The pathological hallmarks of Alzheimer 's disease (AD) include selective neuronal loss, numerous extra-cellular deposits termed senile plaques, and neuro-fibril tangles in the patients brain. The major component of senile plaques is a 39- to 43-amino acid peptide termed β-amyloid protein (AβP). A growing number of reports suggest that elevated levels of extra cellular Alzheimer's β-amyloid alters the homeostasis of intracellular free calcium. In line with previous results, we have previously shown that Hypothalamic neurons exposed to AβP [ 1-40] leads to the spontaneous formation of cation selective channels across the plasma membrane. The unregulated Ca²⁺ and Na+ entry leads in to neuronal apoptosis. In this study, we loaded human astrocytes (cell line 132 1 N 1) with a free Calcium reporter dye and proceeded to expose the 132 1 N 1 cells to AβP [1-40], after pre-incubation in the absence of D-glucose or in its physiological level (5. 5 mM). We found and report here that, a 15 min exposure of the astrocytes to a medium devoid of D-glucose causes a fast entry of Ca²⁺. By constrast, application of the same dos e of AβP [1-40] to the 132 1 N 1 cells which were exposed to physiological levels of D-glucose (5.5 mM), Ca²⁺ and Na+ entry was substantially reduced. Since, hypoglycemia impairs ATP synthesis, the ATP level will drop and, therefore, all plasma membrane ATP-ases, such as cation pumps, would be unable to n1aintain Na•, Ca²⁺ and K+ homeostasis.
Brito, J. ., Alarcón, J. M. ., Sciaraffia, C. ., & Rojas, E. . (2001). En astrocitos humanos, el estrés hipoglicémico facilita la inserción de amiloide beta (AbP [1-40]) que forma un canal de calcio no regulado. Revista Hospital Clínico Universidad De Chile, 12(3), pp. 172–8. https://doi.org/10.5354/2735-7996.2001.79759
