Ca2+ Influx through Store-operated Ca2+ Channels Reduces Alzheimer Disease β-Amyloid Peptide Secretion

Ca2+ dysregulation in the endoplasmic reticulum related to Alzheimer’s disease: A review on experimental progress and computational modeling

“…For example, an increased level of cytosolic Ca 2+ followed treatment with high levels of thapsigargin, an inhibitor of SERCA, leading to decreased Ab formation (Buxbaum et al, 1994). This is consistent with results from a recent study, which suggests increase Ca 2+ influx via SOCE significantly by overexpression of STIM1 can actually inhibit Ab secretion (Zeiger et al, 2013). These contradicting observations may result from different experimental conditions, such as cell lines chosen, or different detection methods (Kurumatani et al, 1998).…”

TRPV1 activation alleviates cognitive and synaptic plasticity impairments through inhibiting AMPAR endocytosis in APP23/PS45 mouse model of Alzheimer’s disease

“…For instance, the levels of calcium activity are increased in AD patients (Johnson et al, ) and elevated Ca 2+ induce BACE1 expression and consequently result in an increase in Aβ production (Cho, Jin, Youn, Huh, & Mook‐Jung, ; Mata, ) and cell death (Pierrot, Ghisdal, Caumont, & Octave, ). However, contradictory results have shown that familial AD‐linked PS1 or PS2 mutation attenuates calcium entry and thus increasing Aβ production (Fedeli, Filadi, Rossi, Mammucari, & Pizzo, ; Yoo et al, ), whereas constitutive activation of Ca 2+ entry reduces Aβ secretion (Zeiger et al, ). Thus, genetic or pharmacological activation of TRPV1 may increase Ca 2+ influx, reduce APP processing, and consequently improve synaptic plasticity and memory in APP23/PS45 model mice of AD.…”

Synaptic plasticity at the interface of health and disease: New insights on the role of endoplasmic reticulum intracellular calcium stores

“…This study further links Ca 2+ stores to AD, and proposes novel strategies for the treatment of the disease. Moreover, it has been suggested that Ca 2+ influx through SOCE reduces the formation of the amyloid beta peptide (Zeiger et al, 2013). Whether activation of SOCE is beneficial or detrimental to synaptic plasticity and cell function in AD, however, remains to be clarified.…”