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Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading TED
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Endoplasmic Reticulum-Based Calcium Dysfunctions in Synucleinopathies.

Gergo Kovacs1,2, Lasse Reimer1,2, Poul Henning Jensen1,2

  • 1Danish Research Institute of Translational Neuroscience - DANDRITE, Aarhus University, Aarhus, Denmark.

Frontiers in Neurology
|November 8, 2021
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Summary

Parkinson's disease (PD) may involve altered calcium handling, where alpha-synuclein aggregates decrease cytosolic calcium by stimulating ER calcium pumps. This research explores new therapeutic targets for PD by examining calcium regulation in neurons and astrocytes.

Keywords:
IP3RParkinson's diseaseRyRSERCAcalciumendoplasmic reticulumα-synuclein

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Neuronal calcium dyshomeostasis is linked to Parkinson's disease (PD), with current research exploring increased cytosolic calcium influx.
  • Previous work suggests an alternative hypothesis: alpha-synuclein aggregates stimulate endoplasmic reticulum (ER) calcium pumps (SERCA), decreasing cytosolic calcium and potentially contributing to PD.
  • This altered calcium state affects signaling pathways and ER calcium concentration, modeling cellular states relevant to PD development.

Purpose of the Study:

  • To discuss a hypothesis where alpha-synuclein aggregates decrease neuronal cytosolic calcium by enhancing ER calcium pumping.
  • To integrate recent findings on Inositol-1,4,5-triphosphate (IP3) kinase B (ITPKB) and its role in ER-mitochondria calcium transfer in PD.
  • To examine alpha-synuclein's impact on ER calcium channels (SERCA, RyR, IP3R) and mitochondrial function in PD patient-derived astrocytes.

Main Methods:

  • Review and discussion of existing literature and mechanistic studies.
  • Analysis of cell models demonstrating alpha-synuclein aggregate effects on SERCA activity and calcium levels.
  • Consideration of studies on patient-derived astrocytes, including genetic mutations (LRRK2-2019S) and their impact on calcium signaling and mitochondrial respiration.

Main Results:

  • Alpha-synuclein aggregates stimulate SERCA, leading to decreased cytosolic calcium and increased ER calcium.
  • Inhibition of SERCA protects neurons and PD models, suggesting SERCA as a therapeutic target.
  • Genetic variations in ITPKB influence ER-mitochondria calcium transfer, potentially explaining its protective role in PD.
  • PD patient-derived astrocytes exhibit altered alpha-synuclein expression, increased ER calcium release, and impaired mitochondrial function.

Conclusions:

  • The study supports a model where alpha-synuclein-induced alterations in ER calcium handling, affecting SERCA, RyR, IP3R, and mitochondrial calcium uniporter (MCU) complex, contribute to PD pathogenesis.
  • Both prolonged cytosolic calcium depletion and ER calcium overload represent potential pathological states in PD.
  • Further investigation into calcium signaling pathways, including store-operated calcium entry (SOCE), is warranted to understand their role in PD development.