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  1. Article ; Online: Impairments in Brain Bioenergetics in Aging and Tau Pathology: A Chicken and Egg Situation?

    Grimm, Amandine

    Cells

    2021  Volume 10, Issue 10

    Abstract: The brain is the most energy-consuming organ of the body and impairments in brain energy metabolism will affect neuronal functionality and viability. Brain aging is marked by defects in energetic metabolism. Abnormal tau protein is a hallmark of ... ...

    Abstract The brain is the most energy-consuming organ of the body and impairments in brain energy metabolism will affect neuronal functionality and viability. Brain aging is marked by defects in energetic metabolism. Abnormal tau protein is a hallmark of tauopathies, including Alzheimer's disease (AD). Pathological tau was shown to induce bioenergetic impairments by affecting mitochondrial function. Although it is now clear that mutations in the tau-coding gene lead to tau pathology, the causes of abnormal tau phosphorylation and aggregation in non-familial tauopathies, such as sporadic AD, remain elusive. Strikingly, both tau pathology and brain hypometabolism correlate with cognitive impairments in AD. The aim of this review is to discuss the link between age-related decrease in brain metabolism and tau pathology. In particular, the following points will be discussed: (i) the common bioenergetic features observed during brain aging and tauopathies; (ii) how age-related bioenergetic defects affect tau pathology; (iii) the influence of lifestyle factors known to modulate brain bioenergetics on tau pathology. The findings compiled here suggest that age-related bioenergetic defects may trigger abnormal tau phosphorylation/aggregation and cognitive impairments after passing a pathological threshold. Understanding the effects of aging on brain metabolism may therefore help to identify disease-modifying strategies against tau-induced neurodegeneration.
    MeSH term(s) Aging/metabolism ; Brain/metabolism ; Cognitive Dysfunction/metabolism ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Humans ; Neurons/metabolism ; Tauopathies/metabolism ; tau Proteins/metabolism
    Chemical Substances tau Proteins
    Language English
    Publishing date 2021-09-24
    Publishing country Switzerland
    Document type Journal Article ; 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/cells10102531
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. 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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  3. 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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  4. 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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  5. 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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  6. 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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  7. Article ; Online: Sex differences in Alzheimer's disease: metabolic reprogramming and therapeutic intervention.

    Demetrius, Lloyd A / Eckert, Anne / Grimm, Amandine

    Trends in endocrinology and metabolism: TEM

    2021  Volume 32, Issue 12, Page(s) 963–979

    Abstract: Studies on the sporadic form of Alzheimer's disease (AD) have revealed three classes of risk factor: age, genetics, and sex. These risk factors point to a metabolic dysregulation as the origin of AD. Adaptive alterations in cerebral metabolism are the ... ...

    Abstract Studies on the sporadic form of Alzheimer's disease (AD) have revealed three classes of risk factor: age, genetics, and sex. These risk factors point to a metabolic dysregulation as the origin of AD. Adaptive alterations in cerebral metabolism are the rationale for the Metabolic Reprogramming (MR) Theory of the origin of AD. The theory contends that the progression toward AD involves three adaptive events: a hypermetabolic phase, a prolonged prodromal phase, and a metabolic collapse. This article exploits the MR Theory to elucidate the effect of hormonal changes on the origin and progression of AD in women. The theory invokes bioenergetic signatures of the menopausal transition to propose sex-specific diagnostic program and therapeutic strategies.
    MeSH term(s) Alzheimer Disease/metabolism ; Energy Metabolism ; Female ; Humans ; Male ; Menopause ; Sex Characteristics
    Language English
    Publishing date 2021-10-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1042384-9
    ISSN 1879-3061 ; 1043-2760
    ISSN (online) 1879-3061
    ISSN 1043-2760
    DOI 10.1016/j.tem.2021.09.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2999: 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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  8. Article ; Conference proceedings: Gelsemium low doses protect against serum deprivation-induced stress on mitochondria in neuronal cells

    Lejri, Imane / Grimm, Amandine / Trempat, Pascal / Boujedaini, Naoual / Eckert, Anne

    Planta Medica

    2023  Volume 89, Issue 14

    Event/congress 71st International Congress and Annual Meeting of the Society for Medicinal Plant and Natural Product Research (GA), Trinity College Dublin Ireland, 2023-07-02
    Language English
    Publishing date 2023-11-01
    Publisher Georg Thieme Verlag KG
    Publishing place Stuttgart ; New York
    Document type Article ; Conference proceedings
    ZDB-ID 123545-x
    ISSN 1439-0221 ; 0032-0943
    ISSN (online) 1439-0221
    ISSN 0032-0943
    DOI 10.1055/s-0043-1774250
    Database Thieme publisher's database

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    In stock of ZB MED Cologne/Königswinter

    Uf I Zs.157: 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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  9. Article: Dietary Mitophagy Enhancer: A Strategy for Healthy Brain Aging?

    Varghese, Nimmy / Werner, Selina / Grimm, Amandine / Eckert, Anne

    Antioxidants. 2020 Sept. 29, v. 9, no. 10

    2020  

    Abstract: Recently, nutritional interventions have received attention as promising approaches to promote human health during a lifespan. The Mediterranean and Okinawan diets have been associated with longevity and decreasing risk for age-related diseases in ... ...

    Abstract Recently, nutritional interventions have received attention as promising approaches to promote human health during a lifespan. The Mediterranean and Okinawan diets have been associated with longevity and decreasing risk for age-related diseases in contrast to the Western diet. The effect might be due to several antioxidative bioactive compounds highly consumed in both diets, namely, resveratrol, hydroxytyrosol, oleuropein, curcumin, and spermidine. This review aims to address the underlying mechanisms of these compounds to enhance mental fitness throughout life with a focus on brain mitophagy. Mitophagy is the autophagic clearance of dysfunctional, redundant, and aged mitochondria. In aging and neurodegenerative disorders, mitophagy is crucial to preserve the autophagy mechanism of the whole cell, especially during oxidative stress. Growing evidence indicates that curcumin, astaxanthin, resveratrol, hydroxytyrosol, oleuropein, and spermidine might exert protective functions via antioxidative properties and as well the enhanced induction of mitophagy mediators. The compounds seem to upregulate mitophagy and thereby alleviate the clearance of dysfunctional and aged mitochondria as well as mitogenesis. Thus, the Mediterranean or Okinawan diet could represent a feasible nutritional approach to reduce the risk of developing age-related cognitive impairment and corresponding disorders via the stimulation of mitophagy and thereby ensure a balanced redox state of brain cells.
    Keywords Western diets ; antioxidant activity ; antioxidants ; astaxanthin ; bioactive compounds ; brain ; cells ; cognitive disorders ; curcumin ; human health ; longevity ; mitochondria ; mitogenesis ; mitophagy ; neurodegenerative diseases ; nutritional intervention ; oleuropein ; oxidative stress ; resveratrol ; risk ; risk reduction ; spermidine
    Language English
    Dates of publication 2020-0929
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    Note NAL-light
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox9100932
    Database NAL-Catalogue (AGRICOLA)

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  10. Article: Dietary Mitophagy Enhancer: A Strategy for Healthy Brain Aging?

    Varghese, Nimmy / Werner, Selina / Grimm, Amandine / Eckert, Anne

    Antioxidants (Basel, Switzerland)

    2020  Volume 9, Issue 10

    Abstract: Recently, nutritional interventions have received attention as promising approaches to promote human health during a lifespan. The Mediterranean and Okinawan diets have been associated with longevity and decreasing risk for age-related diseases in ... ...

    Abstract Recently, nutritional interventions have received attention as promising approaches to promote human health during a lifespan. The Mediterranean and Okinawan diets have been associated with longevity and decreasing risk for age-related diseases in contrast to the Western diet. The effect might be due to several antioxidative bioactive compounds highly consumed in both diets, namely, resveratrol, hydroxytyrosol, oleuropein, curcumin, and spermidine. This review aims to address the underlying mechanisms of these compounds to enhance mental fitness throughout life with a focus on brain mitophagy. Mitophagy is the autophagic clearance of dysfunctional, redundant, and aged mitochondria. In aging and neurodegenerative disorders, mitophagy is crucial to preserve the autophagy mechanism of the whole cell, especially during oxidative stress. Growing evidence indicates that curcumin, astaxanthin, resveratrol, hydroxytyrosol, oleuropein, and spermidine might exert protective functions via antioxidative properties and as well the enhanced induction of mitophagy mediators. The compounds seem to upregulate mitophagy and thereby alleviate the clearance of dysfunctional and aged mitochondria as well as mitogenesis. Thus, the Mediterranean or Okinawan diet could represent a feasible nutritional approach to reduce the risk of developing age-related cognitive impairment and corresponding disorders via the stimulation of mitophagy and thereby ensure a balanced redox state of brain cells.
    Language English
    Publishing date 2020-09-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox9100932
    Database MEDical Literature Analysis and Retrieval System OnLINE

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