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  1. Book: Qualitätsprüfung Tagespflege

    Albert, Natalie / Eckert, Anne / Matzker, Eva-Maria / Rusche, Nicole

    der kompetente Begleiter für die Qualitätsprüfung Tagespflege

    2022  

    Author's details Albert Natalie, Anne Eckert, Eva-Maria Matzker, Nicole Rusche
    Keywords Ergebnisorientiertes Qualitätsmodell ; Ergebnisqualität in der Pflege ; Tagespflege ; externe Qualitätsprüfung ; SIS ; NBI ; Qualitätsprüfrichtlinie ; teilstationäre Pflege ; Qualitätsaspekte ; Qualitätsprüfung ; Indikatorengestützte Qualitätssystem ; QPR ; Qualitätsindikatoren ; MDK ; MDK-Prüfung ; Altentagespflege ; Medizinischer Dienst der Krankenversicherung
    Subject Krankenversicherung ; Vertrauensärztlicher Dienst ; MDK ; Tagespflege
    Language German
    Size 192 Seiten, Illustrationen, 21 cm x 15 cm, 250 g
    Publisher dck media
    Publishing place Münster
    Publishing country Germany
    Document type Book
    HBZ-ID HT021384305
    ISBN 978-3-9818541-6-9 ; 3-9818541-6-0
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2022 A 693 available for loan (reading room) Lesesaal EG

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  2. Book ; Online: Interphase Between Aging and Neurodegenerative Diseases

    Müller, Walter E. / Eckert, Anne / Hemachandra Reddy, P.

    2020  

    Keywords Science: general issues ; Neurosciences ; neurodegenerative diseases ; aging ; Parkinson's disease ; Alzheimer's disease ; neurodegeneration ; β-amyloid ; Aβ
    Size 1 electronic resource (129 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230581
    ISBN 9782889634569 ; 2889634566
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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    Inter-library loan at ZB MED

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  3. Book: Alzheimer - unabwendbares Schicksal?

    Eckert, Anne / Flöel, Agnes

    Moderne Wege zu mentaler Gesundheit

    2013  

    Author's details hrsg. von Agnes Flöel. Unter Mitarb. von Anne Eckert
    Keywords Alzheimerkrankheit
    Subject Alzheimer-Krankheit ; Alzheimersche Krankheit ; Alzheimer-Demenz ; Morbus Alzheimer ; Greisenblödsinn ; Alzheimer's Disease
    Language German
    Size XII, 130 S., Ill., graph. Darst., 240 mm x 165 mm
    Publisher Schattauer
    Publishing place Stuttgart
    Publishing country Germany
    Document type Book
    HBZ-ID HT017365643
    ISBN 978-3-7945-2910-0 ; 3-7945-2910-3
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2009 A 10741 order for loan Magazin

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  4. Article ; Online: Translocator protein (TSPO) ligands attenuate mitophagy deficits in the SH-SY5Y cellular model of Alzheimer's disease via the autophagy adaptor P62.

    Fairley, Lauren H / Grimm, Amandine / Herff, Steffen A / Eckert, Anne

    Biochimie

    2024  

    Abstract: Mitochondrial dysfunction has been widely implicated in the pathogenesis of Alzheimer's disease (AD), with accumulation of damaged and dysfunctional mitochondria occurring early in the disease. Mitophagy, which governs mitochondrial turnover and quality ... ...

    Abstract Mitochondrial dysfunction has been widely implicated in the pathogenesis of Alzheimer's disease (AD), with accumulation of damaged and dysfunctional mitochondria occurring early in the disease. Mitophagy, which governs mitochondrial turnover and quality control, is impaired in the AD brain, and strategies aimed at enhancing mitophagy have been identified as promising therapeutic targets. The translocator protein (TSPO) is an outer mitochondrial membrane protein that is upregulated in AD, and ligands targeting TSPO have been shown to exert neuroprotective effects in mouse models of AD. However, whether TSPO ligands modulate mitophagy in AD has not been explored. Here, we provide evidence that the TSPO-specific ligands Ro5-4864 and XBD173 attenuate mitophagy deficits and mitochondrial fragmentation in a cellular model of AD overexpressing the human amyloid precursor protein (APP). Ro5-4864 and XBD173 appear to enhance mitophagy via modulation of the autophagic cargo receptor P62/SQSTM1, in the absence of an effect on PARK2, PINK1, or LC3 level. Taken together, these findings indicate that TSPO ligands may be promising therapeutic agents for ameliorating mitophagy deficits in AD.
    Language English
    Publishing date 2024-01-26
    Publishing country France
    Document type Journal Article
    ZDB-ID 120345-9
    ISSN 1638-6183 ; 0300-9084
    ISSN (online) 1638-6183
    ISSN 0300-9084
    DOI 10.1016/j.biochi.2024.01.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.135: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Spermidine Rescues Bioenergetic and Mitophagy Deficits Induced by Disease-Associated Tau Protein.

    Fairley, Lauren H / Lejri, Imane / Grimm, Amandine / Eckert, Anne

    International journal of molecular sciences

    2023  Volume 24, Issue 6

    Abstract: Abnormal tau build-up is a hallmark of Alzheimer's disease (AD) and more than 20 other serious neurodegenerative diseases. Mitochondria are paramount organelles playing a predominant role in cellular bioenergetics, namely by providing the main source of ... ...

    Abstract Abnormal tau build-up is a hallmark of Alzheimer's disease (AD) and more than 20 other serious neurodegenerative diseases. Mitochondria are paramount organelles playing a predominant role in cellular bioenergetics, namely by providing the main source of cellular energy via adenosine triphosphate generation. Abnormal tau impairs almost every aspect of mitochondrial function, from mitochondrial respiration to mitophagy. The aim of our study was to investigate the effects of spermidine, a polyamine which exerts neuroprotective effects, on mitochondrial function in a cellular model of tauopathy. Recent evidence identified autophagy as the main mechanism of action of spermidine on life-span prolongation and neuroprotection, but the effects of spermidine on abnormal tau-induced mitochondrial dysfunction have not yet been investigated. We used SH-SY5Y cells stably expressing a mutant form of human tau protein (P301L tau mutation) or cells expressing the empty vector (control cells). We showed that spermidine improved mitochondrial respiration, mitochondrial membrane potential as well as adenosine triphosphate (ATP) production in both control and P301L tau-expressing cells. We also showed that spermidine decreased the level of free radicals, increased autophagy and restored P301L tau-induced impairments in mitophagy. Overall, our findings suggest that spermidine supplementation might represent an attractive therapeutic approach to prevent/counteract tau-related mitochondrial impairments.
    MeSH term(s) Humans ; tau Proteins/metabolism ; Mitophagy ; Spermidine/pharmacology ; Neuroblastoma ; Alzheimer Disease/metabolism ; Energy Metabolism ; Adenosine Triphosphate/metabolism
    Chemical Substances tau Proteins ; Spermidine (U87FK77H25) ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2023-03-10
    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/ijms24065297
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Mitochondria Transfer in Brain Injury and Disease.

    Fairley, Lauren H / Grimm, Amandine / Eckert, Anne

    Cells

    2022  Volume 11, Issue 22

    Abstract: Intercellular mitochondria transfer is a novel form of cell signalling in which whole mitochondria are transferred between cells in order to enhance cellular functions or aid in the degradation of dysfunctional mitochondria. Recent studies have observed ... ...

    Abstract Intercellular mitochondria transfer is a novel form of cell signalling in which whole mitochondria are transferred between cells in order to enhance cellular functions or aid in the degradation of dysfunctional mitochondria. Recent studies have observed intercellular mitochondria transfer between glia and neurons in the brain, and mitochondrial transfer has emerged as a key neuroprotective mechanism in a range of neurological conditions. In particular, artificial mitochondria transfer has sparked widespread interest as a potential therapeutic strategy for brain disorders. In this review, we discuss the mechanisms and effects of intercellular mitochondria transfer in the brain. The role of mitochondrial transfer in neurological conditions, including neurodegenerative disease, brain injury, and neurodevelopmental disorders, is discussed as well as therapeutic strategies targeting mitochondria transfer in the brain.
    MeSH term(s) Humans ; Neurodegenerative Diseases/metabolism ; Mitochondria/metabolism ; Brain Injuries/metabolism ; Brain/metabolism ; Neurons/metabolism
    Language English
    Publishing date 2022-11-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11223603
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Rhodiola Rosea Extract Counteracts Stress in an Adaptogenic Response Curve Manner via Elimination of ROS and Induction of Neurite Outgrowth.

    Agapouda, Anastasia / Grimm, Amandine / Lejri, Imane / Eckert, Anne

    publication RETRACTED

    Oxidative medicine and cellular longevity

    2022  Volume 2022, Page(s) 5647599

    Abstract: Background: Sustained stress with the overproduction of corticosteroids has been shown to increase reactive oxygen species (ROS) leading to an oxidative stress state. Mitochondria are the main generators of ROS and are directly and detrimentally ... ...

    Abstract Background: Sustained stress with the overproduction of corticosteroids has been shown to increase reactive oxygen species (ROS) leading to an oxidative stress state. Mitochondria are the main generators of ROS and are directly and detrimentally affected by their overproduction. Neurons depend almost solely on ATP produced by mitochondria in order to satisfy their energy needs and to form synapses, while stress has been proven to alter synaptic plasticity. Emerging evidence underpins that
    Methods: In this study, the effect of
    Results: RRE increased bioenergetics as well as cell viability and scavenged ROS with a similar efficacy in both cells lines and counteracted the respective corticosteroid-induced dysregulation. The effect of RRE, both under dexamethasone-stress and under normal conditions, resulted in biphasic U-shape and inverted U-shape dose response curves, a characteristic feature of adaptogenic plant extracts. Additionally, RRE treatment promoted neurite outgrowth and induced an increase in BDNF levels.
    Conclusion: These findings indicate that RRE may constitute a candidate for the prevention of stress-induced pathophysiological processes as well as oxidative stress. Therefore, it could be employed against stress-associated mental disorders potentially leading to the development of a condition-specific supplementation.
    MeSH term(s) Animals ; Brain-Derived Neurotrophic Factor ; Dexamethasone ; Humans ; Mice ; Neuronal Outgrowth ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Reactive Oxygen Species ; Rhodiola
    Chemical Substances Brain-Derived Neurotrophic Factor ; Plant Extracts ; Reactive Oxygen Species ; Dexamethasone (7S5I7G3JQL)
    Language English
    Publishing date 2022-05-13
    Publishing country United States
    Document type Journal Article ; Retracted Publication
    ZDB-ID 2455981-7
    ISSN 1942-0994 ; 1942-0994
    ISSN (online) 1942-0994
    ISSN 1942-0994
    DOI 10.1155/2022/5647599
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Spermidine Rescues Bioenergetic and Mitophagy Deficits Induced by Disease-Associated Tau Protein

    Lauren H. Fairley / Imane Lejri / Amandine Grimm / Anne Eckert

    International Journal of Molecular Sciences, Vol 24, Iss 5297, p

    2023  Volume 5297

    Abstract: Abnormal tau build-up is a hallmark of Alzheimer’s disease (AD) and more than 20 other serious neurodegenerative diseases. Mitochondria are paramount organelles playing a predominant role in cellular bioenergetics, namely by providing the main source of ... ...

    Abstract Abnormal tau build-up is a hallmark of Alzheimer’s disease (AD) and more than 20 other serious neurodegenerative diseases. Mitochondria are paramount organelles playing a predominant role in cellular bioenergetics, namely by providing the main source of cellular energy via adenosine triphosphate generation. Abnormal tau impairs almost every aspect of mitochondrial function, from mitochondrial respiration to mitophagy. The aim of our study was to investigate the effects of spermidine, a polyamine which exerts neuroprotective effects, on mitochondrial function in a cellular model of tauopathy. Recent evidence identified autophagy as the main mechanism of action of spermidine on life-span prolongation and neuroprotection, but the effects of spermidine on abnormal tau-induced mitochondrial dysfunction have not yet been investigated. We used SH-SY5Y cells stably expressing a mutant form of human tau protein (P301L tau mutation) or cells expressing the empty vector (control cells). We showed that spermidine improved mitochondrial respiration, mitochondrial membrane potential as well as adenosine triphosphate (ATP) production in both control and P301L tau-expressing cells. We also showed that spermidine decreased the level of free radicals, increased autophagy and restored P301L tau-induced impairments in mitophagy. Overall, our findings suggest that spermidine supplementation might represent an attractive therapeutic approach to prevent/counteract tau-related mitochondrial impairments.
    Keywords tau ; mitochondria ; spermidine ; bioenergetics ; autophagy ; mitophagy ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 571
    Language English
    Publishing date 2023-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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  9. Article ; Online: Genetically Engineered Triple

    Szabo, Leonora / Grimm, Amandine / García-León, Juan Antonio / Verfaillie, Catherine M / Eckert, Anne

    Cells

    2023  Volume 12, Issue 10

    Abstract: Pathological abnormalities in the tau protein give rise to a variety of neurodegenerative diseases, conjointly termed tauopathies. Several tau mutations have been identified in the tau-encoding ... ...

    Abstract Pathological abnormalities in the tau protein give rise to a variety of neurodegenerative diseases, conjointly termed tauopathies. Several tau mutations have been identified in the tau-encoding gene
    MeSH term(s) Humans ; tau Proteins/genetics ; tau Proteins/metabolism ; Induced Pluripotent Stem Cells/metabolism ; Mutation/genetics ; Mitochondria/metabolism ; Energy Metabolism
    Chemical Substances tau Proteins ; MAPT protein, human
    Language English
    Publishing date 2023-05-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12101385
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Psychiatric manifestations of post-COVID-19 syndrome: the potential benefit of Silexan.

    Kasper, Siegfried / Eckert, Anne / Möller, Hans-Jürgen / Volz, Hans-Peter / Seifritz, Erich

    International journal of psychiatry in clinical practice

    2023  Volume 27, Issue 3, Page(s) 285–291

    Abstract: Objective: ...

    Abstract Objective:
    MeSH term(s) Humans ; Post-Acute COVID-19 Syndrome ; COVID-19/complications ; Plant Oils ; Oils, Volatile/pharmacology
    Chemical Substances lavender oil (ZBP1YXW0H8) ; Plant Oils ; Oils, Volatile
    Language English
    Publishing date 2023-04-06
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1465531-7
    ISSN 1471-1788 ; 1365-1501
    ISSN (online) 1471-1788
    ISSN 1365-1501
    DOI 10.1080/13651501.2023.2187308
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4995: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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