Copper-zinc superoxide dismutase activity in red blood cells in probable Alzheimer's patients and their first-degree relatives

Serra, Jorge A.; Famulari, A.; Kohan, Silvia; Marschoff, Enrique; Domínguez, Raúl; Lustig, Eugenia Sacerdote de

doi:10.1016/0022-510x(94)90297-6

Cited by 27 publications

(11 citation statements)

References 29 publications

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“…As in previous studies, the analysis of the differences of the duplicates indicated that this source of variability is nonsignificant [2].…”

Section: Blood Samplingmentioning

confidence: 88%

“…The technique used was previously reported [2]. The protein concentration was determined with the Folin reagent [23], using bovine serum albumin as standard.…”

Section: Sod Assaymentioning

confidence: 99%

“…Oxidative stress has been demonstrated in blood profiles of living neurological patients in association with probable dementia of the Alzheimer's type (DAT) and vascular dementia (VD) among other neurological disorders [1][2][3][4], both diseases presenting characteristic antioxidant profiles by means of which it is possible to differentiate and identify the pathologies, with the activity values of the Cu -Zn superoxide dismutase (SOD) acting as a leading and early marker.…”

Section: Introductionmentioning

confidence: 99%

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Oxidative stress in Alzheimer's and vascular dementias: masking of the antioxidant profiles by a concomitant Type II diabetes mellitus condition

Serra

Marschoff

Domínguez³

et al. 2004

Journal of the Neurological Sciences

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“…As in previous studies, the analysis of the differences of the duplicates indicated that this source of variability is nonsignificant [2].…”

Section: Blood Samplingmentioning

confidence: 88%

“…The technique used was previously reported [2]. The protein concentration was determined with the Folin reagent [23], using bovine serum albumin as standard.…”

Section: Sod Assaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative stress in Alzheimer's and vascular dementias: masking of the antioxidant profiles by a concomitant Type II diabetes mellitus condition

Serra

Marschoff

Domínguez³

et al. 2004

Journal of the Neurological Sciences

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“…Cu-Zn Superoxide Dismutase (SOD) Activity Assay RBC from 5 ml blood samples were hemolyzed with 5 ml of distilled water and hemoglobin was separated by addition of a 2:1 volume of chloroform-ethanol (3:5) at 0°C and centrifugation [6,27]. The remaining solution was assayed for SOD by measuring the ability of the extract to inhibit the auto-oxidation of epinephrine at pH 10.2 and at 30°C [28].…”

Section: Plasma Antioxidant Capacity (Trap) Assaymentioning

confidence: 99%

“…Accordingly to both criteria-plasmatic and antioxidant enzymes markers-a significantly systemic oxidative stress has been observed in Alzheimer's patients (AD), in non-degenerative vascular dementia (VD) and in Parkinson's disease (PD) [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Systemic Oxidative Stress Associated with the Neurological Diseases of Aging

et al. 2009

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Markers of oxidative stress were measured in blood samples of 338 subjects (965 observations): Alzheimer's, vascular dementia, diabetes (type II) superimposed to dementias, Parkinson's disease and controls. Patients showed increased thiobarbituric acid reactive substances (+21%; P < 0.05), copper-zinc superoxide dismutase (+64%; P < 0.001) and decreased antioxidant capacity (-28%; P < 0.001); pairs of variables resulted linearly related across groups (P < 0.001). Catalase and glutathione peroxidase, involved in discrimination between diseases, resulted non-significant. When diabetes is superimposed with dementias, changes resulted less marked but significant. Also, superoxide dismutase resulted not linearly correlated with any other variable or age-related (pure Alzheimer's peaks at 70 years, P < 0.001). Systemic oxidative stress was significantly associated (P << 0.001) with all diseases indicating a disbalance in peripheral/adaptive responses to oxidative disorders through different free radical metabolic pathways. While other changes - methionine cycle, insulin correlation - are also associated with dementias, the responses presented here show a simple linear relation between prooxidants and antioxidant defenses.

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A unifying hypothesis of Alzheimer's disease. II. Pathophysiological processes

Heininger

1999

Hum. Psychopharmacol. Clin. Exp.

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The age-related loss of hormonal balance puts the homeostatic calcium±energy±antioxidant triangle under stress. The energetic compromise enhances b-amyloid protein formation and tau protein hyperphosphorylation, both cellular stress responses, which may give rise to diuse plaque and neuro®brillary tangle formation during normal ageing. Facilitated by a multitude of risk factors (discussed in part III of this series), the age-related processes lead into the pathophysiological events of Alzheimer's disease (AD). In AD, the hormonal imbalance is further aggravated with progressively detrimental sequelae for the calcium±energy±redox homeostasis and for both amyloid protein precursor and tau protein metabolism. The immune system as an integral component of the neuroendocrine immunological network is subject to the deteriorating endocrinological balance and displays a cellular and humoral acute phase-type reaction. In an orchestrated action, an in¯ammatory response is mounted in which activated micro-and astro-glia and their secreted in¯ammatory mediators and matrix constituents elicit the transformation of diuse into neuritic plaques which, secondarily, may induce further tissue damage. Importantly, the AD brain is characterized by the microglial inability to clear the brain of the deposited material. The pathophysiological processes lead to functional and structural impairments of neuronal plasticity, a compromise of the neuronal network and, eventually, to cell death. Conspicuously, these alterations do not uniformly aect all brain regions but manifest with a temporal and topographical speci®city vulnerable areas and nerve cell populations. Copyright # 1999 John Wiley & Sons, Ltd.KEY WORDS Ð Alzheimer's disease; calcium; energy metabolism; oxidative stress; mitochondria; glucocorticoids; neuropeptide Y; DHEA; oestrogen; melatonin; somatostatin; nerve growth factors; insulin; b-amyloid; tau; immune system; signal transduction; apoptosis; vulnerability AGEING AND ALZHEIMER'S DISEASE In part I of this series it was posited that the agerelated imbalance of neuropeptides and hormones puts the neurons under metabolic stress [Heininger, 1999]. Hence, it is outlined how this compromise of cellular homeostasis may lead to the production of amyloid b-protein (Ab) and hyperphosphorylation of tau protein (P-tau). These processes occur already during normal ageing. Both Ab and senile plaques (SP) as well as P-tau and neuro®brillary tangles (NFT) are found in the normal aged brain in a spatial distribution suggesting their independent formation and potentially representing a preclinical stage of the disease [Beach et al., 1997;Braak and Braak, 1997;Troncoso et al., 1998;Price and Morris, 1999].Nevertheless, since these changes are the hallmark of the pathomorphological diagnosis [Khachaturian, 1985; Ball et al., 1997] and, for the sake of the argument, they have been grouped as pathophysiological AD processes. However, it should be borne in mind that these processes are not ADspeci®c and that only by some additional quantitative...

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Copper-zinc superoxide dismutase activity in red blood cells in probable Alzheimer's patients and their first-degree relatives

Cited by 27 publications

References 29 publications

Oxidative stress in Alzheimer's and vascular dementias: masking of the antioxidant profiles by a concomitant Type II diabetes mellitus condition

Oxidative stress in Alzheimer's and vascular dementias: masking of the antioxidant profiles by a concomitant Type II diabetes mellitus condition

Systemic Oxidative Stress Associated with the Neurological Diseases of Aging

A unifying hypothesis of Alzheimer's disease. II. Pathophysiological processes

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