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Yasuo Terayama - One of the best experts on this subject based on the ideXlab platform.

  • levels of reduced and oxidized coenzyme q 10 and 8 hydroxy 2 deoxyguanosine in the csf of patients with alzheimer s disease demonstrate that mitochondrial oxidative damage and or oxidative dna damage contributes to the Neurodegenerative Process
    Journal of Neurology, 2010
    Co-Authors: Chiaki Isobe, Takashi Abe, Yasuo Terayama
    Abstract:

    To investigate the possibility that mitochondrial oxidative damage, oxidative DNA damage or both contribute to the Neurodegenerative Process of Alzheimer's disease (AD), we employed high-performance liquid chromatography using an electrochemical detector to measure the concentrations of the reduced and oxidized forms of coenzyme Q-10 (CoQ-10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 30 patients with AD and in 30 age-matched controls with no neurological disease. The percentage of oxidized/total CoQ-10 (%CoQ-10) in the CSF of the AD group (78.2 +/- 18.8%) was significantly higher than in the control group (41.3 +/- 10.4%) (P < 0.0001). The concentration of 8-OHdG in the CSF of AD patients was greater than in the CSF of controls (P < 0.0001) and was positively correlated with the duration of illness (r(s) = 0.95, P < 0.0001). The %CoQ-10 was correlated with concentrations of 8-OHdG in the CSF of AD patients (r(s) = 0.66, P < 0.001). The present study suggests that both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of early AD development.

  • levels of reduced and oxidized coenzymeq 10 and 8 hydroxy 2 deoxyguanosine in the cerebrospinal fluid of patients with living parkinson s disease demonstrate that mitochondrial oxidative damage and or oxidative dna damage contributes to the neurodege
    Neuroscience Letters, 2010
    Co-Authors: Chiaki Isobe, Takashi Abe, Yasuo Terayama
    Abstract:

    The aim of this study was to investigate the possibility that mitochondrial oxidative damage, oxidative DNA damage or both contribute to the Neurodegenerative Process of Parkinson's disease (PD). We employed high-performance liquid chromatography (HPLC) using an electrochemical detector to measure concentrations of the reduced and oxidized forms of coenzyme Q-10 (CoQ-10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 20 patients with PD and 20 age-matched controls with no neurological disease. The percentage of oxidized to total CoQ-10 (%CoQ-10) in the CSF of the PD group (80.3+/-17.9%) was significantly higher than in the control group (68.2+/-20.4%, P<0.05). In addition, the concentration of 8-OHdG in the CSF of PD patients was greater than in the CSF of controls (P<0.0001) and was positively correlated with the duration of illness (r(s)=0.87, P<0.001). Finally, the %CoQ-10 was correlated with concentrations of 8-OHdG in the CSF of PD patients (r(s)=0.56, P<0.01). The present study suggests that both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of early PD development.

  • Levels of reduced and oxidized coenzymeQ-10 and 8-hydroxy-2′-deoxyguanosine in the cerebrospinal fluid of patients with living Parkinson's disease demonstrate that mitochondrial oxidative damage and/or oxidative DNA damage contributes to the neurodeg
    Neuroscience letters, 2009
    Co-Authors: Chiaki Isobe, Takashi Abe, Yasuo Terayama
    Abstract:

    The aim of this study was to investigate the possibility that mitochondrial oxidative damage, oxidative DNA damage or both contribute to the Neurodegenerative Process of Parkinson's disease (PD). We employed high-performance liquid chromatography (HPLC) using an electrochemical detector to measure concentrations of the reduced and oxidized forms of coenzyme Q-10 (CoQ-10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 20 patients with PD and 20 age-matched controls with no neurological disease. The percentage of oxidized to total CoQ-10 (%CoQ-10) in the CSF of the PD group (80.3+/-17.9%) was significantly higher than in the control group (68.2+/-20.4%, P

  • Levels of reduced and oxidized coenzyme Q-10 and 8-hydroxy-2′-deoxyguanosine in the CSF of patients with Alzheimer’s disease demonstrate that mitochondrial oxidative damage and/or oxidative DNA damage contributes to the Neurodegenerative Process
    Journal of neurology, 2009
    Co-Authors: Chiaki Isobe, Takashi Abe, Yasuo Terayama
    Abstract:

    To investigate the possibility that mitochondrial oxidative damage, oxidative DNA damage or both contribute to the Neurodegenerative Process of Alzheimer's disease (AD), we employed high-performance liquid chromatography using an electrochemical detector to measure the concentrations of the reduced and oxidized forms of coenzyme Q-10 (CoQ-10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 30 patients with AD and in 30 age-matched controls with no neurological disease. The percentage of oxidized/total CoQ-10 (%CoQ-10) in the CSF of the AD group (78.2 +/- 18.8%) was significantly higher than in the control group (41.3 +/- 10.4%) (P < 0.0001). The concentration of 8-OHdG in the CSF of AD patients was greater than in the CSF of controls (P < 0.0001) and was positively correlated with the duration of illness (r(s) = 0.95, P < 0.0001). The %CoQ-10 was correlated with concentrations of 8-OHdG in the CSF of AD patients (r(s) = 0.66, P < 0.001). The present study suggests that both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of early AD development.

  • increased mitochondrial oxidative damage and oxidative dna damage contributes to the Neurodegenerative Process in sporadic amyotrophic lateral sclerosis
    Free Radical Research, 2008
    Co-Authors: Takahiko Murata, Chigumi Ohtsuka, Yasuo Terayama
    Abstract:

    To investigate the possibility that mitochondrial oxidative damage or oxidative DNA damage or both contribute to the Neurodegenerative Process of sporadic amyotrophic lateral sclerosis (sALS), this study used high-performance liquid chromatography with an electrochemical detector to measure the concentrations of the reduced and oxidized forms of coenzyme Q10 (CoQ10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 17 patients with sALS and 17 age-matched controls with no neurological diseases. The percentage of oxidized CoQ10 in the CSF of sALS patients was greater than that in the CSF of controls (p<0.002) and was negatively correlated with the duration of illness (rho=-0.61, p<0.01). The concentration of 8-OHdG in the CSF of sALS patients was greater than that in the CSF of controls (p<0.005) and was positively correlated with the duration of illness (rho=0.53, p<0.005). The percentage of oxidized CoQ10 was correlated with the concentrations of 8-OHdG in the CSF of sALS patients (rho=-0.53, p<0.05). These results suggest that both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of sporadic amyotrophic lateral sclerosis.

Takahiko Murata - One of the best experts on this subject based on the ideXlab platform.

  • increased mitochondrial oxidative damage and oxidative dna damage contributes to the Neurodegenerative Process in sporadic amyotrophic lateral sclerosis
    Free Radical Research, 2008
    Co-Authors: Takahiko Murata, Chigumi Ohtsuka, Yasuo Terayama
    Abstract:

    To investigate the possibility that mitochondrial oxidative damage or oxidative DNA damage or both contribute to the Neurodegenerative Process of sporadic amyotrophic lateral sclerosis (sALS), this study used high-performance liquid chromatography with an electrochemical detector to measure the concentrations of the reduced and oxidized forms of coenzyme Q10 (CoQ10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 17 patients with sALS and 17 age-matched controls with no neurological diseases. The percentage of oxidized CoQ10 in the CSF of sALS patients was greater than that in the CSF of controls (p<0.002) and was negatively correlated with the duration of illness (rho=-0.61, p<0.01). The concentration of 8-OHdG in the CSF of sALS patients was greater than that in the CSF of controls (p<0.005) and was positively correlated with the duration of illness (rho=0.53, p<0.005). The percentage of oxidized CoQ10 was correlated with the concentrations of 8-OHdG in the CSF of sALS patients (rho=-0.53, p<0.05). These results suggest that both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of sporadic amyotrophic lateral sclerosis.

  • Increased mitochondrial oxidative damage and oxidative DNA damage contributes to the Neurodegenerative Process in sporadic amyotrophic lateral sclerosis.
    Free radical research, 2008
    Co-Authors: Takahiko Murata, Chigumi Ohtsuka, Yasuo Terayama
    Abstract:

    To investigate the possibility that mitochondrial oxidative damage or oxidative DNA damage or both contribute to the Neurodegenerative Process of sporadic amyotrophic lateral sclerosis (sALS), this study used high-performance liquid chromatography with an electrochemical detector to measure the concentrations of the reduced and oxidized forms of coenzyme Q10 (CoQ10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 17 patients with sALS and 17 age-matched controls with no neurological diseases. The percentage of oxidized CoQ10 in the CSF of sALS patients was greater than that in the CSF of controls (p

Ann-kathrine Granérus - One of the best experts on this subject based on the ideXlab platform.

  • depressive illness in parkinson s disease indication of a more advanced and widespread Neurodegenerative Process
    Acta Neurologica Scandinavica, 2008
    Co-Authors: Sven Pålhagen, Martin Carlsson, E. Curman, Jan Wålinder, Ann-kathrine Granérus
    Abstract:

    Objective –  The aims were to study if the type and complexity of Parkinsonian symptoms, as well as treatment, could be related to the occurrence and severity of later depressive symptoms. Furthermore, the aim was to study if there is a different depressive symptomatology in Parkinson’s disease (PD) patients compared with depressive illness in an age-matched group of patients with major depression but without Parkinson’s disease. Methods –  Eleven PD-patients with major depression (MD) were compared to 14 PD-patients without depression and to 12 MD patients without PD. Results –  PD patients who later developed a depressive illness were younger at the debut of PD than patients without depression (P < 0.05). At inclusion the depressed PD patients were more disabled than PD patients without depression with higher level in the H&Y scale (P<0.05), and they had more involuntary movements according to Unified Parkinson’s Disease Rating Scale (UPDRS IV) (P < 0.01). A family history of depression was found in one third of the depressed non-parkinsonian patients but in none of the PD groups. Sleep disturbances were significantly more common among depressed PD patients than in PD patients without depression but even more common in depressed patients without PD. Conclusions –  Depressed PD patients had a longer duration of PD and more severe motor symptoms than PD patients without depression, although tremor as an initial symptom seemed to be more common in PD without a later depression. It cannot be excluded that depression in PD reflects a more advanced and widespread neurodegeneration, including serotonergic as well as dopaminergic neurons. Sleep disturbances is common and could be overlooked as an expression of depression.

  • Depressive illness in Parkinson’s disease – indication of a more advanced and widespread Neurodegenerative Process?
    Acta neurologica Scandinavica, 2008
    Co-Authors: Sven Pålhagen, Martin Carlsson, E. Curman, Jan Wålinder, Ann-kathrine Granérus
    Abstract:

    Objective –  The aims were to study if the type and complexity of Parkinsonian symptoms, as well as treatment, could be related to the occurrence and severity of later depressive symptoms. Furthermore, the aim was to study if there is a different depressive symptomatology in Parkinson’s disease (PD) patients compared with depressive illness in an age-matched group of patients with major depression but without Parkinson’s disease. Methods –  Eleven PD-patients with major depression (MD) were compared to 14 PD-patients without depression and to 12 MD patients without PD. Results –  PD patients who later developed a depressive illness were younger at the debut of PD than patients without depression (P < 0.05). At inclusion the depressed PD patients were more disabled than PD patients without depression with higher level in the H&Y scale (P

Sven Pålhagen - One of the best experts on this subject based on the ideXlab platform.

  • depressive illness in parkinson s disease indication of a more advanced and widespread Neurodegenerative Process
    Acta Neurologica Scandinavica, 2008
    Co-Authors: Sven Pålhagen, Martin Carlsson, E. Curman, Jan Wålinder, Ann-kathrine Granérus
    Abstract:

    Objective –  The aims were to study if the type and complexity of Parkinsonian symptoms, as well as treatment, could be related to the occurrence and severity of later depressive symptoms. Furthermore, the aim was to study if there is a different depressive symptomatology in Parkinson’s disease (PD) patients compared with depressive illness in an age-matched group of patients with major depression but without Parkinson’s disease. Methods –  Eleven PD-patients with major depression (MD) were compared to 14 PD-patients without depression and to 12 MD patients without PD. Results –  PD patients who later developed a depressive illness were younger at the debut of PD than patients without depression (P < 0.05). At inclusion the depressed PD patients were more disabled than PD patients without depression with higher level in the H&Y scale (P<0.05), and they had more involuntary movements according to Unified Parkinson’s Disease Rating Scale (UPDRS IV) (P < 0.01). A family history of depression was found in one third of the depressed non-parkinsonian patients but in none of the PD groups. Sleep disturbances were significantly more common among depressed PD patients than in PD patients without depression but even more common in depressed patients without PD. Conclusions –  Depressed PD patients had a longer duration of PD and more severe motor symptoms than PD patients without depression, although tremor as an initial symptom seemed to be more common in PD without a later depression. It cannot be excluded that depression in PD reflects a more advanced and widespread neurodegeneration, including serotonergic as well as dopaminergic neurons. Sleep disturbances is common and could be overlooked as an expression of depression.

  • Depressive illness in Parkinson’s disease – indication of a more advanced and widespread Neurodegenerative Process?
    Acta neurologica Scandinavica, 2008
    Co-Authors: Sven Pålhagen, Martin Carlsson, E. Curman, Jan Wålinder, Ann-kathrine Granérus
    Abstract:

    Objective –  The aims were to study if the type and complexity of Parkinsonian symptoms, as well as treatment, could be related to the occurrence and severity of later depressive symptoms. Furthermore, the aim was to study if there is a different depressive symptomatology in Parkinson’s disease (PD) patients compared with depressive illness in an age-matched group of patients with major depression but without Parkinson’s disease. Methods –  Eleven PD-patients with major depression (MD) were compared to 14 PD-patients without depression and to 12 MD patients without PD. Results –  PD patients who later developed a depressive illness were younger at the debut of PD than patients without depression (P < 0.05). At inclusion the depressed PD patients were more disabled than PD patients without depression with higher level in the H&Y scale (P

Chigumi Ohtsuka - One of the best experts on this subject based on the ideXlab platform.

  • increased mitochondrial oxidative damage and oxidative dna damage contributes to the Neurodegenerative Process in sporadic amyotrophic lateral sclerosis
    Free Radical Research, 2008
    Co-Authors: Takahiko Murata, Chigumi Ohtsuka, Yasuo Terayama
    Abstract:

    To investigate the possibility that mitochondrial oxidative damage or oxidative DNA damage or both contribute to the Neurodegenerative Process of sporadic amyotrophic lateral sclerosis (sALS), this study used high-performance liquid chromatography with an electrochemical detector to measure the concentrations of the reduced and oxidized forms of coenzyme Q10 (CoQ10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 17 patients with sALS and 17 age-matched controls with no neurological diseases. The percentage of oxidized CoQ10 in the CSF of sALS patients was greater than that in the CSF of controls (p<0.002) and was negatively correlated with the duration of illness (rho=-0.61, p<0.01). The concentration of 8-OHdG in the CSF of sALS patients was greater than that in the CSF of controls (p<0.005) and was positively correlated with the duration of illness (rho=0.53, p<0.005). The percentage of oxidized CoQ10 was correlated with the concentrations of 8-OHdG in the CSF of sALS patients (rho=-0.53, p<0.05). These results suggest that both mitochondrial oxidative damage and oxidative DNA damage play important roles in the pathogenesis of sporadic amyotrophic lateral sclerosis.

  • Increased mitochondrial oxidative damage and oxidative DNA damage contributes to the Neurodegenerative Process in sporadic amyotrophic lateral sclerosis.
    Free radical research, 2008
    Co-Authors: Takahiko Murata, Chigumi Ohtsuka, Yasuo Terayama
    Abstract:

    To investigate the possibility that mitochondrial oxidative damage or oxidative DNA damage or both contribute to the Neurodegenerative Process of sporadic amyotrophic lateral sclerosis (sALS), this study used high-performance liquid chromatography with an electrochemical detector to measure the concentrations of the reduced and oxidized forms of coenzyme Q10 (CoQ10) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the cerebrospinal fluid (CSF) of 17 patients with sALS and 17 age-matched controls with no neurological diseases. The percentage of oxidized CoQ10 in the CSF of sALS patients was greater than that in the CSF of controls (p