Serum levels of zinc and copper in patients with Parkinson's disease

Jiménez‐Jiménez, Félix Javier; Fernández–Calle, Pilar; Martínez-Vanaclocha, Marcos; Herrero, E.; Molina, José Antonio; Vázquez, Antonio; Codoceo, Rosa

doi:10.1016/0022-510x(92)90127-7

Cited by 47 publications

(25 citation statements)

References 28 publications

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“…This is in contrast with earlier studies which found normal or raised CP concentration in the serum of PD patients, compared with the controls [22][23][24]. Yet, Hochstrasser et al (2005) found increased iron levels in substantia nigra and lower CP activity in the serum of PD patients with known mutations in the CP gene [25], possibly indicating defective iron metabolism in the CNS as a result of lower CP activity.…”

Section: Parkinson's Diseasecontrasting

confidence: 85%

Case–control studies on ceruloplasmin and superoxide dismutase (SOD1) in neurodegenerative diseases: A short review

Tórsdóttir

Kristinsson

Snædal

et al. 2010

Journal of the Neurological Sciences

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Section: Parkinson's Diseasecontrasting

confidence: 85%

Case–control studies on ceruloplasmin and superoxide dismutase (SOD1) in neurodegenerative diseases: A short review

Tórsdóttir

Kristinsson

Snædal

et al. 2010

Journal of the Neurological Sciences

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“…A 1992 publication found no correlation between ceruloplasmin and age of onset or duration of PD [8]. This was refuted by Tórsdóttir et al [9], who found that serum ceruloplasmin and ceruloplasmin oxidative activity were lower in PD patients compared to age-and gender-matched controls.…”

Section: Introductionmentioning

confidence: 92%

Lower serum ceruloplasmin levels correlate with younger age of onset in Parkinson’s disease

Bharucha

Vincent³

et al. 2008

J Neurol

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Ceruloplasmin functions as a ferroxidase in iron metabolism. Parkinson's disease (PD) is characterized by an increase in brain iron. We postulated that lower circulating ceruloplasmin levels in PD would result in rapid brain iron accumulation and an earlier age of onset. Consecutive PD patients were separated into subgroups with younger (< or = 60 years, n = 62) and older ages of onset (> 60, n = 29), and compared to non-PD controls (n = 40). A one-way ANOVA comparing ceruloplasmin levels showed a very robust effect [F(2,128) = 46.4, p < 1e-99]. Post hoc analysis demonstrated that the younger-onset PD subgroup [22.0 mg/dl +/- 6.5 SD] had a lower mean ceruloplasmin level compared to the older-onset PD subgroup [35.7 +/- 10.4] and controls [35.6 +/- 8.4], whose levels did not differ from each other. Ceruloplasmin levels showed robust correlation with age of onset in all 91 PD patients [r = 0.56, r(2) = 0.31, p < 0.0001] but not in the non-PD controls [r = 0.16, r(2) = 0.03, not significant]. Mode of onset and duration of PD showed no relationship to ceruloplasmin. Serum copper and ferritin, available in most patients, did not differ between the PD subgroups. Younger-onset PD patients have significantly lower levels of serum ceruloplasmin compared to those with older-onset PD. Ceruloplasmin may play a role in the etiopathogenesis of younger-onset PD patients and merits further study.

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“…between exposure to agricultural pesticides and a higher risk for late onset PD (3)(4)(5)(6)(7)(8)(9). A prime candidate is the widely used herbicide 1,1Ј-dimethyl-4,4Ј-bipyridium (paraquat/PQ) because it can cause selective degeneration of tyrosine hydroxylase immuno-positive (TH ϩ ) neurons in the SNpc, and long term exposure was shown to increase PD risk 6-fold in a Taiwan population that sprays it on rice fields (10 -12).…”

mentioning

confidence: 99%

Paraquat Neurotoxicity Is Mediated by a Bak-dependent Mechanism

Fei

McCormack

Monte

et al. 2008

Journal of Biological Chemistry

105

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Paraquat (PQ) causes selective degeneration of dopaminergic neurons in the substantia nigra pars compacta, reproducing an important pathological feature of Parkinson disease. Oxidative stress, c-Jun N-terminal kinase activation, and ␣-synuclein aggregation are each induced by PQ, but details of the cell death mechanisms involved remain unclear. We have identified a Bak-dependent cell death mechanism that is required for PQ-induced neurotoxicity. PQ induced morphological and biochemical features that were consistent with apoptosis, including dose-dependent cytochrome c release, with subsequent caspase-3 and poly(ADP-ribose) polymerase cleavage. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. Evaluation of Bcl-2 family members showed that PQ induced high levels of Bak, Bid, BNip3, and Noxa. Small interfering RNA-mediated knockdown of BNip3, Noxa, and Bak each protected cells from PQ, but Bax knockdown did not. Finally, we tested the sensitivity of Bakdeficient mice and found them to be resistant to PQ treatments that depleted tyrosine hydroxylase immuno-positive neurons in the substantia nigra pars compacta of wild-type mice.

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Serum levels of zinc and copper in patients with Parkinson's disease

Cited by 47 publications

References 28 publications

Case–control studies on ceruloplasmin and superoxide dismutase (SOD1) in neurodegenerative diseases: A short review

Case–control studies on ceruloplasmin and superoxide dismutase (SOD1) in neurodegenerative diseases: A short review

Lower serum ceruloplasmin levels correlate with younger age of onset in Parkinson’s disease

Paraquat Neurotoxicity Is Mediated by a Bak-dependent Mechanism

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