Abstract
Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. To date, there is no effective treatment that halts its progression. Increasing evidence indicates that mitochondria play an important role in the development of PD. Hence mitochondria-targeted approaches or agents may have therapeutic promise for treatment of the disease. Neuropeptide CART (cocaine-amphetamine-regulated transcript), a hypothalamus and midbrain enriched neurotransmitter with an antioxidant property, can be found in mitochondria, which is the main source of reactive oxygen species. Systemic administration of CART has been found to ameliorate dopaminergic neuronal loss and improve motor functions in a mouse model of PD. In this article, we summarize recent progress in studies investigating the relationship between CART, dopamine, and the pathophysiology of PD, with a focus on mitochondria-related topics.
Highlights
Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease (AD), is a severe, progressive disease that affects approximately 1-2% of persons older than 40 years of age [1]
Given the important role that mitochondria play in neuronal function, survival, and protection of CART from ischemia, our results strongly suggest an interaction between CART and SDH as a mechanism of neuroprotection [10]
Using a neuroprotective mouse model for PD, we found that pre-treatment of mice with CART, followed by daily administration of the neurotoxin MPTP for 7 days, resulted in a reduced loss of dopamine nerve cells in the substantia nigra pars compacta, compared to mice that were treated only with the MPTP [11]
Summary
Parkinson’s disease (PD), the second most common neurodegenerative disorder after Alzheimer’s disease (AD), is a severe, progressive disease that affects approximately 1-2% of persons older than 40 years of age [1]. It is characterized by muscle rigidity, tremor, a slowing of physical movement, and in extreme cases, a loss of physical movement. We found that the brain-rich neuropeptide CART (cocaine- and amphetamine- regulated transcript) is preferentially localized to mitochondria with both mitochondria activating and antioxidative properties in vitro and in vivo [10,11] These findings suggest that CART may be a new candidate for therapeutic agents targeting PD. We summarize recent progress made in investigating characteristics of CART as a potential therapeutic agent for PD, focusing on CART in relationship to mitochondria function
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