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  1. Article ; Online: In vivo brain imaging of mitochondrial Ca

    Calvo-Rodriguez, Maria / Kharitonova, Elizabeth K / Bacskai, Brian J

    Biochimica et biophysica acta. Molecular cell research

    2021  Volume 1868, Issue 6, Page(s) 118998

    Abstract: Mitochondria are involved in a large number of essential roles related to neuronal function. ... ...

    Abstract Mitochondria are involved in a large number of essential roles related to neuronal function. Ca
    MeSH term(s) Animals ; Brain/diagnostic imaging ; Brain/metabolism ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling ; Disease Models, Animal ; Humans ; Mice ; Microscopy, Fluorescence, Multiphoton/methods ; Mitochondria/metabolism ; Neurodegenerative Diseases/diagnostic imaging ; Neurodegenerative Diseases/metabolism
    Chemical Substances Calcium Channels ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-03-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2021.118998
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.247: Show issues Location:
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  2. Article ; Online: Resistant CMV infection in a transplant patient. Letermovir and withdrawal of immunosuppression.

    Crucio López, María / Fernández Rivera, Constantino / Calvo Rodríguez, María / Alonso Hernández, Ángel

    Nefrologia

    2023  Volume 43, Issue 5, Page(s) 661–662

    MeSH term(s) Humans ; Cytomegalovirus Infections/drug therapy ; Antiviral Agents/adverse effects ; Acetates ; Immunosuppression Therapy/adverse effects
    Chemical Substances letermovir (1H09Y5WO1F) ; Antiviral Agents ; Acetates
    Language English
    Publishing date 2023-11-10
    Publishing country Spain
    Document type Letter
    ZDB-ID 2837917-2
    ISSN 2013-2514 ; 2013-2514
    ISSN (online) 2013-2514
    ISSN 2013-2514
    DOI 10.1016/j.nefroe.2023.10.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: High mitochondrial calcium levels precede neuronal death

    Calvo-Rodriguez, Maria / Bacskai, Brian J

    Cell stress

    2020  Volume 4, Issue 7, Page(s) 187–190

    Abstract: Alzheimer's disease (AD), the most common cause of dementia, affects millions of people worldwide. Suggested mechanisms of neurotoxicity in AD include impaired calcium ( ... ...

    Abstract Alzheimer's disease (AD), the most common cause of dementia, affects millions of people worldwide. Suggested mechanisms of neurotoxicity in AD include impaired calcium (Ca
    Language English
    Publishing date 2020-06-18
    Publishing country Austria
    Document type Journal Article ; Comment
    ISSN 2523-0204
    ISSN (online) 2523-0204
    DOI 10.15698/cst2020.07.226
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  4. Article ; Online: Therapeutic Strategies to Target Calcium Dysregulation in Alzheimer's Disease.

    Calvo-Rodriguez, Maria / Kharitonova, Elizabeth K / Bacskai, Brian J

    Cells

    2020  Volume 9, Issue 11

    Abstract: Alzheimer's disease (AD) is the most common form of dementia, affecting millions of people worldwide. Unfortunately, none of the current treatments are effective at improving cognitive function in AD patients and, therefore, there is an urgent need for ... ...

    Abstract Alzheimer's disease (AD) is the most common form of dementia, affecting millions of people worldwide. Unfortunately, none of the current treatments are effective at improving cognitive function in AD patients and, therefore, there is an urgent need for the development of new therapies that target the early cause(s) of AD. Intracellular calcium (Ca
    MeSH term(s) Alzheimer Disease/physiopathology ; Alzheimer Disease/therapy ; Calcium/metabolism ; Calcium Signaling/immunology ; Homeostasis ; Humans
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-11-20
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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/cells9112513
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  5. Article ; Online: Mitochondria and Calcium in Alzheimer's Disease: From Cell Signaling to Neuronal Cell Death.

    Calvo-Rodriguez, Maria / Bacskai, Brian J

    Trends in neurosciences

    2020  Volume 44, Issue 2, Page(s) 136–151

    Abstract: Mitochondrial dysfunction has been implicated in the pathogenesis of almost all neurological diseases, including Alzheimer's disease (AD). Historically, a primary focus in this context has been the link between mitochondrial dynamics and amyloid β ... ...

    Abstract Mitochondrial dysfunction has been implicated in the pathogenesis of almost all neurological diseases, including Alzheimer's disease (AD). Historically, a primary focus in this context has been the link between mitochondrial dynamics and amyloid β toxicity. Recent evidence suggests that dysregulation of mitochondrial calcium homeostasis is also related to tau and other risk factors in AD, although an ongoing challenge in the field is that data collected from different models or experimental settings have not always been consistent. We examine recent literature on mitochondrial dysregulation in AD, with special emphasis on mitochondrial calcium. We include data from in vitro systems, genetic animal models, and AD-derived human tissue, and discuss whether mitochondrial calcium transporters should be proposed as therapeutic candidates for the development of neuroprotective drugs against AD.
    MeSH term(s) Alzheimer Disease ; Amyloid beta-Peptides ; Animals ; Calcium ; Cell Death ; Humans ; Mitochondria ; Signal Transduction
    Chemical Substances Amyloid beta-Peptides ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-11-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 282488-7
    ISSN 1878-108X ; 0378-5912 ; 0166-2236
    ISSN (online) 1878-108X
    ISSN 0378-5912 ; 0166-2236
    DOI 10.1016/j.tins.2020.10.004
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1442: Show issues Location:
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    Zs.MG 53: Show issues

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  6. Article ; Online: Mitochondria-ER contacts and glucose: the powerhouse of Alzheimer's disease?

    Garcia-Alloza, Monica / Bacskai, Brian J / Calvo-Rodriguez, Maria

    Cell calcium

    2021  Volume 97, Page(s) 102434

    Abstract: A mechanism involving endoplasmic reticulum-mitochondria contacts noted in diabetes mellitus may explain the neurodegeneration and amyloidogenesis observed in these patients. Urolithin A, a metabolite found in the gut microbiome, is proposed as a ... ...

    Abstract A mechanism involving endoplasmic reticulum-mitochondria contacts noted in diabetes mellitus may explain the neurodegeneration and amyloidogenesis observed in these patients. Urolithin A, a metabolite found in the gut microbiome, is proposed as a therapeutic strategy for the treatment of the diabetes-related dementia.
    Language English
    Publishing date 2021-06-12
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2021.102434
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    Zs.A 1596: Show issues Location:
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  7. Article: Amyloid Beta Oligomers-Induced Ca

    Caballero, Erica / Hernando-Pérez, Elena / Tapias, Victor / Calvo-Rodríguez, María / Villalobos, Carlos / Núñez, Lucía

    Biomedicines

    2022  Volume 10, Issue 5

    Abstract: The molecular basis of amyloid toxicity in Alzheimer's disease (AD) remains controversial. Amyloid β (Aβ) oligomers promote ... ...

    Abstract The molecular basis of amyloid toxicity in Alzheimer's disease (AD) remains controversial. Amyloid β (Aβ) oligomers promote Ca
    Language English
    Publishing date 2022-05-17
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10051153
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  8. Article ; Online: Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer's disease.

    Calvo-Rodriguez, Maria / Kharitonova, Elizabeth K / Snyder, Austin C / Hou, Steven S / Sanchez-Mico, Maria Virtudes / Das, Sudeshna / Fan, Zhanyun / Shirani, Hamid / Nilsson, K Peter R / Serrano-Pozo, Alberto / Bacskai, Brian J

    Molecular neurodegeneration

    2024  Volume 19, Issue 1, Page(s) 6

    Abstract: Background: Reactive oxidative stress is a critical player in the amyloid beta (Aβ) toxicity that contributes to neurodegeneration in Alzheimer's disease (AD). Damaged mitochondria are one of the main sources of reactive oxygen species and accumulate in ...

    Abstract Background: Reactive oxidative stress is a critical player in the amyloid beta (Aβ) toxicity that contributes to neurodegeneration in Alzheimer's disease (AD). Damaged mitochondria are one of the main sources of reactive oxygen species and accumulate in Aβ plaque-associated dystrophic neurites in the AD brain. Although Aβ causes neuronal mitochondria reactive oxidative stress in vitro, this has never been directly observed in vivo in the living mouse brain. Here, we tested for the first time whether Aβ plaques and soluble Aβ oligomers induce mitochondrial oxidative stress in surrounding neurons in vivo, and whether this neurotoxic effect can be abrogated using mitochondrial-targeted antioxidants.
    Methods: We expressed a genetically encoded fluorescent ratiometric mitochondria-targeted reporter of oxidative stress in mouse models of the disease and performed intravital multiphoton microscopy of neuronal mitochondria and Aβ plaques.
    Results: For the first time, we demonstrated by direct observation in the living mouse brain exacerbated mitochondrial oxidative stress in neurons after both Aβ plaque deposition and direct application of soluble oligomeric Aβ onto the brain, and determined the most likely pathological sequence of events leading to oxidative stress in vivo. Oxidative stress could be inhibited by both blocking calcium influx into mitochondria and treating with the mitochondria-targeted antioxidant SS31. Remarkably, the latter ameliorated plaque-associated dystrophic neurites without impacting Aβ plaque burden.
    Conclusions: Considering these results, combination of mitochondria-targeted compounds with other anti-amyloid beta or anti-tau therapies hold promise as neuroprotective drugs for the prevention and/or treatment of AD.
    MeSH term(s) Mice ; Animals ; Amyloid beta-Peptides/metabolism ; Alzheimer Disease/metabolism ; Oxidative Stress/physiology ; Antioxidants/pharmacology ; Antioxidants/metabolism ; Oxidation-Reduction ; Mitochondria/metabolism ; Disease Models, Animal
    Chemical Substances Amyloid beta-Peptides ; Antioxidants
    Language English
    Publishing date 2024-01-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 2244557-2
    ISSN 1750-1326 ; 1750-1326
    ISSN (online) 1750-1326
    ISSN 1750-1326
    DOI 10.1186/s13024-024-00702-2
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  9. Article ; Online: Role of Toll Like Receptor 4 in Alzheimer's Disease.

    Calvo-Rodriguez, Maria / García-Rodríguez, Carmen / Villalobos, Carlos / Núñez, Lucía

    Frontiers in immunology

    2020  Volume 11, Page(s) 1588

    Abstract: Long-term evidence has confirmed the involvement of an inflammatory component in neurodegenerative disorders including Alzheimer's disease (AD). This view is supported, in part, by data suggesting that selected non-steroidal anti-inflammatory drugs ( ... ...

    Abstract Long-term evidence has confirmed the involvement of an inflammatory component in neurodegenerative disorders including Alzheimer's disease (AD). This view is supported, in part, by data suggesting that selected non-steroidal anti-inflammatory drugs (NSAIDs) provide protection. Additionally, molecular players of the innate immune system have recently been proposed to contribute to these diseases. Toll-like receptors (TLRs) are transmembrane pattern-recognition receptors of the innate immune system that recognize different pathogen-derived and tissue damage-related ligands. TLR4 mediated signaling has been reported to contribute to the pathogenesis of age-related neurodegenerative diseases, including AD. Although the pathophysiology of AD is not clear, soluble aggregates (oligomers) of the amyloid β peptide (Aβo) have been proven to be key players in the pathology of AD. Among others, Aβo promote Ca
    MeSH term(s) Aging/metabolism ; Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Animals ; Calcium/metabolism ; Calcium Signaling ; Disease Susceptibility ; Hippocampus/metabolism ; Hippocampus/pathology ; Humans ; Protein Aggregates ; Protein Aggregation, Pathological ; Pyramidal Cells/metabolism ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism
    Chemical Substances Amyloid beta-Peptides ; Protein Aggregates ; Toll-Like Receptor 4 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-08-26
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2020.01588
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  10. Article ; Online: Toll-like receptors in neuroinflammation, neurodegeneration, and alcohol-induced brain damage.

    Pascual, María / Calvo-Rodriguez, Maria / Núñez, Lucía / Villalobos, Carlos / Ureña, Juan / Guerri, Consuelo

    IUBMB life

    2021  Volume 73, Issue 7, Page(s) 900–915

    Abstract: Toll-like receptors (TLRs) or pattern recognition receptors respond to pathogen-associated molecular patterns (PAMPs) or internal damage-associated molecular patterns (DAMPs). TLRs are integral membrane proteins with both extracellular leucine-rich and ... ...

    Abstract Toll-like receptors (TLRs) or pattern recognition receptors respond to pathogen-associated molecular patterns (PAMPs) or internal damage-associated molecular patterns (DAMPs). TLRs are integral membrane proteins with both extracellular leucine-rich and cytoplasmic domains that initiate downstream signaling through kinases by activating transcription factors like AP-1 and NF-κB, which lead to the release of various inflammatory cytokines and immune modulators. In the central nervous system, different TLRs are expressed mainly in microglia and astroglial cells, although some TLRs are also expressed in oligodendroglia and neurons. Activation of TLRs triggers signaling cascades by the host as a defense mechanism against invaders to repair damaged tissue. However, overactivation of TLRs disrupts the sustained immune homeostasis-induced production of pro-inflammatory molecules, such as cytokines, miRNAs, and inflammatory components of extracellular vesicles. These inflammatory mediators can, in turn, induce neuroinflammation, and neural tissue damage associated with many neurodegenerative diseases. This review discusses the critical role of TLRs response in Alzheimer's disease, Parkinson's disease, ischemic stroke, amyotrophic lateral sclerosis, and alcohol-induced brain damage and neurodegeneration.
    MeSH term(s) Alcoholism/etiology ; Alcoholism/physiopathology ; Animals ; Brain/drug effects ; Brain/physiopathology ; Exosomes/pathology ; Exosomes/physiology ; Gene Expression ; Humans ; Immunity, Innate ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/therapy ; Neuroinflammatory Diseases/etiology ; Neuroinflammatory Diseases/therapy ; Toll-Like Receptors/physiology
    Chemical Substances MicroRNAs ; Toll-Like Receptors
    Language English
    Publishing date 2021-06-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1492141-8
    ISSN 1521-6551 ; 1521-6543
    ISSN (online) 1521-6551
    ISSN 1521-6543
    DOI 10.1002/iub.2510
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    Zs.A 1611: Show issues Location:
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