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Calcium channelopathies and Alzheimer's disease: insight into therapeutic success and failures

Shreaya Chakroborty1, Grace E Stutzmann1

  • 1Department of Neuroscience, Rosalind Franklin University of Medicine and Science, The Chicago Medical School, 3333 Green Bay Road, North Chicago, IL 60064, USA.

European Journal of Pharmacology
|December 10, 2013
PubMed

Insights

Calcium signaling disruptions, termed calciumopathies, are implicated in Alzheimer's disease (AD) pathogenesis. Targeting early calcium channel issues offers a promising therapeutic strategy for preserving memory and synaptic function in AD.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Calcium ions (Ca2+) are crucial intracellular signals regulating diverse cellular functions.
  • Precise calcium signaling is vital for cellular health; dysregulation can lead to cell death.
  • Impaired calcium channel function causes "calciumopathies," multi-system disorders affecting various cell types.

Purpose of the Study:

  • To review the role of calcium signaling in Alzheimer's disease (AD) pathophysiology.
  • To summarize current therapeutic strategies for AD.
  • To highlight the potential of targeting calcium channelopathies as an alternative therapeutic approach for AD.

Main Methods:

  • Literature review focusing on calcium signaling in AD.
  • Analysis of existing therapeutic options and clinical trial outcomes for AD.
  • Discussion of calcium channelopathies in the context of AD pathogenesis.

Main Results:

  • Calcium signaling plays a multifaceted role in the pathophysiology of Alzheimer's disease.
  • Current AD therapies have shown disappointing results in clinical trials for cognitive outcomes.
  • Early calcium channelopathies are centrally linked to AD pathogenesis.

Conclusions:

  • Disruptions in calcium signaling are a significant factor in AD.
  • There is an urgent need for novel therapeutic strategies beyond current approaches.
  • Targeting early calcium channelopathies presents a promising avenue for preserving synaptic and memory functions in AD.
Keywords:
Alzheimer's diseaseAmyloidBrainCalciumClinical trialsERIP3RNeurodegenerationNeuronRyanodine receptorSynaptic plasticity

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