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Structural Damage to The Substantia Nigra of The Midbrain Dffects Sequential Working Memory in Parkinson's Patients

The Journal of Neuroscience published an online research paper entitled "The structural integrity of the substantia nigra in Parkinson's disease is related to sequential working memory". Combining neuromelanin-sensitive magnetic resonance imaging and task-state functional magnetic resonance imaging, studies have found that structural damage to the substantia nigra compact part of the midbrain affects the function of the basal ganglia and sequential working memory in patients with Parkinson's disease (PD).

PD is a common neurodegenerative disease in middle-aged and elderly people. Its core pathological feature is the degeneration and death of dopaminergic neurons in the substantia nigra compact area of the midbrain. It is mainly manifested by motor symptoms such as tremor, muscle rigidity, and slow movement, accompanied by cognition. A series of non-motor symptoms such as hypofunction, sleep disorders, and autonomic dysfunction. Cognitive impairment is one of the common non-motor symptoms of PD, which seriously affects the quality of life of patients. So far, there is no effective means to cure PD. Clinically, compound levodopa, dopamine receptor agonists and other drugs are mainly used to relieve motor symptoms.

People have to deal with a large amount of sequence information every day. When talking, they must decide what to say first and then what to say, and when working, they must decide what to do first and then do. In the brains of healthy adults, the prefrontal lobe-basal ganglia network is responsible for the processing of sequence information. The basal ganglia include important structures such as the striatum, globus pallidus, and subthalamic nucleus. The researchers found in previous work that the sequential working memory impairment of PD patients is related to the excessive activation of the subthalamic nucleus and the weakening of the functional connection between the subthalamic nucleus and the striatum.

In order to further explore the underlying mechanism of PD sequence working memory impairment, the study used neuromelanin-sensitive magnetic resonance imaging technology to detect the area of the neuromelanin high-signal area in the dense substantia nigra of the midbrain in 29 PD patients and 29 healthy controls.

Meanwhile, utilizing task-state functional magnetic resonance imaging technology, the behavior and brain activities of these subjects in the digital sequence task were detected. This task requires the subjects to remember 4 consecutive numbers in ascending order. In half of the trials, the numbers appear in ascending order, and the subjects only need to remember the original sequence. In the other half of the trial, the numbers appeared in a random order, and the subjects had to rearrange the numbers and remember the new sequence. The comparison of these two trials tested the subjects' ability to process and update sequence information.

The study found that compared with healthy controls, the neuromelanin high signal area of the substantia nigra compact in PD patients was significantly reduced, indicating that the structure of the substantia nigra compact in the patient was damaged. In the digital back task, compared with healthy controls, PD patients’ subthalamic nucleus was over-activated, and striatum and globus pallidus were under-activated. The functional connection between the substantia nigra of the midbrain and the subthalamic nucleus, striatum and globus pallidus gradually weakened.

In PD patients, the smaller the neuromelanin high signal area in the substantia nigra compact region of the midbrain, the weaker the activation of the striatum related to sequence processing, and the worse the ability to process sequence information. Although commonly used clinical anti-Parkinson drugs (such as dopamine receptor agonists) can regulate the activation of the subthalamic nucleus, they cannot effectively improve the sequence processing ability of PD patients.

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