Presenilin-2 modulation of ER-mitochondria interactions: FAD mutations, mechanisms and pathological consequences.

@article{Zampese2011Presenilin2MO,
  title={Presenilin-2 modulation of ER-mitochondria interactions: FAD mutations, mechanisms and pathological consequences.},
  author={Enrico Zampese and Cristina Fasolato and Tullio Pozzan and Paola Pizzo},
  journal={Communicative & integrative biology},
  year={2011},
  volume={4 3},
  pages={357-60}
}
Presenilin (PS) mutations are the main cause of Familial Alzheimer's Disease (FAD) and have been demonstrated to cause an imbalance of intracellular Ca(2+) homeostasis. Though PS1 and 2 are generally considered to behave similarly in terms of their effects on Ca(2+) handling, we have recently described a novel function, which is unique to PS2, i.e., the modulation of ER-mitochondria juxtaposition. Accordingly, PS2, but not PS1, affects the Ca(2+) cross-talk between these organelles, a key… CONTINUE READING
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