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nature portfolio privacy policy r_{{\mathrm{min}}}}}{{r_{{\mathrm{max}}} thermo scientific pierce /pharmacology/bers/maxchelator/caegta-nist advertising open data sharing wtcm/tgcm/aβ-depleted tgcm/tgcm+ru360/ru360 chicken anti-gfp igy time-lapse images showing calcium-induced permeability transition sapphire mode-locked laser reprints ad libitum access age-matched wt-littermate controls nupage bis-tris gels rabbit anti-glutamine synthetase pan-neuronal marker map2 app/ps1 tg mouse app/ps1 tg mice steroidal anti-inflammatory drugs article calvo-rodriguez anti-β-amyloid antibody source data file aβ-induced mitochondrial fragmentation nature 476 nature 467 nature 427 nature 443 nature research design open question mouse anti-vdac1/porin purified anti-β-amyloid disease maria calvo-rodriguez mouse anti-β-tubulin disease research custom-written matlab scripts upenn vector core fokker-planck diffusion maps mitochondrial ca2+-related genes ca2+-related mitochondrial genes supplementary information files monica garcia-alloza aging-related neurodegenerative disorders9 yfp/cfp ratio greater increased resting [ca2+]mit higher yfp/cfp ratios averaged yfp/cfp ratios yfp/cfp ratio significantly

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         headline:Increased mitochondrial calcium levels associated with neuronal death in a mouse model of Alzheimer’s disease
         description:Mitochondria contribute to shape intraneuronal Ca2+ signals. Excessive Ca2+ taken up by mitochondria could lead to cell death. Amyloid beta (Aβ) causes cytosolic Ca2+ overload, but the effects of Aβ on mitochondrial Ca2+ levels in Alzheimer’s disease (AD) remain unclear. Using a ratiometric Ca2+ indicator targeted to neuronal mitochondria and intravital multiphoton microscopy, we find increased mitochondrial Ca2+ levels associated with plaque deposition and neuronal death in a transgenic mouse model of cerebral β-amyloidosis. Naturally secreted soluble Aβ applied onto the healthy brain increases Ca2+ concentration in mitochondria, which is prevented by blockage of the mitochondrial calcium uniporter. RNA-sequencing from post-mortem AD human brains shows downregulation in the expression of mitochondrial influx Ca2+ transporter genes, but upregulation in the genes related to mitochondrial Ca2+ efflux pathways, suggesting a counteracting effect to avoid Ca2+ overload. We propose lowering neuronal mitochondrial Ca2+ by inhibiting the mitochondrial Ca2+ uniporter as a novel potential therapeutic target against AD. Calvo-Rodriguez et al. show elevated calcium levels in neuronal mitochondria in a mouse model of cerebral β-amyloidosis after plaque deposition, which precede rare neuron death events in this model. The mechanism involves toxic extracellular Aβ oligomers and the mitochondrial calcium uniporter.
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      headline:Increased mitochondrial calcium levels associated with neuronal death in a mouse model of Alzheimer’s disease
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