Cytochrome c oxidase is decreased in Alzheimer’s disease platelets

Cardoso, Sandra M.; Proença, Maria Teresa; Santos, Sancha; Santana, Isabel; Oliveira, Catarina R.

doi:10.1016/s0197-4580(03)00033-2

Cited by 259 publications

(185 citation statements)

References 35 publications

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“…Complex III was decreased slightly in their study, and other groups finding ETC Complex IV deficiency did not also examine Complex III (Bosetti et al, 2002;Cardoso et al, 2004a). The disparity between our results and Parker et al could be ascribed to methodological differences in our assays, particularly in the selection of ubiquinol analogs: they cite usage of ubiquinol-2 (Q 2 ) while we employed decylubiquinol.…”

Section: Discussioncontrasting

confidence: 81%

“…Parker's original finding of reduced platelet Complex IV activity in AD has been replicated (Parker et al, 1994a;Bosetti et al, 2002;Cardoso et al, 2004a), yet the role of mitochondrial abnormalities remains largely undefined. Amyloid-β (Aβ), the protein that makes up the amyloid plaques in the brain of AD patients, has been shown to interact directly with mitochondria and inhibit Complex IV activity (Crouch et al, 2005) and induce oxidative stress (Lustbader et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Impaired platelet mitochondrial activity in Alzheimer’s disease and mild cognitive impairment

et al. 2006

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Mitochondrial abnormalities are found in Alzheimer's disease (AD), but previous reports haven't examined at-risk groups. In subjects with AD, mild cognitive impairment (MCI), and nondemented aged controls, platelet and lymphocyte mitochondria were isolated and analyzed for Complexes I, III, and IV of the electron transport chain. Western blots were used to control for differential enrichment of samples. Results demonstrated significant declines in Complexes III and IV in AD, and a significant decline in Complex IV in MCI. This report confirms mitochondrial deficiencies in AD, extends them to MCI, and suggests they are present at the earliest symptomatic stages of disease.

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Section: Discussioncontrasting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Impaired platelet mitochondrial activity in Alzheimer’s disease and mild cognitive impairment

et al. 2006

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“…Previous studies have suggested that a decrease in brain bioenergetics may be a useful biomarker to predict disease decades before symptoms [33][34][35][36]. Decreases in mitochondrial bioenergetics, metabolic enzyme expression and activity, cerebral glucose metabolism, along with increased oxidative stress, Aβ deposits within mitochondria, and expression of ABAD are associated with the prodromal state of AD [34,[37][38][39][40][41][42].…”

Section: Current Strategies Targeting Mitochondria and Bioenergetics mentioning

confidence: 99%

“…A decline in mitochondrial function can occur decades prior to clinical diagnosis of AD and thus may serve as a biomarker of AD risk, as well as a therapeutic target [12,24,32,67]. Preclinical in vitro and in vivo AD models have demonstrated a decline in mitochondrial function, including reduced mitochondrial respiration, decreased metabolic enzyme expression and activity, increased oxidative stress, and increased mitochondrial Aβ load and ABAD expression, prior to AD pathology [12,13,15,24,34,38]. A series of mitochondrial enhancer candidates have been proposed and investigated in preclinical and clinical studies for AD prevention and treatment ( Table 2).…”

Section: Mitochondrial Bioenergetics As a Therapeutic Targetmentioning

confidence: 99%

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

2015

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Alzheimer's disease (AD) has a complex and progressive neurodegenerative phenotype, with hypometabolism and impaired mitochondrial bioenergetics among the earliest pathogenic events. Bioenergetic deficits are well documented in preclinical models of mammalian aging and AD, emerge early in the prodromal phase of AD, and in those at risk for AD. This review discusses the importance of early therapeutic intervention during the prodromal stage that precedes irreversible degeneration in AD. Mechanisms of action for current mitochondrial and bioenergetic therapeutics for AD broadly fall into the following categories: 1) glucose metabolism and substrate supply; 2) mitochondrial enhancers to potentiate energy production; 3) antioxidants to scavenge reactive oxygen species and reduce oxidative damage; 4) candidates that target apoptotic and mitophagy pathways to either remove damaged mitochondria or prevent neuronal death. Thus far, mitochondrial therapeutic strategies have shown promise at the preclinical stage but have had little-to-no success in clinical trials. Lessons learned from preclinical and clinical therapeutic studies are discussed. Understanding the bioenergetic adaptations that occur during aging and AD led us to focus on a systems biology approach that targets the bioenergetic system rather than a single component of this system. Bioenergetic system-level therapeutics personalized to bioenergetic phenotype would target bioenergetic deficits across the prodromal and clinical stages to prevent and delay progression of AD.

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“…Zamudio method: take a film sample (liquid film) 0.6mL in the cuvette plus the reaction solution at a wavelength of 420nm at the mixing ratio of color, to add to NADH as a starting point, the recording starts within 6 minutes of the reaction OD values (Cardoso et al,2004).…”

Section: Nadh-measured Activity Of Cytochrome C Oxidoreductasementioning

confidence: 99%

Solanum Nigrum Polysaccharide (SNL) Extract Effects in Transplanted Tumor-bearing Mice - Erythrocyte Membrane Fluidity and Blocking of Functions

Yuan¹,

Liu²

2015

Asian Pacific Journal of Cancer Prevention

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Background: Solanum nigrum L. has been used in traditional Chinese medicine because of its diuretic and antipyretic effects. The present research concerned effects of crude polysaccharides isolated from Solanum nigrum L. on erythrocyte membranes of tumor-bearing S 180 and H 22 in mice. Materials and Methods: Fluorescencelabeled red blood cell membranes were used with DPH fluorescence spectrophotometry to examine erythrocyte membrane fluidity, and colorimetry to determine degree of erythrocyte surface membrane blocking. Extent of reaction by tumor-bearing mice with the enzyme erythrocyte membrane bubble shadow detection of red cell membrane variation in the degree of closure before and after administration. Results: Solanum nigrum polysaccharide could significantly improve the S 180 and H 22 tumor-bearing mice erythrocyte membrane fluidity, compared with the control group, the difference was significant (p<0.01), SNL can significantly improve the red blood cell membrane and then S 180 tumor-bearing mice sealing ability, compared with the negative control group, the difference was significant(p<0.05, p<0.01). H 22 tumor-bearing mice can increase red cell membrane and then sealing ability, the difference was significant (p<0.05). Solanum nigrum polysaccharide degree of fluidity and blocking two transplanted tumors in mice restored the ability to raise the red cell membrane has a significant effect. Conclusions: Solanum nigrum L.-type mice transplanted tumor can affect the red blood cell membrane fluidity and re-closed, through the red cell membrane of red blood cells to enhance the immune function of the possibility of erythrocyte immunity against tumor formation garland provide experimental basis.

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Cytochrome c oxidase is decreased in Alzheimer’s disease platelets

Cited by 259 publications

References 35 publications

Impaired platelet mitochondrial activity in Alzheimer’s disease and mild cognitive impairment

Impaired platelet mitochondrial activity in Alzheimer’s disease and mild cognitive impairment

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

Solanum Nigrum Polysaccharide (SNL) Extract Effects in Transplanted Tumor-bearing Mice - Erythrocyte Membrane Fluidity and Blocking of Functions

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