Literature DB >> 17508283

Iron: the Redox-active center of oxidative stress in Alzheimer disease.

Rudy J Castellani1, Paula I Moreira, Gang Liu, Jon Dobson, George Perry, Mark A Smith, Xiongwei Zhu.   

Abstract

Although iron is essential in maintaining the function of the central nervous system, it is a potent source of reactive oxygen species. Excessive iron accumulation occurs in many neurodegenerative diseases including Alzheimer disease (AD), Parkinson's disease, and Creutzfeldt-Jakob disease, raising the possibility that oxidative stress is intimately involved in the neurodegenerative process. AD in particular is associated with accumulation of numerous markers of oxidative stress; moreover, oxidative stress has been shown to precede hallmark neuropathological lesions early in the disease process, and such lesions, once present, further accumulate iron, among other markers of oxidative stress. In this review, we discuss the role of iron in the progression of AD.

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Year:  2007        PMID: 17508283     DOI: 10.1007/s11064-007-9360-7

Source DB:  PubMed          Journal:  Neurochem Res        ISSN: 0364-3190            Impact factor:   3.996


  78 in total

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5.  Increased peroxidation and reduced antioxidant enzyme activity in Alzheimer's disease.

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Review 6.  Recent advances in disorders of iron metabolism: mutations, mechanisms and modifiers.

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7.  Structural characteristics of human substantia nigra neuromelanin and synthetic dopamine melanins.

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9.  Ischemic stress induces deposition of amyloid beta immunoreactivity in human brain.

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  54 in total

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Review 4.  Iron-chelating backbone coupled with monoamine oxidase inhibitory moiety as novel pluripotential therapeutic agents for Alzheimer's disease: a tribute to Moussa Youdim.

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5.  Serum ferritin is a candidate biomarker of disease aggravation in amyotrophic lateral sclerosis.

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6.  Iron enhances the neurotoxicity of amyloid β.

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7.  Brain Anatomy in Latino Farmworkers Exposed to Pesticides and Nicotine.

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8.  Acetylcholinesterase-independent protective effects of huperzine A against iron overload-induced oxidative damage and aberrant iron metabolism signaling in rat cortical neurons.

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Review 9.  What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer's disease, about the therapeutic strategies in Alzheimer's research.

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10.  Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases.

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