Nanoparticle iron chelators: A new therapeutic approach in Alzheimer disease and other neurologic disorders associated with trace metal imbalance

Liu, Gang; Men, Ping; Harris, Peggy L.R.; Rolston, Raj K.; Perry, George; Smith, Mark A.

doi:10.1016/j.neulet.2006.07.020

Cited by 170 publications

(84 citation statements)

References 23 publications

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“…However, in general, abnormal body iron stores (low or high) appear unlikely to have clinically significant effects on cognition or dementia risk in community-dwelling older people. These findings should be taken into account in any consideration of whether to limit treatments for iron deficiency anemia or use venesection or chelation to protect against cognitive effects in older people [3][4][5][6]. .…”

Section: Discussionmentioning

confidence: 99%

“…There has been considerable speculation that both iron deficiency and excess affect cognitive or motor performance and contribute to neurodegenerative disease, leading to proposals that chelation or other approaches may be of therapeutic relevance in this context [3][4][5][6]. This is supported by a limited amount of intriguing, but largely circumstantial, evidence derived from animal models and small patient groups [1,[7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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A Cross-Sectional Community Study of Serum Iron Measures and Cognitive Status in Older Adults

Milward

Bruce

Knuiman

et al. 2010

JAD

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Abstract.The relationship of iron status with cognition and dementia risk in older people is contentious. We have examined the longitudinal relationship between serum ferritin and cognition in 800 community-dwelling Australians 60 years or older. In participants without dementia (n = 749), neither serum ferritin in 1994/5 or 2003/4 nor change in serum ferritin between these times was related to total CAMCOG or executive function scores, with or without adjustment for gender, age, National Adult reading test, or stroke history (all p > 0.05). No relationships were observed between ferritin and cognition for participants with possible or probable dementia (n = 51). All participants identified as HFE C282Y homozygous or with serum ferritin > 1,000 ng/ml had normal CAMCOG scores. We conclude abnormal body iron stores (low or high) are unlikely to have clinically significant effects on cognition or dementia risk in community-dwelling older people.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A Cross-Sectional Community Study of Serum Iron Measures and Cognitive Status in Older Adults

Milward

Bruce

Knuiman

et al. 2010

JAD

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“…180 The M-30, a compound synthesized from VK-28, but with an additional monoamine oxidase moiety, has been found to attenuate the dopamine-depleting action of MPTP in mice; it has also been found to increase striatal levels of dopamine, serotonin and norepinephrine, while decreasing their metabolites. 181 Interestingly, Liu et al 182 have synthesized a chelator attached to a nanoparticle that complexes with iron. They demonstrate that this addition is likely to promote BBB absorption.…”

Section: Iron-related Neurotherapeuticsmentioning

confidence: 99%

“…They demonstrate that this addition is likely to promote BBB absorption. 182 Thus, clearly the neurotherapeutic pipeline for iron-related neurotherapies is actively growing in depth and breadth.…”

Section: Iron-related Neurotherapeuticsmentioning

confidence: 99%

Iron in Chronic Brain Disorders: Imaging and Neurotherapeutic Implications

et al. 2007

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Summary:Iron is important for brain oxygen transport, electron transfer, neurotransmitter synthesis, and myelin production. Though iron deposition has been observed in the brain with normal aging, increased iron has also been shown in many chronic neurological disorders including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. In vitro studies have demonstrated that excessive iron can lead to free radical production, which can promote neurotoxicity. However, the link between observed iron deposition and pathological processes underlying various diseases of the brain is not well understood. It is not known whether excessive in vivo iron directly contributes to tissue damage or is solely an epiphenomenon. In this article, we focus on the imaging of brain iron and the underlying physiology and metabolism relating to iron deposition. We conclude with a discussion of the potential implications of iron-related toxicity to neurotherapeutic development.

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“…This property plays a central role in the development of iron oxide nanoparticles for contrast enhancement, targeted delivery of drugs or genes, tissue engineering, cancer thermal therapy, magnetic transfection, chelation therapy, and tissue engineering. [1][2][3][4][5][6][7] Given the widespread potential applications of iron oxide nanoparticles and their impending commercialization, exposure of humans and animals to iron oxide nanoparticles is likely to increase significantly in the near future. Therefore, evaluation of the health impact of iron oxide nanoparticles is important.…”

Section: Introductionmentioning

confidence: 99%

Iron oxide nanoparticles suppressed T helper 1 cell-mediated immunity in a murine model of delayed-type hypersensitivity

Shen¹,

Liang²,

Liao³

et al. 2012

IJN

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Background: It was recently reported that iron oxide nanoparticles attenuated antigen-specific humoral responses and T cell cytokine expression in ovalbumin-sensitized mice. It is presently unclear whether iron oxide nanoparticles influence T helper 1 cell-mediated immunity. The present study aimed to investigate the effect of iron oxide nanoparticles on delayed-type hypersensitivity (DTH), whose pathophysiology requires the participation of T helper 1 cells and macrophages. Methods: DTH was elicited by a subcutaneous challenge with ovalbumin to the footpads of mice sensitized with ovalbumin. Iron oxide nanoparticles (0.2-10 mg iron/kg) were administered intravenously 1 hour prior to ovalbumin sensitization. Local inflammatory responses were examined by footpad swelling and histological analysis. The expression of cytokines by splenocytes was measured by enzyme-linked immunosorbent assay. Results: Administration of iron oxide nanoparticles, in a dose-dependent fashion, significantly attenuated inflammatory reactions associated with DTH, including the footpad swelling, the infiltration of T cells and macrophages, and the expression of interferon-γ, interleukin-6, and tumor necrosis factor-α in the inflammatory site. Iron oxide nanoparticles also demonstrated a suppressive effect on ovalbumin-stimulated production of interferon-γ by splenocytes and the phagocytic activity of splenic CD11b + cells. Conclusion:These results demonstrated that a single dose of iron oxide nanoparticles attenuated DTH reactions by suppressing the infiltration and functional activity of T helper 1 cells and macrophages in response to antigen stimulation.

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Nanoparticle iron chelators: A new therapeutic approach in Alzheimer disease and other neurologic disorders associated with trace metal imbalance

Cited by 170 publications

References 23 publications

A Cross-Sectional Community Study of Serum Iron Measures and Cognitive Status in Older Adults

A Cross-Sectional Community Study of Serum Iron Measures and Cognitive Status in Older Adults

Iron in Chronic Brain Disorders: Imaging and Neurotherapeutic Implications

Iron oxide nanoparticles suppressed T helper 1 cell-mediated immunity in a murine model of delayed-type hypersensitivity

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