and central nervous system level. In this review, we recapitulate the role of LRRK2 in central and peripheral inflammation in PD and inflammatory disease models. Moreover, we discuss how LRRK2 inhibitors and anti- inflammatory drugs may be beneficial at reducing disease risk/progression in LRRK2-mutation carriers and manifesting PD patients, thus supporting LRRK2 as a promising disease-modifying PD strategy.
MeSH term(s)	Animals ; Humans ; Immune System ; Inflammation/genetics ; Inflammation/immunology ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/immunology ; Mutation ; Parkinson Disease/genetics ; Parkinson Disease/immunology
Chemical Substances	LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1)
Language	English
Publishing date	2022-04-12
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105724
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Zs.A 4444: Show issues

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Article ; Online: Correction: Human frataxin, the Friedreich ataxia deficient protein, interacts with mitochondrial respiratory chain.

Doni, Davide / Cavion, Federica / Bortolus, Marco / Baschiera, Elisa / Muccioli, Silvia / Tombesi, Giulia / d'Ettorre, Federica / Ottaviani, Daniele / Marchesan, Elena / Leanza, Luigi / Greggio, Elisa / Ziviani, Elena / Russo, Antonella / Bellin, Milena / Sartori, Geppo / Carbonera, Donatella / Salviati, Leonardo / Costantini, Paola

Cell death & disease

2024 Volume 15, Issue 1, Page(s) 93

Language	English
Publishing date	2024-01-29
Publishing country	England
Document type	Published Erratum
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-024-06459-2
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Article ; Online: Too much for your own good: Excessive dopamine damages neurons and contributes to Parkinson's disease: An Editorial Highlight for "Enhanced tyrosine hydroxylase activity induces oxidative stress, causes accumulation of autotoxic catecholamine metabolites, and augments amphetamine effects in vivo".

Masato, Anna / Bubacco, Luigi / Greggio, Elisa

Journal of neurochemistry

2021 Volume 158, Issue 4, Page(s) 833–836

Abstract: Dopamine dyshomeostasis is a driving factor of nigrostriatal degeneration in Parkinson's disease (PD). Accumulation of cytosolic dopamine at striatal projections results in the buildup of autoxidation products, which generates protein adducts and ... ...

Abstract	Dopamine dyshomeostasis is a driving factor of nigrostriatal degeneration in Parkinson's disease (PD). Accumulation of cytosolic dopamine at striatal projections results in the buildup of autoxidation products, which generates protein adducts and exacerbate oxidative stress. Moreover, an excessive rate of dopamine degradation results in accumulation of 3,4-dihydroxyphenylacetaldehyde (DOPAL), a toxic metabolite which rapidly reacts with other proteins. These events lead to protein misfolding and cross-linking as well as mitochondrial and lysosomal dysfunction, the main pathological mechanisms underscoring dopaminergic neuron loss in PD. In this issue of Journal of Neurochemistry, Vecchio et al. generated and characterized a new in vivo model of chronic dopamine accumulation through the overexpression of a hyperactive form of tyrosine hydroxylase (TH-HI), the rate-limiting step enzyme in dopamine biosynthesis. At 3-5 months of age, TH-HI mice displayed increased striatal dopamine content, exacerbated dopamine catabolism, and augmented responses to amphetamine. This correlated with enhanced oxidative stress and DOPAL buildup, highlighting a catechol-induced neurotoxic vicious cycle that may anticipate a parkinsonian-like phenotype in aged mice. This novel TH-HI animal model represents an exciting new tool to unravel the molecular mechanisms underlying dopamine disequilibrium, catecholamine autotoxicity, and neurodegeneration in PD.
MeSH term(s)	Amphetamine ; Animals ; Catecholamines ; Dopamine ; Dopaminergic Neurons ; Mice ; Oxidative Stress ; Parkinson Disease ; Tyrosine 3-Monooxygenase
Chemical Substances	Catecholamines ; Amphetamine (CK833KGX7E) ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2021-06-28
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15442
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Article ; Online: Role of LRRK2 kinase activity in the pathogenesis of Parkinson's disease.

Greggio, Elisa

Biochemical Society transactions

2012 Volume 40, Issue 5, Page(s) 1058–1062

Abstract: Interest in studying the biology of LRRK2 (leucine-rich repeat kinase 2) started in 2004 when missense mutations in the LRRK2 gene were linked to an inherited form of Parkinson's disease with clinical and pathological presentation resembling the sporadic ...

Abstract	Interest in studying the biology of LRRK2 (leucine-rich repeat kinase 2) started in 2004 when missense mutations in the LRRK2 gene were linked to an inherited form of Parkinson's disease with clinical and pathological presentation resembling the sporadic syndrome. LRRK2 is a complex molecule containing domains implicated in protein interactions, as well as kinase and GTPase activities. The observation that the common G2019S mutation increases kinase activity in vitro suggests that altered phosphorylation of LRRK2 targets may have pathological outcomes. Given that protein kinases are ideal targets for drug therapies, much effort has been directed at understanding the role of LRRK2 kinase activity on disease onset. However, no clear physiological substrates have been identified to date, indicating that much research is still needed to fully understand the signalling pathways orchestrated by LRRK2 and deregulated under pathological conditions.
MeSH term(s)	Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 ; Mutation ; Parkinson Disease/enzymology ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Parkinson Disease/pathology ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism
Chemical Substances	LRRK2 protein, human (EC 2.7.11.1) ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2012-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20120054
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Zs.A 944: Show issues

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Article ; Online: The Regulation of MiTF/TFE Transcription Factors Across Model Organisms: from Brain Physiology to Implication for Neurodegeneration.

Agostini, Francesco / Agostinis, Rossella / Medina, Diego L / Bisaglia, Marco / Greggio, Elisa / Plotegher, Nicoletta

Molecular neurobiology

2022 Volume 59, Issue 8, Page(s) 5000–5023

Abstract: The microphthalmia/transcription factor E (MiTF/TFE) transcription factors are responsible for the regulation of various key processes for the maintenance of brain function, including autophagy-lysosomal pathway, lipid catabolism, and mitochondrial ... ...

Abstract	The microphthalmia/transcription factor E (MiTF/TFE) transcription factors are responsible for the regulation of various key processes for the maintenance of brain function, including autophagy-lysosomal pathway, lipid catabolism, and mitochondrial homeostasis. Among them, autophagy is one of the most relevant pathways in this frame; it is evolutionary conserved and crucial for cellular homeostasis. The dysregulation of MiTF/TFE proteins was shown to be involved in the development and progression of neurodegenerative diseases. Thus, the characterization of their function is key in the understanding of the etiology of these diseases, with the potential to develop novel therapeutics targeted to MiTF/TFE proteins and to the autophagic process. The fact that these proteins are evolutionary conserved suggests that their function and dysfunction can be investigated in model organisms with a simpler nervous system than the mammalian one. Building not only on studies in mammalian models but also in complementary model organisms, in this review we discuss (1) the mechanistic regulation of MiTF/TFE transcription factors; (2) their roles in different regions of the central nervous system, in different cell types, and their involvement in the development of neurodegenerative diseases, including lysosomal storage disorders; (3) the overlap and the compensation that occur among the different members of the family; (4) the importance of the evolutionary conservation of these protein and the process they regulate, which allows their study in different model organisms; and (5) their possible role as therapeutic targets in neurodegeneration.
MeSH term(s)	Animals ; Humans ; Autophagy/physiology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Brain/metabolism ; Lysosomes/metabolism ; Mammals/metabolism ; Microphthalmia-Associated Transcription Factor/genetics ; Microphthalmia-Associated Transcription Factor/metabolism ; Microphthalmos/metabolism
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Microphthalmia-Associated Transcription Factor ; MITF protein, human
Language	English
Publishing date	2022-06-04
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/s12035-022-02895-3
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Zs.A 2411: Show issues

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Article ; Online: Prospective Role of PAK6 and 14-3-3γ as Biomarkers for Parkinson's Disease.

Giusto, Elena / Maistrello, Lorenza / Iannotta, Lucia / Giusti, Veronica / Iovino, Ludovica / Bandopadhyay, Rina / Antonini, Angelo / Bubacco, Luigi / Barresi, Rita / Plotegher, Nicoletta / Greggio, Elisa / Civiero, Laura

Journal of Parkinson's disease

2024 Volume 14, Issue 3, Page(s) 495–506

Abstract: ... quantitative ELISA tests. We analyzed samples obtained from 39 healthy subjects, 40 patients with sporadic ...

Abstract	Background: Parkinson's disease is a progressive neurodegenerative disorder mainly distinguished by sporadic etiology, although a genetic component is also well established. Variants in the LRRK2 gene are associated with both familiar and sporadic disease. We have previously shown that PAK6 and 14-3-3γ protein interact with and regulate the activity of LRRK2. Objective: The aim of this study is to quantify PAK6 and 14-3-3γ in plasma as reliable biomarkers for the diagnosis of both sporadic and LRRK2-linked Parkinson's disease. Methods: After an initial quantification of PAK6 and 14-3-3γ expression by means of Western blot in post-mortem human brains, we verified the presence of the two proteins in plasma by using quantitative ELISA tests. We analyzed samples obtained from 39 healthy subjects, 40 patients with sporadic Parkinson's disease, 50 LRRK2-G2019S non-manifesting carriers and 31 patients with LRRK2-G2019S Parkinson's disease. Results: The amount of PAK6 and 14-3-3γ is significantly different in patients with Parkinson's disease compared to healthy subjects. Moreover, the amount of PAK6 also varies with the presence of the G2019S mutation in the LRRK2 gene. Although the generalized linear models show a low association between the presence of Parkinson's disease and PAK6, the kinase could be added in a broader panel of biomarkers for the diagnosis of Parkinson's disease. Conclusions: Changes of PAK6 and 14-3-3γ amount in plasma represent a shared readout for patients affected by sporadic and LRRK2-linked Parkinson's disease. Overall, they can contribute to the establishment of an extended panel of biomarkers for the diagnosis of Parkinson's disease.
MeSH term(s)	Humans ; Parkinson Disease/blood ; Parkinson Disease/diagnosis ; Parkinson Disease/genetics ; 14-3-3 Proteins/blood ; Male ; p21-Activated Kinases/blood ; p21-Activated Kinases/metabolism ; p21-Activated Kinases/genetics ; Female ; Aged ; Biomarkers/blood ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2/genetics ; Middle Aged ; Aged, 80 and over ; Prospective Studies ; Adult ; Mutation
Chemical Substances	14-3-3 Proteins ; p21-Activated Kinases (EC 2.7.11.1) ; Biomarkers ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (EC 2.7.11.1) ; LRRK2 protein, human (EC 2.7.11.1) ; PAK6 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2024-04-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2620609-2
ISSN	1877-718X ; 1877-7171
ISSN (online)	1877-718X
ISSN	1877-7171
DOI	10.3233/JPD-230402
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Article: Ceramides in Parkinson's Disease: From Recent Evidence to New Hypotheses.

Plotegher, Nicoletta / Bubacco, Luigi / Greggio, Elisa / Civiero, Laura

Frontiers in neuroscience

2019 Volume 13, Page(s) 330

Abstract: Ceramides (Cer) constitute a class of lipids present in the cell membranes where they act as structural components, but they can also work as signaling molecules. Increasing genetic and biochemical evidence supports a link between deregulation of ... ...

Abstract	Ceramides (Cer) constitute a class of lipids present in the cell membranes where they act as structural components, but they can also work as signaling molecules. Increasing genetic and biochemical evidence supports a link between deregulation of ceramide metabolism in the brain and neurodegeneration. Here, we provide an overview of the genes and cellular pathways that link Cer with Parkinson's disease and discuss how ceramide pathobiology is gaining increasing interest in the understanding of the pathological mechanisms that contribute to the disease and in the clinical and therapeutic side.
Language	English
Publishing date	2019-04-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2019.00330
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