Alteration of calcium signaling as one of the mechanisms of Alzheimer's disease and diabetic polyneuropathy

2010 ◽  
Vol 56 (4) ◽  
pp. 130-138 ◽  
Author(s):  
OP Kostiuk ◽  
◽  
TIu Korol' ◽  
SV Korol' ◽  
SV Romanenko ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Calcium Signaling ◽  
Diabetic Polyneuropathy

scholarly journals Capacitative Calcium Entry Deficits and Elevated Luminal Calcium Content in Mutant Presenilin-1 Knockin Mice

2000 ◽  
Vol 149 (4) ◽  
pp. 793-798 ◽  
Author(s):  
Malcolm A. Leissring ◽  
Yama Akbari ◽  
Christopher M. Fanger ◽  
Michael D. Cahalan ◽  
Mark P. Mattson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Calcium Signaling ◽  
Intracellular Calcium ◽  
Brain Aging ◽  
Calcium Entry ◽  
Calcium Stores ◽  
Capacitative Calcium Entry ◽  
Intracellular Calcium Stores ◽  
Agonist Stimulation

Dysregulation of calcium signaling has been causally implicated in brain aging and Alzheimer's disease. Mutations in the presenilin genes (PS1, PS2), the leading cause of autosomal dominant familial Alzheimer's disease (FAD), cause highly specific alterations in intracellular calcium signaling pathways that may contribute to the neurodegenerative and pathological lesions of the disease. To elucidate the cellular mechanisms underlying these disturbances, we studied calcium signaling in fibroblasts isolated from mutant PS1 knockin mice. Mutant PS1 knockin cells exhibited a marked potentiation in the amplitude of calcium transients evoked by agonist stimulation. These cells also showed significant impairments in capacitative calcium entry (CCE, also known as store-operated calcium entry), an important cellular signaling pathway wherein depletion of intracellular calcium stores triggers influx of extracellular calcium into the cytosol. Notably, deficits in CCE were evident after agonist stimulation, but not if intracellular calcium stores were completely depleted with thapsigargin. Treatment with ionomycin and thapsigargin revealed that calcium levels within the ER were significantly increased in mutant PS1 knockin cells. Collectively, our findings suggest that the overfilling of calcium stores represents the fundamental cellular defect underlying the alterations in calcium signaling conferred by presenilin mutations.

Altered Calcium Signaling and Neuronal Injury: Stroke and Alzheimer's Disease as Examples

1993 ◽  
Vol 679 (1 Markers of Ne) ◽  
pp. 1-21 ◽  
Author(s):  
M. P. MATTSON ◽  
R. E. RYDEL ◽  
I. LIEBERBURG ◽  
V. L. SMITH-SWINTOSKY
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Calcium Signaling ◽  
Neuronal Injury

scholarly journals Calcium signaling in Alzheimer's disease & therapies

2018 ◽  
Vol 1865 (11) ◽  
pp. 1745-1760 ◽  
Author(s):  
Benjamin Chun-Kit Tong ◽  
Aston Jiaxi Wu ◽  
Min Li ◽  
King-Ho Cheung
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Calcium Signaling
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