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Disruption of zinc neuromodulation by Aß oligomers: therapeutic implications

Emily C Vogler, Jorge Busciglio1

  • 1Department of Neurobiology and Behavior, Institute for Memory Impairment and Neurological Disorders, Center for the Neurobiology of Learning and Memory, University of California- Irvine, Irvine, California 92697. jbuscigl@uci.edu.

Current Pharmaceutical Design
|July 18, 2013
PubMed

Insights

Alzheimer's disease treatments targeting amyloid beta have failed. This review explores the role of zinc in neurotransmission and its interaction with amyloid beta oligomers (AβO) as a novel therapeutic target.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Alzheimer's disease (AD) therapeutics targeting amyloid beta have shown limited success.
  • Novel therapeutic targets are needed to halt or slow AD progression.
  • Soluble amyloid beta in oligomeric forms (AβO) interact with zinc.

Purpose of the Study:

  • To review the interaction between AβO and zinc.
  • To explore the role of zinc in neurotransmission and its neurotoxic effects.
  • To discuss potential AD treatments modulating zinc homeostasis and hyperexcitability.

Main Methods:

  • Literature review of existing studies on AβO, zinc, and neurotransmission.
  • Analysis of experimental data from animal models of AD.
  • Exploration of therapeutic strategies targeting zinc modulation.

Main Results:

  • AβO bind with high affinity to zinc released during synaptic activity.
  • Zinc plays a role in neurotransmission and may contribute to neurotoxicity in AD.
  • Animal models suggest modulation of hyperexcitability and zinc homeostasis as potential treatments.

Conclusions:

  • Targeting the AβO-zinc interaction represents a promising therapeutic strategy for AD.
  • Modulating zinc homeostasis and neuronal hyperexcitability may offer new avenues for AD treatment.
  • Further research into zinc's role in AD pathogenesis is warranted.

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