Unaltered Respiratory Chain Enzyme Activity and Mitochondrial DNA in Skeletal Muscle from Patients with Idiopathic Parkinson’s Syndrome

Reichmann, Heinz; Janetzky, Bernd; Bischof, F.; Seibel, Peter; Schöls, Lüdger; Kühn, Wilfried; Przuntek, H.

doi:10.1159/000117053

Cited by 24 publications

(15 citation statements)

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“…In these studies complex I deficiency and impairment in other complexes have been variably described (Parker et al, 1989;Bindoff et al, 1991;Shoffner et al, 1991;Bravi et al, 1992;Mann et al, 1992;Nakagawa-Hattori et al, 1992;Yoshino et al, 1992;Anderson et al, 1993;Barroso et al, 1993;Benecke et al, 1993;Cardellach et al, 1993;Blin et al, 1994;Di Donato et al, 1993;Krige et al, 1993;Janetzky et al, 1994;Reichmann et al, 1994;Haas et al, 1995;Martin et al, 1996;Blake et al, 1997). Reduction in platelet complex I activity was found by the majority, but not by all groups (Bravi et al, 1992;Mann et al, 1992;Blake et al, 1997;Aomi et al 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Conflicting results have been reported regarding activities of respiratory complexes I and IV. Decreased (Bindoff et al, 1991;Shoffner et al, 1991;NakagawaHattori et al, 1992;Cardellach et al, 1993;Blin et al, 1994) or normal (Mann et al, 1992;Anderson et al, 1993;Di Donato et al, 1993;Reichmann et al, 1994) activities for skeletal muscles, decreased (Barroso et al, 1993) or normal (Yoshino et al, 1992;Martin et al, 1996) values for lymphocyte mitochondria have been reported. Complex I defect in platelets has revealed relatively more consistent results than in other peripheral tissues.…”

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confidence: 99%

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Mitochondrial Complex I, Ii/Iii, and Iv Activities in Familial and Sporadic Parkinson's Disease

Hanağası

Ayribas

Baysal

et al. 2005

International Journal of Neuroscience

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A possible role of mitochondrial respiratory chain dysfunction in the pathogenesis of sporadic Parkinson's disease (PD) has been described. There are only a few reports concerning mitochondrial involvement in familial Parkinson's disease. The present study investigated mitochondrial complex I-IV activity in patients with sporadic and familial PD, compared to controls. Platelets were isolated from venous blood and platelet mitochondria were obtained through sonication and differential centrifugation. Complex I, II/III, and IV activities were measured in 17 patients with family history of Parkinson's disease (PDF), 15 patients with sporadic Parkinson disease (PDS), and 17 age-matched, healthy controls. The mitochondrial enzyme activities did not differ significantly between patient groups and controls. In addition, there was no correlation between mitochondrial complex activities and age, severity of disease, or age at onset of disease in the patient groups. In this study, the data indicate no significant differences in mitochondrial complex I-IV activities in PDF and PDS.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Mitochondrial Complex I, Ii/Iii, and Iv Activities in Familial and Sporadic Parkinson's Disease

Hanağası

Ayribas

Baysal

et al. 2005

International Journal of Neuroscience

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“…Others could not confirm this finding [38], but a recent study also reported some abnormalities in assembly and oxidation of complex I subunits in PD cortex mitochondria [36]. Several studies showed impaired complex I, II+III, and IV in PD muscle [39–41], whereas others reported no differences [29,42,43], and findings on the ETC deficiency in PD lymphocytes [20,44] are counter-balanced by the evidence on the absence of such deficiencies [45]. Such inconsistency in the experimental data could likely be explained by significant methodological differences in all these studies, e.g.…”

Section: Mitochondrial Dysfunction In the Idiopathic Form Of Diseasementioning

confidence: 99%

Mitochondrial dysfunction in the limelight of Parkinson's disease pathogenesis

Banerjee

Starkov

Beal

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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185

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Parkinson's disease (PD) is a progressive neurodegenerative movement disorder with unknown etiology. It is marked by widespread neurodegeneration in the brain with profound loss of A9 midbrain dopaminergic neurons in substantia nigra pars compacta. Several theories of biochemical abnormalities have been linked to pathogenesis of PD of which mitochondrial dysfunction due to an impairment of mitochondrial complex I and subsequent oxidative stress seems to take the center stage in experimental models of PD and in postmortem tissues of sporadic forms of illness. Recent identification of specific gene mutations and their influence on mitochondrial functions has further reinforced the relevance of mitochondrial abnormalities in disease pathogenesis. In both sporadic and familial forms of PD abnormal mitochondrial paradigms associated with disease include impaired functioning of the mitochondrial electron transport chain, aging associated damage to mitochondrial DNA, impaired calcium buffering, and anomalies in mitochondrial morphology and dynamics. Here we provide an overview of specific mitochondrial functions affected in sporadic and familial PD that play a role in disease pathogenesis. We propose to utilize these gained insights to further streamline and focus the research to better understand mitochondria's role in disease development and exploit potential mitochondrial targets for therapeutic interventions in PD pathogenesis.

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“…On the other side, defective OXPHOS has been suggested to occur also in skeletal muscle; however, this alteration have been more difficult to identified, probably because of the used assays to measure complex I activity are insensitive to subtle defects (i.e., 20% of activity reduction) [94,101,102]. Finally, other mitochondrial enzymes involved in energy metabolism, includingketoglutarate dehydrogenase and pyruvate dehydrogenase, have been demonstrated to have reduced activity in brain from PD patients [101,103].…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

The Intranasal Administration of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP): A New Rodent Model to Test Palliative and Neuroprotective Agents for Parkinson's disease

Prediger

Aguiar²,

Moreira³

et al. 2011

Current Pharmaceutical Design

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Parkinson's disease (PD) is the second most common neurodegenerative disorder affecting approximately 1% of the population older than 60 years. Classically, PD is considered to be a motor system disease and its diagnosis is based on the presence of a set of cardinal motor signs that are consequence of a pronounced death of dopaminergic neurons in the substantia nigra pars compacta (SNc). Nowadays there is considerable evidence showing that non-dopaminergic degeneration also occurs in other brain areas which seems to be responsible for the deficits in olfactory, emotional and memory functions that precede the classical motor symptoms in PD. Dopamine-replacement therapy has dominated the treatment of PD and although the currently approved antiparkinsonian agents offer effective relief of the motor deficits, they have not been found to alleviate the non-motor features as well as the underlying dopaminergic neuron degeneration and thus drug efficacy is gradually lost. Another major limitation of chronic dopaminergic therapy is the numerous adverse effects such as dyskinesias, psychosis and behavioral disturbance. The development of new therapies in PD depends on the existence of representative animal models to facilitate the evaluation of new pharmacological agents before they are applied in clinical trials. We have recently proposed a new experimental model of PD consisting of a single intranasal (i.n.) administration of the proneurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP, 1 mg/nostril) in rodents. Our findings demonstrated that rats and mice treated intranasally with MPTP suffer impairments in olfactory, cognitive, emotional and motor functions conceivably analogous to those observed during different stages of PD. Such infusion causes time-dependent loss of tyrosine hydroxylase in the olfactory bulb and SNc, resulting in significant dopamine depletion in different brain areas. We have also identified some pathogenic mechanisms possibly involved in the neurodegeneration induced by i.n. administration of MPTP including mitochondrial dysfunction, oxidative stress, activation of apoptotic cell death mechanisms and glutamatergic excitotoxicity. Therefore, the present review attempts to provide a comprehensive picture of the i.n. MPTP model and to highlight recent findings from our group showing its potential as a valuable rodent model for testing novel drugs that may provide alternative or adjunctive treatment for both motor and non-motor symptoms relief with a reduced side-effect profile as well as the discovery of compounds to modify the course of PD.

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Unaltered Respiratory Chain Enzyme Activity and Mitochondrial DNA in Skeletal Muscle from Patients with Idiopathic Parkinson’s Syndrome

Cited by 24 publications

References 0 publications

Mitochondrial Complex I, Ii/Iii, and Iv Activities in Familial and Sporadic Parkinson's Disease

Mitochondrial Complex I, Ii/Iii, and Iv Activities in Familial and Sporadic Parkinson's Disease

Mitochondrial dysfunction in the limelight of Parkinson's disease pathogenesis

The Intranasal Administration of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP): A New Rodent Model to Test Palliative and Neuroprotective Agents for Parkinson's disease

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