title: Disruption of zinc neuromodulation by Aß oligomers: therapeutic implications.
abstract: So far, therapeutics focusing on reducing levels of amyloid beta for treatment of Alzheimer's disease have not been successful in completing clinical trials to come to market, suggesting the need of a wider perspective and the consideration of novel targets of intervention to slow or halt the progression of this disease. One such target is soluble amyloid beta in oligomeric forms, which have been demonstrated to bind with high affinity to zinc released during synaptic activity. This review considers the interaction of AβO and zinc and the role of zinc in neurotransmission along with possible neurotoxic effects of this interaction. Finally, it also discusses recent experimental data in animal models that have translated into potential treatments for AD based on the modulation of hyperexcitability and zinc homeostasis.
authors.forename: Emily C
authors.initials: EC
authors.lastname: Vogler
authors.affiliation: Department 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.
authors.forename: Jorge
authors.initials: J
authors.lastname: Busciglio
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000209:etiology; D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D006624:Hippocampus / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D055503:Protein Multimerization; D013569:Synapses / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*; D015032:Zinc / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D016229:Amyloid beta-Peptides; D015032:Zinc