Mitochondrial Dysfunction in Parkinson’s Disease: From Mechanistic Insights to Therapy

Published on June 20, 2022

Imagine a bustling city with a brilliant, electric energy. But deep within, there’s a glitch in the power grid that threatens to plunge the entire city into darkness. This is similar to what happens in Parkinson’s disease (PD), where a faulty powerhouse called the mitochondrion wreaks havoc on the brain. Mitochondrial dysfunction, which impairs the energy production needed for the brain’s movement-controlling neurons, is at the heart of PD. Just like fixing the power grid is crucial to restoring order and functionality to a city, understanding and repairing mitochondrial dysfunction holds promise for treating PD. Scientists have discovered specific genes associated with familial PD and factors linked to sporadic PD that contribute to mitochondrial dysfunction. They have also delved into how the maintenance of mitochondrial quality control is disrupted in PD. Excitingly, researchers are exploring therapeutic strategies that target mitochondria to protect neurodegeneration in PD. By unraveling and addressing this key player in the disease, we may open doors to innovative treatments and interventions that could halt or slow down its progression. To find out more about this fascinating area of research, dive deeper into the full article!

Parkinson’s disease (PD) is one of the most common neurodegenerative movement disorders worldwide. There are currently no cures or preventative treatments for PD. Emerging evidence indicates that mitochondrial dysfunction is closely associated with pathogenesis of sporadic and familial PD. Because dopaminergic neurons have high energy demand, cells affected by PD exhibit mitochondrial dysfunction that promotes the disease-defining the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The mitochondrion has a particularly important role as the cellular “powerhouse” of dopaminergic neurons. Therefore, mitochondria have become a promising therapeutic target for PD treatments. This review aims to describe mitochondrial dysfunction in the pathology of PD, outline the genes associated with familial PD and the factors related to sporadic PD, summarize current knowledge on mitochondrial quality control in PD, and give an overview of therapeutic strategies for targeting mitochondria in neuroprotective interventions in PD.

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