Back to article: High mitochondrial calcium levels precede neuronal death in vivo in Alzheimer’s disease

FIGURE 2: Major effects of Aβ aggregates on mitochondrial Ca2+ homeostasis in neurons. In physiological conditions, mitochondria take up Ca2+ from the cytosol via the MCU to produce ATP among other functions. In AD, Aβ aggregates (particularly soluble Aβ) increase mitochondrial Ca2+ via the MCU in vivo. This leads to mitochondrial Ca2+ overload and activates mPTP and caspases, which can trigger neuronal cell death via apoptosis. Blocking the MCU with Ru360 inhibits mitochondrial Ca2+ uptake, pointing to the MCU as a potential target for therapeutics aimed at preventing or reversing the progression of AD.

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