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Nitric Oxide Links Mitochondrial Fission to Alzheimer's Disease

Mitochondrial dysfunction is a hallmark of β-amyloid (Aβ)–induced neuronal injury in the pathogenesis of Alzheimer’s disease. Neurotoxic Aβ peptide, thought to be a key mediator of Alzheimer’s disease, may be imported into human brain mitochondria, where it inhibits key enzymes of respiratory metabolism. Nitric oxide (NO) produced in response to Aβ induces S-nitrosylation of the mitochondrial division protein, dynamin-related protein 1 (Drp-1), which leads to excessive mitochondrial fission, synaptic loss, and neuronal damage. Furthermore, brains of patients with Alzheimer’s disease contain high amounts of S-nitrosylated Drp-1. Aβ-dependent mitochondrial fragmentation likely enhances the decline in bioenergetic capacity of damaged mitochondria and therefore contributes to neuronal injury and pathogenesis of Alzheimer’s disease.

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Classifications


Resource Type: Bibliography, Diagram, Illustration, Journal article/Issue, Review
Audience Level: Undergraduate upper division 15-16, Graduate, Professional (degree program)

Author and Copyright


Authors and Editors: Benedikt Westermann of Institut fur Zellbiologie and Bayreuther Zentrum fur Molekulare Biowissenschaften, Universitat Bayreuth
Publisher: American Association for the Advancement of Science
Format: application/pdf, image/gif, image/jpeg, text/html
Copyright and other restrictions: Yes
Cost: Yes

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Collection:
STKE/Science Signaling


     
   

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