As many as 10 million people worldwide are estimated to be living with Parkinson’s disease, a progressive neurological disorder that affects movement control. As the global population ages, Parkinson’s disease remains a significant public health concern, making ongoing medical research an urgent priority. Now, a new study published in the journal Brain may shed light on the progression of Parkinson’s disease, transforming the way medical professionals approach treatment.
Understanding Parkinson’s Disease Progression
Clinicians typically evaluate the progression of Parkinson’s disease in five distinct stages:
- Stage 1:Mild symptoms may include slight tremors and changes in gait. These symptoms generally will not interfere with daily life.
- Stages 2 and 3:Individuals can still live independently; however, symptoms such as tremors, postural instability, loss of balance, and stiffness may start to interfere with daily activities.
- Advanced Parkinson’s Disease (Stages 4 and 5):Individuals will likely need significant help with daily activities due to impaired mobility, tremors, and the risk of frequent falls. Individuals may also experience mood fluctuations and cognitive changes.
The progression of Parkinson’s disease can vary widely from person to person, with some individuals experiencing gradual changes over the course of decades. This highly individual progression is due to a number of factors, including genetic and environmental interference. But now, the aforementioned research led by Jeffrey Kordower, director of the ASU-Banner Neurodegenerative Disease Research Center, has identified another factor that could influence disease progression: the tau protein, which was already known to be associated with Alzheimer’s disease.
How the Tau Protein Contributes to Disease Progression
Kordower’s groundbreaking research centers on the tau protein, which is primarily associated with Alzheimer’s disease. In neurodegenerative conditions like Parkinson’s and Alzheimer’s diseases, abnormal tau protein is shown to accumulate in the brain, forming structures that contribute to cell death.
In Alzheimer’s disease, the tau protein mainly accumulates in two regions of the brain: the substantia nigra and putamen. The former is responsible for the production of dopamine, which helps regulate movement and cognitive executive function; the latter is crucial to motor function, as well as numerous cognitive processes. Now, in a fascinating twist, Kordower’s study suggests that the tau protein may be one of the earliest causes of neuronal damage and cell death in patients with Parkinson’s disease.
Re-Evaluating Parkinson’s Disease Pathology
Kordower’s team began by evaluating postmortem brain tissue from older adults with mild motor impairments that could be indicative of early-stage Parkinson’s disease. The researchers first checked the subjects for signs of α-synuclein, a protein that accumulates in the brains of individuals with neurodegenerative disorders including Parkinson’s. Specifically, they looked for Lewy bodies, which are abnormal accumulations of α-synuclein. But they found something surprising: Even in patients without Lewy bodies, researchers observed significant tau pathology in the brain tissue — significant enough to match those of people with advanced illness, suggesting that tau’s role occurs early in the disease’s evolution.
The new study suggests that the tau protein may be one of the earliest causes of neuronal damage and cell death in patients with Parkinson’s disease. Given that takeaway, tau intervention in the early stages of the illness could be crucial to slowing the disease’s progression.
Implications for Disease Treatment
Ultimately, the study challenges previous assumptions about Parkinson’s disease pathology. While further research is needed, one thing is certain: The previous focus on α-synuclein as a diagnostic hallmark of Parkinson’s disease may be misguided. With this in mind, scientists can dramatically shift the focus of Parkinson’s disease research and treatment, potentially improving outcomes for everyone affected by this disease.
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