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Topology of the Mitochondrial Inner Membrane: Dynamics and Bioenergetic Implications
Computer modeling studies using the “Virtual Cell” program suggest that the shape of the inner membrane can influence mitochondrial function, and simulations indicate that narrow cristae junctions restrict diffusion between intracristal and external compartments, causing depletion of ADP and decreased ATP output inside the crists.
Mitochondrial amyloid-beta levels are associated with the extent of mitochondrial dysfunction in different brain regions and the degree of cognitive impairment in Alzheimer's transgenic mice.
- N. Dragičević, M. Mamcarz, P. Bradshaw
- Biology, PsychologyJournal of Alzheimer's disease : JAD
- 3 June 2010
The association between mitochondrial Abeta levels and mitochondrial dysfunction in mouse models of AD supports a primary role for mitochondria from AbetaPP/PS1 brain regions in AD pathology, and the degree of cognitive impairment in AD transgenic mice can be linked to the extent of synaptic mitochondrial dysfunction and mitochondrialAbeta levels, suggesting that a mitochondrial Abeta-induced signaling cascade may contribute to cognitive impairment.
Properties of a Cyclosporin-insensitive Permeability Transition Pore in Yeast Mitochondria*
Yeast mitochondria (Saccharomyces cerevisiae) contain a permeability transition pore which is regulated differently than the pore in mammalian mitochondria, and this suggests that the same pore is induced in both cases and is comparable in size with the permeability Transition pore of heart and liver mitochondria.
The Role of Mitochondrial DNA Mutations in Mammalian Aging
Evidence supporting a causative role for mtDNA mutations in mammalian aging is examined and potential mechanisms for the generation of these mutations and the means by which they may mediate their pathological consequences are discussed.
Green tea epigallocatechin-3-gallate (EGCG) and other flavonoids reduce Alzheimer's amyloid-induced mitochondrial dysfunction.
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.
Ketone bodies mimic the life span extending properties of caloric restriction
It is proposed that the life span extension produced by caloric restriction can be duplicated by the metabolic changes induced by ketosis and that calorie restriction extends life span at least in part through increasing the levels of ketone bodies.
Melatonin treatment restores mitochondrial function in Alzheimer’s mice: a mitochondrial protective role of melatonin membrane receptor signaling
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.
Mechanisms of amino acid-mediated lifespan extension in Caenorhabditis elegans
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.
Metabolome and proteome changes with aging in Caenorhabditis elegans