Brain Iron and Zinc Contents of German Patients with Alzheimer Disease

Andrási, Erzsébet; Farkas, É.; Gawlik, D.; Rösick, U.; Βrätter, P.

doi:10.3233/jad-2000-2103

Cited by 44 publications

(24 citation statements)

References 27 publications

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“…Several studies have shown an increase in zinc in AD neocortex [7, 13, 61, 62] while others have found no significant increase [11, 63] and two have found a decrease in zinc [8, 64]. Our result demonstrates that zinc is increased in AD only in grey matter.…”

Section: Discussionsupporting

confidence: 56%

Effect of Cerebral Amyloid Angiopathy on Brain Iron, Copper, and Zinc in Alzheimer's Disease

Schrag

Crofton

Zabel

et al. 2011

JAD

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Cerebral amyloid angiopathy (CAA) is a vascular lesion associated with Alzheimer’s disease (AD) present in up to 95% of AD patients and produces MRI-detectable microbleeds in many of these patients. It is possible that CAA-related microbleeding is a source of pathological iron in the AD brain. Because the homeostasis of copper, iron, and zinc are so intimately linked, we determined whether CAA contributes to changes in the brain levels of these metals. We obtained brain tissue from AD patients with severe CAA to compare to AD patients without evidence of vascular amyloid-β. Patients with severe CAA had significantly higher non-heme iron levels. Histologically, iron was deposited in the walls of large CAA-affected vessels. Zinc levels were significantly elevated in grey matter in both the CAA and non-CAA AD tissue, but no vascular staining was noted in CAA cases. Copper levels were decreased in both CAA and non-CAA AD tissues and copper was found to be prominently deposited on the vasculature in CAA. Together, these findings demonstrate that CAA is a significant variable affecting transition metals in AD.

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Section: Discussionsupporting

confidence: 56%

Effect of Cerebral Amyloid Angiopathy on Brain Iron, Copper, and Zinc in Alzheimer's Disease

Schrag

Crofton

Zabel

et al. 2011

JAD

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“…From our data (Table 3) it can be seen that corresponding regions from the two hemispheres of three human brains revealed similar concentrations in general, which is in accordance with other essential element studies [26,27]. Interestingly, in certain cases (e.g.…”

Section: Resultssupporting

confidence: 90%

“…NIST 1571 Orchard leaves b 160±20 [16] 175±6 173±4 [29] 177±8 [30] remained in brain tissue [26]. The present finding indicates the high lipid solubility of iodine and its complexes.…”

Section: Resultsmentioning

confidence: 51%

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Iodine concentration in different human brain parts

Andrási¹,

Bélavári²,

Stibilj³

et al. 2004

Analytical and Bioanalytical Chemistry

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Iodine is one of the most important essential elements as demonstrated by the fact that its deficiency can cause goitre. Nevertheless, quantitative data on its concentration in biological materials, especially in the human brain, are scarce. There is therefore a demand for accurate and reliable information on iodine in these types of samples. The purpose of the present work was to determine the concentration of total iodine in some control human brain parts by rapid radiochemical neutron activation analysis. Our second goal was to determine I distribution between lipid fraction and in brain tissue without lipid by applying two types of solvent extraction methods. The results were checked by the analysis of biological standard reference materials with certified or literature values for iodine and good agreement was found.

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“…Normal processing of APP by α-secretase cleavage in the Golgi complex leads to formation of sAPP, a neurotrophic factor [198]. Additional proteolytic processing of APP by β-secretase (BACE) at the β-cleavage site [5,31,94,171,189] occurs in endosomes [107,115], where acidic pH necessary for β-secretase activity is possible [198]. Further processing by the γ-secretase complex at the plasma membrane (reviewed [172]) leads to formation of Aβ, a 40 or 42 amino acid peptide that is the major component of SP in AD [168].…”

Section: Zinc and Amyloid Beta (Aβ) Peptide Processing And Aggregationmentioning

confidence: 99%

A Potential Role for Alterations of Zinc and Zinc Transport Proteins in the Progression of Alzheimer's Disease

Lovell

2009

JAD

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Although multiple studies have suggested a role for alterations of zinc (Zn) and zinc transport (ZnT) proteins in the pathogenesis of Alzheimer's disease (AD), the exact role of this essential trace element in the progression of AD remains unclear. The following review discusses the normal role of Zn and ZnT proteins in brain and the potential effects of their alteration in the pathogenesis of AD particularly in the processing of the amyloid precursor protein and amyloid beta peptide generation and aggregation. Keywords zinc; zinc transport proteins; mild cognitive impairment; early Alzheimer's disease AD and MCIAlzheimer's disease (AD) is the fourth leading cause of death in the United States and in 2000 affected 4.5 million Americans [87]. Estimates indicate that ~3% of Americans between ages 65 and 74, 19% ages 75 -84, and 47% over age 85 are victims of the disease [67] and that 6 0% of nursing home patients over age 65 suffer from AD. Clinically AD is characterized by a progressive decline in multiple cognitive functions and is thought to begin with amnestic mild cognitive impairment (MCI), widely considered to be a transition between normal aging and dementia. Current data suggest that conversion from MCI to dementia occurs at a rate of 10 to 15% per year [156] with ~80% conversion by the sixth year of followup; although ~5% of MCI subjects remain stable or convert back to normal [13,52]. Progression from MCI leads to early AD (EAD) which is clinically characterized by a) a decline in cognitive function from a previous higher level, b). decline in one or more areas of cognition in addition to memory, c) a clinical dementia rating scale score of 0.5 to 1, d) impaired ADLs, and e) a clinical evaluation that excludes other causes of dementia. The disease eventually progresses to late stage AD (LAD) characterized by severe dementia with disorientation, profound memory impairment, global cognitive deficits and immobility. Without preventive strategies, there may be 14 million Americans with AD by the year 2040 [87].Pathologically AD is characterized by an abundance of neurofibrillary tangles (NFT), senile plaques (SP), neuropil thread formation, and Aβ deposition; neuron and synapse loss; and proliferation of reactive astrocytes, particularly in the hippocampus, amygdala, entorhinal cortex, and neocortex. NFT are composed of intracellular deposits of paired helical filaments Zinc and Zinc Homeostasis in BrainZinc is an essential trace element [159] that is redox inert with structural, catalytic, and regulatory roles [17,80,186] and functions as a crucial component in over 300 enzymes and transcription factors where it serves as an essential cofactor for catalytic activity [70] or by conferring structural stability to Zn finger domains of DNA binding proteins [42] including stimulating protein-1 (sp-1), a transcription factor responsible for ~30% of APP transcription [18,48,49]. In addition to its structural and catalytic roles, recent studies suggest free Zn has important signaling functions including i...

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Brain Iron and Zinc Contents of German Patients with Alzheimer Disease

Cited by 44 publications

References 27 publications

Effect of Cerebral Amyloid Angiopathy on Brain Iron, Copper, and Zinc in Alzheimer's Disease

Effect of Cerebral Amyloid Angiopathy on Brain Iron, Copper, and Zinc in Alzheimer's Disease

Iodine concentration in different human brain parts

A Potential Role for Alterations of Zinc and Zinc Transport Proteins in the Progression of Alzheimer's Disease

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