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The effect of insulin on calcium regulation in hippocampal neurons: Potential treatment of cognitive disorders

1. Abstract/review Some cognitive disorders like the Alzheimer disease are associated with aging and the changes in bodily conditions and processes. Research suggests that an observed increase of intracellular calcium concentration and calcium-dependent afterhyperpolarization (AHP) in hippocampal neurons may be connected with some cognitive deficiencies. Further, research has also associated alterations in the functioning of insulin receptors with cognitive disorders because untreated insulin-resistant patients have a high-risk of developing various cognitive disorders. However, the mechanisms that underlie the influence of insulin management on the prevention of memory loss still remain unknown. To address the observed gap in knowledge, the authors of this study examined the effects of insulin on hippocampal neurons’ voltage-gated calcium channels (VGCC) and ryanodine (Rya) receptors. Researchers used fluorescent imaging to monitor spontaneous and depolarization-mediated transients of calcium and whole-cell patch-clamp technique to investigate neuronal calcium currents. Results suggest zinc-free insulin in the concentrations administered during inhalation therapy induces the reduction of calcium transients. Insulin was also found to influence the activity of VGCC and Rya receptors by reducing afterhyperpolarization and cellular concentration of calcium for approx. 20-30%. These results correlate with previous scientific findings which report a connection between cognition loss and varying levels of calcium within neural cells. Keywords: insulin, memory impairment, memory loss, nerve impulse, Voltage-gated calcium channels, Ryanodine receptors 2. Background/introduction Alzheimer disease (AD) is a cognitive disorder that primarily affects people over the age of 65. According to reports, the disease has an estimated incidence of 1-3% and prevalence of 10-30% (Masters 2015). AD is primarily associated with extracellular accumulation of amyloid¬β (Aβ) protein in the cerebral cortex and hippocampus (Masters 2015), but also with some metabolic disorders like diabetes mellitus (Leibson 1997, De Felice 2013, Neth 2017).


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