Calcium dyshomeostasis and intracellular signalling in alzheimer's disease

By F. LaFerla. Nature Reviews Neuroscience, 2002

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Physiology and pathophysiology of the calcium store in the endoplasmic reticulum of neurons. (2005, background): “Most importantly however, cellular Ca(2) dishomeostasis occurs at the initial stages of AD (142), and studies on transgenic mice with APP or PS mutations found that impaired Ca(2) handling occurs long before any histopathological changes (195, 323).”
Neurodegenerative diseases and oxidative stress (2004, background): “The excessive generation of ROS leads to dysregulation of intracellular calcium signalling, and such dysregulation has been widely observed in neurodegenerative diseases in which aberrant calcium levels stimulate multiple pathways that ultimately induce an apoptotic cascade (reviewed in Ref”
ER stress and neurodegenerative diseases (2006, background): “The reasons for the altered processing of APP in sporadic AD is not known but increased intracellular levels of calcium together with other insults probably play a role.(39) Fibrillar Ab is toxic to neuronal cells and produces high amounts of ROS with the impairment of the mitochondrial redox activi”
Presenilins form ER Ca2+ leak channels, a function disrupted by familial Alzheimer's disease-linked mutations. (2006, background): “, 1994), in FAD cellular and animal models (LaFerla, 2002; Smith et al., 2005), and in cells from PS1 and PS2 knockout mice (Herms et al.”