Calcium handling: a strategy to fight neurodegeneration in Alzheimer’s disease

Calcium homeostasis mechanisms: The cytosolic calcium concentration depends on calcium influx from the extracellular space and efflux from intracellular stores, two finely regulated mechanisms. The extracellular calcium influx is mediated by different types of calcium channels as the voltage-gated calcium channels, N-methylD-aspartic acid, and α-amino-3-hydroxy-5-methyl4-isoxazole propionic acid receptors. Calcium is also released into the cytosol from endoplasmic reticulum (ER) stores through the ryanodine receptors and the inositol 1,4,5-triphosphate receptors, and from the mitochondria via the sodium/calcium exchanger. This cytosolic calcium increase is counteracted by the sarcoendoplasmic reticulum calcium transport ATPase pump and the mitochondrial calcium uniporter. Neurons display also intrinsic calcium buffering ways to control calcium levels, thanks to the expression of calciumbinding proteins (i.e., calbindin and calretinin), calcium sensors (such as calmodulin), and a tied interplay between the ER and mitochondria. The functional consequence of this intricate machinery is the tight control of physiological calcium oscillations, crucial for the activity of DA neurons in VTA.

• Publication year

  2023

• Venue

  Neural Regeneration Research

• Publication date

  2023-04-20

• Fields of study

  Medicine

• Identifiers
  DOI 10.4103/1673-5374.374004PMID 37449622PMCID 10358684
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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