Metabolic Syndrome: An Important Risk Factor for Parkinson’s Disease

Zhang, Pei; Tian, Bo

doi:10.1155/2014/729194

Cited by 62 publications

(62 citation statements)

References 100 publications

(81 reference statements)

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“…Many studies have shown that metabolic stress also causes dopaminereleasing neurons to prematurely die along with the cell death, leading to neuronal toxicity and subsequent onset of Parkinson's symptoms [92]. Further, a growing number of studies revealed that MetS like obesity in middle age individuals also augment the risk of PD and decrease life expectancy [93]. Additionally, adiposity and body mass index along with other risk factors also lead in the advancement of PD [94].…”

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 99%

“…Moreover, increasing inflammatory molecules, mitochondrial dysfunction, oxidative stress and lipid metabolism has all been shown to occur due to high-fat feeding. Most importantly, hypertension as a component of MetS is less frequent in PD, suggesting the need for exploring the possible link between PD and hypertension [93]. Furthermore, abnormalities in cholesterol homeostasis or lipid metabolism have also been associated with the neurodegenerative process of PD, and such abnormalities are occurred due to metabolic imbalances, injuries, therapeutics and autoimmune diseases [95].…”

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 99%

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Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

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

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Mounting evidence suggests a link between metabolic syndrome (MetS) such as diabetes, obesity, non-alcoholic fatty liver disease in the progression of Alzheimer's disease (AD), Parkinson's disease (PD) and other neurodegenerative diseases (NDDs). For instance, accumulated Aβ oligomer is enhancing neuronal Ca release and neural NO where increased NO level in the brain through post translational modification is modulating the level of insulin production. It has been further confirmed that irrespective of origin; brain insulin resistance triggers a cascade of the neurodegeneration phenomenon which can be aggravated by free reactive oxygen species burden, ER stress, metabolic dysfunction, neuorinflammation, reduced cell survival and altered lipid metabolism. Moreover, several studies confirmed that MetS and diabetic sharing common mechanisms in the progression of AD and NDDs where mitochondrial dynamics playing a critical role. Any mutation in mitochondrial DNA, exposure of environmental toxin, high-calorie intake, homeostasis imbalance, glucolipotoxicity is causative factors for mitochondrial dysfunction. These cumulative pleiotropic burdens in mitochondria leads to insulin resistance, increased ROS production; enhanced stress-related enzymes that is directly linked MetS and diabetes in neurodegeneration. Since, the linkup mechanism between mitochondrial dysfunction and disease phenomenon of both MetS and NDDs is quite intriguing, therefore, it is pertinent for the researchers to identify and implement the therapeutic interventions for targeting MetS and NDDs. Herein, we elucidated the pertinent role of MetS induced mitochondrial dysfunction in neurons and their consequences in NDDs. Further, therapeutic potential of well-known biomolecules and chaperones to target altered mitochondria has been comprehensively documented. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.

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Section: Amyotrophic Lateral Sclerosismentioning

confidence: 99%

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 99%

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Jha

Kumar

et al. 2017

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

View full text Add to dashboard Cite

show abstract

“…ER-mitochondria contact sites transfer Ca 2+ from ER to mitochondria to sustain cell metabolism and bioenergetics [28, 37, 38]. Recent studies suggest PD to be linked to other metabolic diseases, such as diabetes or metabolic syndrome [39]. For instance, epidemiological evidence links type 2 diabetes mellitus (T2DM) with the pathogenesis of PD, since mitochondrial dysfunction and ER-stress leads to insulin resistance [40].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial control of cell bioenergetics in Parkinson’s disease

Requejo-Aguilar

Bolaños

2016

Free Radical Biology and Medicine

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Parkinson disease (PD) is a neurodegenerative disorder characterized by a selective loss of dopaminergic neurons in the substantia nigra. The earliest biochemical signs of the disease involve failure in mitochondrial-endoplasmic reticulum cross talk and lysosomal function, mitochondrial electron chain impairment, mitochondrial dynamics alterations, and calcium and iron homeostasis abnormalities. These changes are associated with increased mitochondrial reactive oxygen species (mROS) and energy deficiency. Recently, it has been reported that, as an attempt to compensate for the mitochondrial dysfunction, neurons invoke glycolysis as a low-efficient mode of energy production in models of PD. Here, we review how mitochondria orchestrate the maintenance of cellular energetic status in PD, with special focus on the switch from oxidative phosphorylation to glycolysis, as well as the implication of endoplasmic reticulum and lysosomes in the control of bioenergetics.

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“…Inflammation and oxidative stress, the central mechanisms underlying MetS, are also putative pathogenetic mechanisms in PD . Given the integral role of oxidative stress and inflammation in the pathogenesis of both PD and MetS, it is not surprising that MetS may increase the risk of developing PD . In this review, we will consider the benefits of physical activity, including exercise, and the adverse metabolic effects of physical inactivity as they relate to Parkinson's disease risk and progression.…”

mentioning

confidence: 99%

The best medicine? The influence of physical activity and inactivity on Parkinson's disease

2016

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The incidence of Parkinson's disease (PD) is expected to increase as our population ages and will likely strain the projected capacity of our health care system. Despite being the most common movement disorder, there have been few noninvasive therapeutic advances for people with PD since the first levodopa clinical trial in 1961. The study of PD pathogenesis, combined with an appreciation for the biochemical mechanisms by which physical activity and exercise may impact physiology, has resulted in emerging hypotheses for new modifiable risk factors for PD. Physical activity and exercise as a means of preventing PD, or maintaining the functionality of people with PD, are a promising area of investigation. Conversely, physical inactivity is implicated in many disease states, some of which are also correlated with the development of PD, such as metabolic syndrome. The primary relationship between these diseases is likely rooted in heightened inflammation and oxidative stress at the cellular level. Physical activity and exercise as a means of attenuating inflammation have led to increased interest in related potential therapeutic targets for PD. Ultimately, these findings may translate into low‐cost, universally available therapies for PD disease modification or prevention. © 2016 International Parkinson and Movement Disorder Society

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Metabolic Syndrome: An Important Risk Factor for Parkinson’s Disease

Cited by 62 publications

References 100 publications

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration

Mitochondrial control of cell bioenergetics in Parkinson’s disease

The best medicine? The influence of physical activity and inactivity on Parkinson's disease

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