RNAA for arsenic, cadmium, copper, and molybdenum in CNS tissues from subjects with age-related neurodegenerative diseases

Tandon, Lav; Ni, B. F.; Ding, Xiaxin; Ehmann, W. D.; Kasarskis, Edward J.; Markesbery, William R.

doi:10.1007/bf02040168

Cited by 22 publications

(14 citation statements)

References 26 publications

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“…Decreased concentration Unchanged concentration Cu Hippocampus, entorhinal cortex, frontal cortex, putamen (102,119) and senile plaques (121) Hippocampus, amygdala (99) , basal ganglia (116) and cortex (117) Hippocampus, cerebellum, cortex (98,99,118) , amygdala (99,118) and hippocampus (114) Fe Senile plaques (121) , amygdala, piriform cortex, olfactory system (109) , hippocampus/amygdala (99,124) , frontal cortex (102) , grey motor cortex (103,124) , temporal cortex (105) , hippocampus (106) , frontal/parietal/temporal lobe (107) , putamen/thalamus/globus pallidus/area occipitalis (108) and cortex (116) Basal ganglia (116) and hippocampus (114,115) Pituitary gland (125) CSF (61) levels of Cu in patients with AD or mild cognitive impairment (93) compared with healthy controls. In these studies, total Cu (78,80,94,139 -141) , ceruloplasmin (140,141) as well as 'free' Cu (ceruloplasmin non-bound Cu) (78,93,140,142,143) have been found at increased rates.…”

Section: Increased Concentrationmentioning

confidence: 99%

Copper and iron in Alzheimer's disease: a systematic review and its dietary implications

Loef

Walach

2011

Br J Nutr

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Fe and Cu could represent dietary risk factors for Alzheimer's disease (AD), which has become a global health concern. To establish the relationship between diets high in Cu and Fe and cognitive decline or AD, we have conducted a systematic review of the literature (up to January 2011). We identified two meta-analyses, two systematic reviews, eleven placebo-controlled trials, five observational studies, forty-five case -control studies, thirty autopsy and five uncontrolled studies, and one case report. There were eleven interventional trials that tried to either supplement or deplete Fe and Cu, but none of them provided clear evidence of a beneficial effect on cognitive performance in patients with AD. The prospective studies revealed an association between a diet simultaneously high in SFA and Cu and cognitive decline. Case -control and autopsy studies showed elevated Fe levels in the brains of AD patients, whereas the evidence was less consistent for Cu. In most of the studies, Cu concentrations were unchanged in the cerebrospinal fluid and the brain but increased in the serum. In conclusion, the existing data suggest that diets excessive in Fe or Cu, together with a high intake of SFA, should be avoided in the elderly who are not at risk of anaemia. Basic studies and, building on this, clinical investigations are needed to further elucidate in which dietary patterns and in which patient groups an Fe-and Cu-rich diet might foster the risk of developing AD.

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Section: Increased Concentrationmentioning

confidence: 99%

Copper and iron in Alzheimer's disease: a systematic review and its dietary implications

Loef

Walach

2011

Br J Nutr

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“…Several original papers were retrieved on Al, Fe, Cu, and Zn determination in brain samples of both AD patients and non-AD controls at the tissue level: Hallgren and Sourander (1958, controls;1960, patients), Crapper McLachlan et al (1973, 1976, and 1980c, Constantinidis et al (1977), McDermott et al (1977 and1979), Trapp et al (1978), Yoshimasu et al (1980), Traub et al (1981), Markesbery et al (1981 and, Hershey et al (1984), Ehmann et al (1984), Yoshimasu (1985, Thompson et al (1988), Plantin et al (1987), Ward and Mason (1987), Jacobs et al (1989), Corrigan et al (1993), Xu et al (1992), Dedman et al (1992), Griffiths and Crossman (1993), Tandon et al (1994), Andrasi et al (1994 and, Samudralwar et al (1995), Deibel et al (1996), Cornett et al (1996Cornett et al ( , 1998aCornett et al ( , and 1998b, Kala and Hasinoff (1996), Bjertness et al (1996), Danscher et al (1997), Stedman and Spyrou (1997), Rao et al (1999 and, Rulon et al (2000), Panayi et al (2000 and. Two original works with only data on patients, VanDalsem et al (1995) and …”

Section: Aluminum Iron Copper and Zinc In Alzheimer's Diseasementioning

confidence: 94%

“…No relation to age was observed. Tandon et al (1994) examined 17 controls (age 33-85) and observed a significant positive correlation between Cu content in bulk brain and age.…”

Section: Ironmentioning

confidence: 96%

“…The original papers retrieved on Al, Fe, Cu, and Zn determination in brain samples from both patients affected by ALS (not better defined) and non-ALS controls were Yoshimasu et al (1976 and, Yase (1978), Yoshida et al (1988), Khare et al (1990), and Tandon et al (1994). The papers with data on controls and patients affected by the Western Pacific variant of ALS were Yoshimasu et al (1982), Traub et al (1981), Yoshida (1987 and, Yasui et al (1991aYasui et al ( , 1991bYasui et al ( , and 1993.…”

Section: Aluminum Iron Copper and Zinc Inmentioning

confidence: 99%

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Metals Distribution and Regionalization in the Brain

Speziali¹,

Orvini²

2003

Metal Ions and Neurodegenerative Disorders

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A review of the literature on trace element levels in normal and diseased human brain is undertaken in an attempt to recognize possible distribution patterns of aluminum, iron, copper, and zinc. Trace element concentration changes are known to occur in brain areas of subjects affected with neurodegenerative diseases. We have considered the levels of the four metals in Alzheimer's disease, Parkinson's disease, and Western Pacific Parkinsonism-dementia along with amyotrophic lateral sclerosis. For each disease, we selected articles that consider well-defined brain sites for which the element values observed in controls were found to be significantly different from those determined in patients. For a more complete picture statistically not significant differences of the same element concentrations in the same regions, whenever available, were also taken into consideration.

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“…Copper ions are normally bound to copper enzymes or proteins like cytochrome oxidase, ceruloplasmin and superoxide dismutase during normal physiological circulation and are released into the synapse upon presynaptic excitation, reaching up to 15 μM in the synaptic cleft [60]. Although found in high concentrations in senile plaques ( 400 μM) [33] compared to the normal brain extracellular concentration of 0.2-1.7 μM [60,61], most studies of bulk tissue have found either no statistical difference [62,63] or a decrease [64] in total copper concentration in AD brain compared to age-matched controls. Interestingly, a recent study examining a pair of elderly monozygotic female twins that were discordant for AD demonstrated that the twin who met the criteria for the diagnosis of AD and who performed significantly worse on all cognitive testing had significantly higher serum copper and total peroxide levels [65].…”

Section: Metalsmentioning

confidence: 99%

Alzheimer Disease and the Role of Free Radicals in the Pathogenesis of the Disease

Moreira

Santos

Oliveira

et al. 2008

CNSNDDT

137

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Oxidative stress occurs early in the progression of Alzheimer disease, significantly before the development of the pathologic hallmarks, neurofibrillary tangles and senile plaques. All classes of macromolecules (sugar, lipids, proteins, and nucleic acids) are affected by oxidative stress leading, inevitably, to neuronal dysfunction. Extensive data from the literature support the notion that mitochondrial and metal abnormalities are key sources of oxidative stress in Alzheimer disease. Furthermore, it has been suggested that in the initial stages of the development of Alzheimer disease, amyloid-beta deposition and hyperphosphorylated tau function as compensatory responses to ensure that neuronal cells do not succumb to oxidative damage. However, during the progression of the disease, the antioxidant activity of both agents is either overwhelmed or, according to others, evolves into pro-oxidant activity resulting in the exacerbation of reactive species production.

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RNAA for arsenic, cadmium, copper, and molybdenum in CNS tissues from subjects with age-related neurodegenerative diseases

Cited by 22 publications

References 26 publications

Copper and iron in Alzheimer's disease: a systematic review and its dietary implications

Copper and iron in Alzheimer's disease: a systematic review and its dietary implications

Metals Distribution and Regionalization in the Brain

Alzheimer Disease and the Role of Free Radicals in the Pathogenesis of the Disease

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