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Green tea epigallocatechin-3-gallate (EGCG) and other flavonoids reduce Alzheimer's amyloid-induced mitochondrial dysfunction.
TLDR
The results of this study lend further credence to the notion that EGCG and other flavonoids, such as luteolin, are 'multipotent therapeutic agents' that not only reduce toxic levels of brain Aβ, but also hold the potential to protect neuronal mitochondrial function in AD.
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Melatonin treatment restores mitochondrial function in Alzheimer’s mice: a mitochondrial protective role of melatonin membrane receptor signaling
TLDR
Mitochondrial dysfunction is a hallmark of Alzheimer’s disease (AD) and is observed in mutant amyloid precursor protein (APP) transgenic mouse models of familial AD, and treatments that stimulate melatonin receptor signaling may be beneficial for restoring mitochondrial function in AD.
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Mechanisms of amino acid-mediated lifespan extension in Caenorhabditis elegans
TLDR
Lifespan extension appears to be caused by altered mitochondrial TCA cycle metabolism and respiratory substrate utilization resulting in the activation of the DAF-16/FOXO and SKN-1/Nrf2 stress response pathways.
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Metabolome and proteome changes with aging in Caenorhabditis elegans
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Caffeine increases mitochondrial function and blocks melatonin signaling to mitochondria in Alzheimer's mice and cells
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D-beta-hydroxybutyrate extends lifespan in C. elegans
TLDR
D-βHB extends lifespan through inhibiting HDACs and through the activation of conserved stress response pathways, which delayed Alzheimer's amyloid-beta toxicity and decreased Parkinson's alpha-synuclein aggregation.
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Malate and Fumarate Extend Lifespan in Caenorhabditis elegans
TLDR
Fumarate reduction, glyoxylate shunt activity, and mild mitochondrial uncoupling likely contribute to the lifespan extension induced by malate and fumarate by increasing the amount of oxidized NAD and FAD cofactors.
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D-beta-Hydroxybutyrate Extends Lifespan in
D-ß-hydroxybutyrate: an anti-aging ketone body
TLDR
This was the first report to identify sHB as a positive modulator of lifespan in wild-type animals and proposes two overlapping pathways for lifespan extension mediated by sHB supplementation as shown in Figure ​Figure1.1.
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The Deanna protocol supplement complex supports mitochondrial energy metabolism and prolongs lifespan in preclinical models of amyotrophic lateral sclerosis (ALS)
TLDR
Targeting energy metabolism with the DP supplement as a metabolic therapy produces a change in the global metabolic profile of ALS mice that support the role of the DP for enhanced mitochondrial energy metabolism and prolongs time to paralysis of ALS C. elegans TDP-43 disease models.
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