Related Experiment Video

Updated: Nov 20, 2025

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
14:57

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

94.7K

Microglial Store-operated Calcium Signaling in Health and in Alzheimer's Disease

James G McLarnon1

  • 1Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, Vancouver BC, V6T1Z3, Canada.

Current Alzheimer Research
|January 19, 2021
PubMed

Insights

Store-operated calcium entry (SOCE) is impaired in microglia from Alzheimer's Disease (AD) brains. This calcium dysregulation in immune cells may contribute to AD pathogenesis and neuroinflammation.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Neuronal calcium signaling dysregulation is implicated in early-onset Alzheimer's Disease (AD).
  • The role of calcium mobilization in microglia, the brain's resident immune cells, remains less understood in AD pathogenesis.
  • Store-operated calcium entry (SOCE) is a key calcium pathway in non-excitable cells like microglia.

Purpose of the Study:

  • To review findings on the alterations of SOCE in microglia from Alzheimer's Disease (AD) brains.
  • To investigate the impact of amyloid-beta (Aβ) on microglial calcium signaling.
  • To explore the potential consequences of altered microglial SOCE on AD pathology.

Main Methods:

  • Review of studies examining calcium (Ca2+) mobilization in human microglia (adult, fetal, cell-line) using platelet-activating factor (PAF) and adenosine triphosphate (ATP) stimulation.
  • Analysis of SOCE properties in microglia from AD brain tissue and in microglia treated with amyloid-beta (Aβ42) peptide.
  • Comparison of Ca2+ release from endoplasmic reticulum (ER) stores in healthy versus AD-affected or Aβ42-treated microglia.

Main Results:

  • Platelet-activating factor (PAF) induces robust SOCE in healthy human microglia by depleting endoplasmic reticulum (ER) Ca2+ stores.
  • Adenosine triphosphate (ATP) stimulation results in attenuated SOCE duration in human microglia, potentially due to purinergic receptor subtypes.
  • Microglia from AD brains and Aβ42-treated microglia exhibit significantly reduced SOCE amplitude and decreased ER Ca2+ release compared to controls.

Conclusions:

  • Alterations in microglial SOCE are observed in Alzheimer's Disease (AD).
  • Reduced SOCE and impaired Ca2+ release in microglia may contribute to neuroinflammation and neurovascular dysfunction in the AD brain.
  • Dysfunctional microglial calcium signaling represents a potential therapeutic target for AD.
Keywords:
Alzheimer's disease (AD)Human microgliaamyloid- beta (Aβ)platelet-activating factor (PAF)prolonged SOCEstore-operated calcium entry (SOCE)

More Related Videos

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis09:36

Primary Cultures of Rat Astrocytes and Microglia and Their Use in the Study of Amyotrophic Lateral Sclerosis

Published on: June 23, 2022

3.7K
Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models10:46

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models

Published on: May 3, 2017

11.5K

Related Concept Videos

Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
5.6K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
3.4K
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
2.8K
Long-term Depression01:05

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
32.4K
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
1.1K