Home » The tau protein in Parkinson’s: unlike synuclein it would guide the initial alterations of movement

The tau protein in Parkinson’s: unlike synuclein it would guide the initial alterations of movement

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The tau protein in Parkinson’s: unlike synuclein it would guide the initial alterations of movement

Introduction

Parkinson’s disease affects approximately 10 million people worldwide. Each year, nearly 90,000 new cases of Parkinson’s disease are diagnosed in the United States. The progression of Parkinson’s disease involves distinct stages, and the timeline can vary significantly between individuals. The typical stages of Parkinson’s, as outlined by the Parkinson’s Foundation, can help patients understand changes as they occur. The disease affects people in different ways, and not everyone will feel all the symptoms or experience them in the same order or intensity. Some may experience changes over 20 years or more; for others, the disease progresses rapidly. The progression of the disease is influenced by a combination of several factors. After a diagnosis, many individuals experience a good response to medications such as levodopa, and this optimal time period can last for many years. As time passes, however, changes to medications are often necessary, and symptoms may intensify.

The molecular vision of Parkinson’s: new vs. old

In a new study, Jeffrey Kordower, director of ASU-Banner’s Neurodegenerative Disease Research Center, and his colleagues reveal fundamental insights into the progression of Parkinson’s disease, presenting new hope for patients battling this severely debilitating disease. The findings suggest that tau protein aggregates can initiate neuronal damage processes and death features of the disease. The findings challenge the conventional view of Parkinson’s disease pathology, which typically focuses on the protein alpha-synuclein as the classic diagnostic hallmark biomarker. The new study illustrates how tau pathology may be actively involved in the degeneration of dopamine-producing neurons in the brain, independent of alpha-synuclein. This revelation could shift the focus of research, diagnosis and treatment of this condition.

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A new vision: the role of the tau protein

A wide range of physical and mental symptoms characterize Parkinson’s disease. These include: rhythmic tremors, which often start in a limb, such as the hand or fingers; slowness of movement, which can lead to difficulty performing simple tasks; muscle stiffness or stiffness; and difficulty with balance. In addition to these physical symptoms, Parkinson’s disease can also cause various mental and emotional changes, including depression and anxiety, sleep disturbances, memory difficulties, tiredness, and emotional changes. Tau protein accumulates in two regions: the substantia nigra and the putamen, both part of the basal ganglia of the brain.

The substantia nigra is responsible for the production of dopamine, which is essential for modulating movement, cognitive executive functions and emotional limbic activity. The putamen, a component of the dorsal striatum, is involved in movement initiation, selection, and decision making, as well as learning, memory, language, and emotion. Dysfunction of the putamen can contribute to various disorders, particularly those related to motor function. The scientists conducted the study using post-mortem brain tissue from older adults who had experienced varying degrees of motor impairment.

The research analyzed brain tissues from individuals with no motor deficits, mild motor deficits with and without Lewy pathology in the nigra region of the brain, and individuals with a clinical diagnosis of Parkinson’s disease. Lewy bodies are abnormal aggregates of alpha-synuclein that accumulate in the brain and are a hallmark of numerous neurodegenerative disorders, including Lewy body dementia. In the case of Parkinson’s, Lewy bodies are found primarily in the substantia nigra, a region of the brain crucial for movement control, leading to characteristic motor symptoms such as stiffness, tremors, and slow movements.

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The study focused on a cohort of subjects with mild motor disabilities, not sufficiently pronounced to diagnose Parkinson’s, but still significant. By dividing these subjects based on the presence or absence of α-synuclein, the researchers found that tau pathology was a common denominator. The researchers observed that brain tissue associated with minimal motor deficit showed accumulations of tau similar to those in advanced Parkinson’s patients, suggesting that the role of tau occurs early in the evolution of the disease. These findings open the door to early diagnosis and intervention, potentially slowing or altering disease progression.

The research also sheds light on parkinsonism, a condition that mimics the symptoms of Parkinson’s disease but is distinct in its underlying mechanisms. The study suggests that tau pathology in the nigrostriatal region of the brain is a shared feature, offering a new lens through which to view and treat various forms of parkinsonism. The findings also highlight the potential of targeting tau pathology as a therapeutic approach in Parkinson’s disease. Because tau aggregation is related to motor deficits and degeneration of dopamine-producing regions of the brain, interventions aimed at reducing tau accumulation could offer new hope for altering the trajectory of the disease.

By Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

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Scientific publications

Chu Y et al. Brain. 2024 Feb; 147(2):444-457.

Lane-Donovan C et al. Neurotherapeutics. 2024 Jan 25:e00321.

Yang JY et al. Front Neurol. 2023; 14:1153305.

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