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  1. Article ; Online: Philanthropy: ice-bucket challenge should jolt funding.

    Carrì, Maria Teresa

    Nature

    2014  Volume 515, Issue 7527, Page(s) 343

    MeSH term(s) Amyotrophic Lateral Sclerosis/economics ; Animals ; Biomedical Research/economics ; Fund Raising/methods ; Humans ; Public Opinion
    Language English
    Publishing date 2014-11-20
    Publishing country England
    Document type Comment ; Letter
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/515343e
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 26: Show issues Location:
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  2. Article: Cysteine Modifications in the Pathogenesis of ALS.

    Valle, Cristiana / Carrì, Maria Teresa

    Frontiers in molecular neuroscience

    2017  Volume 10, Page(s) 5

    Abstract: Several proteins are found misfolded and aggregated in sporadic and genetic forms of amyotrophic lateral sclerosis (ALS). These include superoxide dismutase (SOD1), transactive response DNA-binding protein (TDP-43), fused in sarcoma/translocated in ... ...

    Abstract Several proteins are found misfolded and aggregated in sporadic and genetic forms of amyotrophic lateral sclerosis (ALS). These include superoxide dismutase (SOD1), transactive response DNA-binding protein (TDP-43), fused in sarcoma/translocated in liposarcoma protein (FUS/TLS), p62, vasolin-containing protein (VCP), Ubiquilin-2 and dipeptide repeats produced by unconventional RAN-translation of the GGGGCC expansion in C9ORF72. Up to date, functional studies have not yet revealed a common mechanism for the formation of such diverse protein inclusions. Consolidated studies have demonstrated a fundamental role of cysteine residues in the aggregation process of SOD1 and TDP43, but disturbance of protein thiols homeostatic factors such as protein disulfide isomerases (PDI), glutathione, cysteine oxidation or palmitoylation might contribute to a general aberration of cysteine residues proteostasis in ALS. In this article we review the evidence that cysteine modifications may have a central role in many, if not all, forms of this disease.
    Language English
    Publishing date 2017-01-23
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2452967-9
    ISSN 1662-5099
    ISSN 1662-5099
    DOI 10.3389/fnmol.2017.00005
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  3. Article ; Online: Which TDP-43 aggregates are toxic in ALS?

    Valle, Cristiana / Carrì, Maria Teresa

    Oncotarget

    2016  Volume 7, Issue 50, Page(s) 81973–81974

    MeSH term(s) Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Animals ; DNA-Binding Proteins/metabolism ; Humans ; Mice
    Chemical Substances DNA-Binding Proteins ; TARDBP protein, human
    Language English
    Publishing date 2016-10-27
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.13461
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  4. Article ; Online: Mitochondria in the nervous system: From health to disease, part II.

    Carrì, Maria Teresa / Polster, Brian M / Beart, Philip M

    Neurochemistry international

    2018  Volume 117, Page(s) 1–4

    Abstract: In Part II of this Special Issue on "Mitochondria in the Nervous System: From Health to Disease", the editors bring together more reviews and original articles from researchers in the field of mitochondrial metabolism in the healthy and diseased nervous ... ...

    Abstract In Part II of this Special Issue on "Mitochondria in the Nervous System: From Health to Disease", the editors bring together more reviews and original articles from researchers in the field of mitochondrial metabolism in the healthy and diseased nervous system. Subjects span from basic mitochondrial physiology to papers on mitochondrial dynamics and to those altered states of the nervous system that can be considered "mitopathologies". Finally, a few papers approach aspects of mitochondrial biology linked to the feasibility and validity of a mitochondrial therapy.
    MeSH term(s) Animals ; Central Nervous System/metabolism ; Central Nervous System/pathology ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Mitochondrial Dynamics/physiology ; Nervous System Diseases/metabolism ; Nervous System Diseases/pathology ; Oxidative Stress/physiology
    Language English
    Publishing date 2018-04-10
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 283190-9
    ISSN 1872-9754 ; 0197-0186
    ISSN (online) 1872-9754
    ISSN 0197-0186
    DOI 10.1016/j.neuint.2018.04.006
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    Zs.A 1610: Show issues Location:
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  5. Article ; Online: Pathways to mitochondrial dysfunction in ALS pathogenesis.

    Carrì, Maria Teresa / D'Ambrosi, Nadia / Cozzolino, Mauro

    Biochemical and biophysical research communications

    2017  Volume 483, Issue 4, Page(s) 1187–1193

    Abstract: Alterations in the structure and functions of mitochondria are a typical trait of Amyotrophic Lateral Sclerosis, a neurodegenerative disease characterized by a prominent degeneration of upper and lower motor neurons. The known gene mutations that are ... ...

    Abstract Alterations in the structure and functions of mitochondria are a typical trait of Amyotrophic Lateral Sclerosis, a neurodegenerative disease characterized by a prominent degeneration of upper and lower motor neurons. The known gene mutations that are responsible for a small fraction of ALS cases point to a complex interplay between different mechanisms in the disease pathogenesis. Here we will briefly overview the genetic and mechanistic evidence that make dysfunction of mitochondria a candidate major player in this process.
    MeSH term(s) Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/physiopathology ; Animals ; Humans ; Mitochondria/metabolism ; Mitochondria/physiology ; Mutation
    Language English
    Publishing date 2017-02-19
    Publishing country United States
    Document type Journal Article ; Review
    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.2016.07.055
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    Zs.A 116: Show issues Location:
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  6. Article ; Online: Mitochondria in the nervous system: From health to disease, Part I.

    Polster, Brian M / Carrì, Maria Teresa / Beart, Philip M

    Neurochemistry international

    2017  Volume 109, Page(s) 1–4

    Abstract: In Part I of this Special Issue on "Mitochondria in the Nervous System: From Health to Disease", the editors bring together contributions from experts in brain mitochondrial research to provide an up-to-date overview of mitochondrial functioning in ... ...

    Abstract In Part I of this Special Issue on "Mitochondria in the Nervous System: From Health to Disease", the editors bring together contributions from experts in brain mitochondrial research to provide an up-to-date overview of mitochondrial functioning in physiology and pathology. The issue provides cutting edge reviews on classical areas of mitochondrial biology that include energy substrate utilization, calcium handling, mitochondria-endoplasmic reticulum communication, and cell death regulation. Additional reviews and original research articles touch upon key mitochondrial defects seen across multiple neurodegenerative conditions, including fragmentation, loss of respiratory capacity, calcium overload, elevated reactive oxygen species generation, perturbed NAD
    Language English
    Publishing date 2017-10
    Publishing country England
    Document type Editorial
    ZDB-ID 283190-9
    ISSN 1872-9754 ; 0197-0186
    ISSN (online) 1872-9754
    ISSN 0197-0186
    DOI 10.1016/j.neuint.2017.09.006
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  7. Article ; Online: Neuroinflammation in Amyotrophic Lateral Sclerosis: Role of Redox (dys)Regulation.

    D'Ambrosi, Nadia / Cozzolino, Mauro / Carrì, Maria Teresa

    Antioxidants & redox signaling

    2017  Volume 29, Issue 1, Page(s) 15–36

    Abstract: Significance: Amyotrophic lateral sclerosis (ALS) is due to degeneration of upper and lower motor neurons in the anterior horn of the spinal cord and in the motor cortex. Mechanisms leading to motor neuron death are complex and currently the disease is ... ...

    Abstract Significance: Amyotrophic lateral sclerosis (ALS) is due to degeneration of upper and lower motor neurons in the anterior horn of the spinal cord and in the motor cortex. Mechanisms leading to motor neuron death are complex and currently the disease is untreatable. Recent Advances: Work in genetic models of ALS indicates that an imbalance in the cross talk that physiologically exists between motor neurons and the surrounding cells is eventually detrimental to motor neurons. In particular, the cascade of events collectively known as neuroinflammation and mainly characterized by a reactive phenotype of astrocytes and microglia, moderate infiltration of peripheral immune cells, and elevated levels of inflammatory mediators has been consistently observed in motor regions of the central nervous system (CNS) in sporadic and familial ALS, constituting a hallmark of the disease. Resident glial cells and infiltrated immune cells are considered among the major producers of reactive species of oxygen and nitrogen in pathological conditions of the CNS, including motor neuron diseases.
    Critical issues: The timing and exact role of oxidative stress-mediated neuroinflammation and damage to motor neurons in ALS are still not fully elucidated.
    Future directions: It is clear that a major challenge in the next future will be to envisage effective strategies to modulate the neuroinflammatory response in the symptomatic stage of disease, to prevent progression of neurodegeneration through the propagation of oxidative damage. Antioxid. Redox Signal. 29, 15-36.
    MeSH term(s) Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Oxidation-Reduction ; Reactive Nitrogen Species/metabolism ; Reactive Oxygen Species/metabolism
    Chemical Substances Reactive Nitrogen Species ; Reactive Oxygen Species
    Language English
    Publishing date 2017-10-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2017.7271
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    Zs.A 5488: Show issues Location:
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  8. Article: Minocycline for patients with ALS.

    Carrì, Maria Teresa

    The Lancet. Neurology

    2007  Volume 7, Issue 2, Page(s) 118–9; author reply 120–1

    MeSH term(s) Amyotrophic Lateral Sclerosis/drug therapy ; Animals ; Anti-Bacterial Agents/adverse effects ; Anti-Bacterial Agents/therapeutic use ; Disease Models, Animal ; Drug Therapy, Combination ; Humans ; Mice ; Mice, Knockout ; Minocycline/adverse effects ; Minocycline/therapeutic use ; Randomized Controlled Trials as Topic ; Superoxide Dismutase/genetics ; Superoxide Dismutase-1 ; Treatment Failure
    Chemical Substances Anti-Bacterial Agents ; SOD1 protein, human ; Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1) ; Minocycline (FYY3R43WGO)
    Language English
    Publishing date 2007-10-04
    Publishing country England
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2081241-3
    ISSN 1474-4422
    ISSN 1474-4422
    DOI 10.1016/S1474-4422(08)70005-X
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    Zs.A 5955: Show issues Location:
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  9. Article: Pathways to mitochondrial dysfunction in ALS pathogenesis

    Carrì, Maria Teresa / D’Ambrosi, Nadia / Cozzolino, Mauro

    Biochemical and biophysical research communications. 2016,

    2016  

    Abstract: Alterations in the structure and functions of mitochondria are a typical trait of Amyotrophic Lateral Sclerosis, a neurodegenerative disease characterized by a prominent degeneration of upper and lower motor neurons. The known gene mutations that are ... ...

    Abstract Alterations in the structure and functions of mitochondria are a typical trait of Amyotrophic Lateral Sclerosis, a neurodegenerative disease characterized by a prominent degeneration of upper and lower motor neurons. The known gene mutations that are responsible for a small fraction of ALS cases point to a complex interplay between different mechanisms in the disease pathogenesis. Here we will briefly overview the genetic and mechanistic evidence that make dysfunction of mitochondria a candidate major player in this process.
    Keywords amyotrophic lateral sclerosis ; genes ; mitochondria ; motor neurons ; mutation ; pathogenesis
    Language English
    Size p. .
    Publishing place Elsevier Inc.
    Document type Article
    Note Pre-press version
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2016.07.055
    Database NAL-Catalogue (AGRICOLA)

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  10. Article ; Online: Old versus New Mechanisms in the Pathogenesis of ALS.

    Rossi, Simona / Cozzolino, Mauro / Carrì, Maria Teresa

    Brain pathology (Zurich, Switzerland)

    2016  Volume 26, Issue 2, Page(s) 276–286

    Abstract: Amyotrophic Lateral Sclerosis (ALS) is recognized as a very complex disease. As we have learned in the past 20 years from studies in patients and in models based on the expression of mutant SOD1, ALS is not a purely motor neuron disease as previously ... ...

    Abstract Amyotrophic Lateral Sclerosis (ALS) is recognized as a very complex disease. As we have learned in the past 20 years from studies in patients and in models based on the expression of mutant SOD1, ALS is not a purely motor neuron disease as previously thought. While undoubtedly motor neurons are lost in patients, a number of alterations in those cell-types that interact functionally with motor neurons (astrocytes, microglia, muscle fibers, oligodendrocytes) take place even long before onset of symptoms. At the same time, disturbance of several, only partly inter-related physiological functions play some role in the onset and progression of the disease. Traditionally, mitochondrial damage and oxidative stress, excitotoxicity, neuroinflammation, altered axonal transport, ER stress, protein aggregation and defective removal of toxic proteins have been considered as key factors in the pathogenesis of ALS, with the relatively recent addition of disturbances in RNA metabolism. This complexity makes the search for an effective treatment extremely difficult and prompts further studies to reveal other possible, previously unappreciated aspects of the pathogenesis of ALS. In this review, we focus on previous knowledge on ALS mechanisms as well as new facets emerging from studies on genetic ALS patients and models that may both provide precious information for a novel therapeutic approach.
    MeSH term(s) Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/physiopathology ; Amyotrophic Lateral Sclerosis/therapy ; Animals ; Humans
    Language English
    Publishing date 2016-01-11
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/bpa.12355
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