Aβ accumulation in choroid plexus is associated with mitochondrial-induced apoptosis

Vargas, Teodoro; Ugalde, Cristina; Spuch, Carlos; Antequera, Desireé; Morán, María; Martín, Miguel A.; Ferrer, Isidro; Bermejo‐Pareja, Félix; Carro, Eva

doi:10.1016/j.neurobiolaging.2008.08.017

Cited by 62 publications

(81 citation statements)

References 75 publications

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“…This would inhibit the entry of nuclear-encoded complex IV subunits IV and Vb into mitochondria, leading to decreased mitochondrial complex IV activity, ATP synthesis and membrane potential (Anandatheerthavarada et al, 2003;Devi et al, 2006). Accordingly, alterations in the assembly and enzyme activities of the RC complexes I and IV were demonstrated in rat choroid plexus epithelial cells treated with Aβ, and also in human choroid plexus cells from patients suffering AD (Vargas et al, 2010). The import blockage of complex IV constituents towards mitochondria could lead to an abnormal assembly of complex IV and the respirasome, which in turn would be responsible for the partial loss of complex I activity (Schagger et al, 2004;Li et al, 2007;Moreno-Lastres et al, 2012).…”

Section: In Alzheimer´s Diseasementioning

confidence: 98%

Mitochondrial respiratory chain dysfunction: Implications in neurodegeneration

Morán

Moreno-Lastres

Marín-Buera

et al. 2012

Free Radical Biology and Medicine

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136

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For decades mitochondria have been considered static round shaped organelles in charge of energy production. On the contrary, they are highly dynamic cellular components that undergo continuous cycles of fusion and fission influenced, for instance, by oxidative stress, cellular energy requirements, or the cell cycle state. New important functions beyond energy production have been attributed to mitochondria, such as the regulation of cell survival due to their role in the modulation of apoptosis, autophagy and aging. Primary mitochondrial diseases due to mutations in genes involved in these new mitochondrial functions, and the implication of mitochondrial dysfunction in multifactorial human pathologies like cancer, Alzheimer's and Parkinson's diseases, or diabetes has been demonstrated. Therefore, mitochondria are set at a central point of the equilibrium between health and disease, and a better understanding of mitochondrial functions will open new fields to explore the role of these mitochondrial pathways in human pathologies. The present review will dissect the relationships between the activity and assembly defects of the mitochondrial respiratory chain, oxidative damage, and alterations in mitochondrial dynamics, with special focus at their implications in neurodegeneration.

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Section: In Alzheimer´s Diseasementioning

confidence: 98%

Mitochondrial respiratory chain dysfunction: Implications in neurodegeneration

Morán

Moreno-Lastres

Marín-Buera

et al. 2012

Free Radical Biology and Medicine

Self Cite

136

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“…Cell death in substantia nigra from mice groups was also detected with a Cell Death Detection ELISAPLUS kit (Roche), according to the manufacturer's protocol. For NO detection, brain tissue was processed using the Nitric Oxide Colorimetric Assay Kit (BioVision, Inc.) according to previously published study [32]. Activation of NFB p65 was determined in substantia nigra from mice groups, and in SH-SY5Y dopaminergic cell line, by ELISA using a commercially available ELISA kit (Active Motif), as described [33].…”

Section: Immunoassaysmentioning

confidence: 99%

Intranasal PRGF-Endoret enhances neuronal survival and attenuates NF-κB-dependent inflammation process in a mouse model of Parkinson's disease

Anitua¹,

Pascual

Pérez‐González

et al. 2015

Journal of Controlled Release

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“…Moreover, this reduction in Ab burden, measured by both immunohistochemistry and ELISA assays, was accompanied by a significant reduction in apoptotic cell death in the hybrid-treated APP/Ps1 mice. This finding is not surprising in view of the ability of Ab 40 and Ab 42 to induce cell death (Yao et al 2005;Vargas et al 2008). …”

Section: Discussionmentioning

confidence: 83%

“…DNA fragmentation from in vivo (APP/Ps1 mice) and in vitro (neuronal cell cultures) samples undergoing apoptosis was also detected using a Cell Death Detection ELISA PLUS kit (Roche Diagnostics), as described previously (Vargas et al 2008). …”

Section: Cell Death Quantificationmentioning

confidence: 99%

A New Tacrine–Melatonin Hybrid Reduces Amyloid Burden and Behavioral Deficits in a Mouse Model of Alzheimer’s Disease

et al. 2009

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Alzheimer's disease (AD) is a progressive degenerative disorder characterized by the presence of amyloid deposits, neurofibrillary tangles and neuron loss. Emerging evidence indicates that antioxidants could be useful either for the prevention or treatment of AD. Tacrine and melatonin are well-known drugs which act as an acetylcholinesterase inhibitor and a free radical scavenger, respectively. In this study, we evaluated the effects of a new tacrine-melatonin hybrid on behavior and the biochemical and neuropathologic changes observed in amyloid precursor protein/presenilin 1 (APP/Ps1) transgenic mice. Our findings showed that direct intracerebral administration of this hybrid decreased amyloid beta peptide (Abeta)-induced cell death and amyloid burden in the brain parenchyma of APP/Ps1 mice. This reduction in Abeta pathology was accompanied by a recovery in cognitive function. Since this tacrine-melatonin hybrid apparently reduces brain Abeta and behavioral deficits, we believe this drug has remarkable and significant neuroprotective effects and might be considered a potential therapeutic strategy in AD.

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Aβ accumulation in choroid plexus is associated with mitochondrial-induced apoptosis

Cited by 62 publications

References 75 publications

Mitochondrial respiratory chain dysfunction: Implications in neurodegeneration

Mitochondrial respiratory chain dysfunction: Implications in neurodegeneration

Intranasal PRGF-Endoret enhances neuronal survival and attenuates NF-κB-dependent inflammation process in a mouse model of Parkinson's disease

A New Tacrine–Melatonin Hybrid Reduces Amyloid Burden and Behavioral Deficits in a Mouse Model of Alzheimer’s Disease

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