Heterogeneity of Letter Fluency Impairment and Executive Dysfunction in Parkinson's Disease

AbstractLetter fluency deficits are commonly detected in non-demented Parkinson's disease (PD) patients but the underlying cause remains uncertain. We investigated the role of slowed processing speed and executive dysfunction. Eighteen non-demented PD participants and nineteen controls were compared on letter fluency using a fluency index (Fi); the average time to “think” of each word, a measure independent of motor speed. Video analyses produced thinking times to switch between word clusters and generate a word within a cluster. Correlational and regression analyses were undertaken with tests of processing speed and executive functioning. The PD group exhibited significantly longer fluency indices than controls across all components. Performance on tests of executive functioning explained a significant proportion of variance whereas performance in processing speed tests did not. Moreover, PD participants with an executive functioning impairment showed significantly worse switching fluency indices only compared with Controls and PD participants without executive dysfunction. PD participants with executive dysfunction exhibited a disproportionate impairment in the time taken to switch between clusters than to think of words within clusters. Executive functioning contributed to fluency performance more than processing speed. Cognitive heterogeneity and motor slowing, may mask the profile of cognitive dysfunction in neurodegenerative disease. (JINS, 2013, 19, 1–9)

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Executive functioning and serum lipid fractions in Parkinson’s disease—a possible sex-effect: the PACOS study

Journal of Neural Transmission ◽

10.1007/s00702-022-02460-1 ◽

2022 ◽

Author(s):

Antonina Luca ◽

Roberto Monastero ◽

Calogero Edoardo Cicero ◽

Roberta Baschi ◽

Giulia Donzuso ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Executive Functioning ◽

Lipid Profile ◽

Serum Lipid ◽

Density Lipoprotein ◽

Positive Association ◽

Executive Dysfunction ◽

Lipoprotein Cholesterol ◽

Lipid Fractions

AbstractThe association between dyslipidemia and cognitive performance in Parkinson’s disease (PD) patients still needs to be clarified. Aim of the study was to evaluate the presence of possible associations between serum lipids fractions and executive dysfunction also exploring the sex-specific contribute of lipids level on cognition. Patients from the PACOS cohort, who underwent a complete serum lipid profile measures (total cholesterol-TC, low-density lipoprotein cholesterol-LDL, high-density lipoprotein cholesterol-HDL and triglycerides-TG) were selected. Adult Treatment Panel III guidelines of the National Cholesterol Education Program were used to classify normal/abnormal lipid fractions. Executive functioning was assessed with the Frontal Assessment Battery (FAB). Logistic regression was performed to assess associations between lipids fractions and FAB score. Correlations between lipids fractions and FAB score were explored. Sex-stratified analysis was performed. Three hundred and forty-eight PD patients (148 women; age 66.5 ± 9.5 years; disease duration 3.9 ± 4.9 years) were enrolled. Women presented significantly higher TC, LDL and HDL than men. In the whole sample, any association between lipid profile measures and FAB score was found. Among women, a positive association between hypertriglyceridemia and FAB score under cutoff was found (OR 3.4; 95%CI 1.29–9.03; p value 0.013). A statistically significant negative correlation was found between the FAB score and triglyceride serum levels (r = − 0.226; p value 0.005). Differently, among men, a statistically significant negative association between hypercholesterolemia and FAB score under cutoff (OR 0.4; 95%CI 0.17–0.84; p value 0.018) and between high LDL levels and FAB score under cutoff (OR 0.4; 95%CI 0.18–0.90; p value 0.027) were found. Our data suggest a sex-specific different role of lipids in executive functioning.

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The role of mitochondria-targeted antioxidant MitoQ in neurodegenerative disease

Molecular and Cellular Therapies ◽

10.13052/2052-8426-2018-01 ◽

2018 ◽

pp. 1-8

Author(s):

Linlin Zhang ◽

Aurelio Reyes ◽

Xiangdong Wang

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neurodegenerative Diseases ◽

Mitochondrial Dysfunction ◽

Neurodegenerative Disease ◽

Amyloid Β ◽

Amyloid Β Peptide ◽

And Oxidative Stress

Abstract: The discovery of charged molecules being able to cross the mitochondrial membrane has prompted many scholars to exploit this idea to find a way of preventing or slowing down aging. In this paper, we will focus on mitochondriatargeted antioxidants, which are cationic derivatives of plastoquinone, and in particular on the mitochondria-targeted antioxidant therapy of neurodegenerative diseases. It is well known that the accumulation of amyloid-β peptide (Aβ) in mitochondria and its related mitochondrial dysfunction are critical signatures of Alzheimer’ s disease (AD). In another neurodegenerative disease, Parkinson’s disease (PD), the loss of dopaminergic neurons in the substantia nigra and the production of Lewy bodies are among their pathological features. Pathogenesis of Parkinson’s disease and Alzheimer’s disease has been frequently linked to mitochondrial dysfunction and oxidative stress. Recent studies show that MitoQ, a mitochondria-targeted antioxidant, may possess therapeutic potential for Aβ-related and oxidative stress-associated neurodegenerative diseases, especially AD. Although MitoQ has been developed to the stage of clinical trials in PD, its true clinical effect still need further verification. This review aims to discuss the role of mitochondrial pathology in neurodegenerative diseases, as well as the recent development of mitochondrial targeted antioxidants as a potential treatment for these diseases by removing excess oxygen free radicals and inhibiting lipid peroxidation in order to improve mitochondrial function.

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The role of mitochondria-targeted antioxidant MitoQ in neurodegenerative disease

Molecular and Cellular Therapies ◽

10.26781/2052-8426-2018-01 ◽

2018 ◽

Vol 6 (1) ◽

Cited By ~ 2

Author(s):

Linlin Zhang ◽

Aurelio Reyes ◽

Xiangdong Wang

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Neurodegenerative Diseases ◽

Mitochondrial Dysfunction ◽

Neurodegenerative Disease ◽

And Oxidative Stress

The discovery of charged molecules being able to cross the mitochondrial membrane has prompted many scholars to exploit this idea to find a way of preventing or slowing down aging. In this paper, we will focus on mitochondria-targeted antioxidants, which are cationic derivatives of plastoquinone, and in particular on the mitochondria-targeted antioxidant therapy of neurodegenerative diseases. It is well known that the accumulation of amyloid-β peptide (Aβ) in mitochondria and its related mitochondrial dysfunction are critical signatures of Alzheimer’s disease (AD). In another neurodegenerative disease, Parkinson’s disease (PD), the loss of dopaminergic neurons in the substantia nigra and the production of Lewy bodies are among their pathological features. Pathogenesis of Parkinson’s disease and Alzheimer’s disease has been frequently linked to mitochondrial dysfunction and oxidative stress. Recent studies show that MitoQ, a mitochondria-targeted antioxidant, may possess therapeutic potential for Aβ-related and oxidative stress-associated neurodegenerative diseases, especially AD. Although MitoQ has been developed to the stage of clinical trials in PD, its true clinical effect still need further verification. This review aims to discuss the role of mitochondrial pathology in neurodegenerative diseases, as well as the recent development of mitochondrial targeted antioxidants as a potential treatment for these diseases by removing excess oxygen free radicals and inhibiting lipid peroxidation in order to improve mitochondrial function.

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The Role of Mental Imagery in Parkinson’s Disease Rehabilitation

Brain Sciences ◽

10.3390/brainsci11020185 ◽

2021 ◽

Vol 11 (2) ◽

pp. 185

Author(s):

Amit Abraham ◽

Ryan P. Duncan ◽

Gammon M. Earhart

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Neurodegenerative Disease ◽

Mental Imagery ◽

Future Research ◽

Motor Rehabilitation ◽

Research Directions ◽

Current Therapies ◽

Future Research Directions

Parkinson’s disease (PD) is a disabling neurodegenerative disease whose manifestations span motor, sensorimotor, and sensory domains. While current therapies for PD include pharmacological, invasive, and physical interventions, there is a constant need for developing additional approaches for optimizing rehabilitation gains. Mental imagery is an emerging field in neurorehabilitation and has the potential to serve as an adjunct therapy to enhance patient function. Yet, the literature on this topic is sparse. The current paper reviews the motor, sensorimotor, and sensory domains impacted by PD using gait, balance, and pain as examples, respectively. Then, mental imagery and its potential for PD motor and non-motor rehabilitation is discussed, with an emphasis on its suitability for addressing gait, balance, and pain deficits in people with PD. Lastly, future research directions are suggested.

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