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What Part Of Brain Does Parkinson Disease Affect

6 min read

What Part Of Brain Does Parkinson Disease Affect – When people talk about Parkinson’s disease, they may mention its effects on the substantia nigra. But did you know that there are other areas of the brain that are affected by this condition?

Parkinson’s disease is a condition that causes the gradual loss of dopamine-producing brain cells in the substantia nigra, the area of ​​the brain just above where the spinal cord meets the midbrain. It is these cells that produce and release the neurotransmitter dopamine, which plays a key role in turning thoughts into action.

What Part Of Brain Does Parkinson Disease Affect

While this definition of the condition is helpful in briefly explaining Parkinson’s disease, the full story is a bit more complicated. Over the past 30 years, it has become accepted that Parkinson’s disease also causes a number of non-motor symptoms, such as changes in sleep, smell, and even thinking, possibly involving other areas of the brain.

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Scientists are now looking at the wider effects of the condition on the brain in an effort to better understand why people experience different symptoms. The discovery could lead to new treatments that go beyond the motor symptoms of the condition.

The substantia nigra is an area of ​​the midbrain located at the top of the spinal cord and there has been a lot of work on the effects of Parkinson’s disease on the center of the brain.

There is a right and left black base, and often one part is affected before the other. Because of this, people with Parkinson’s disease often have symptoms mainly in one part of the body, especially in the early stages. Indeed, this common feature of the condition often helps distinguish Parkinson’s disease from other similar conditions.

When it comes to confirming a diagnosis, the black dye handed over for research is where pathologists look for changes in brain tissue at the end of life. And the loss of dopamine-producing cells in this area of ​​the brain, accompanied by clumps of the protein alpha-synuclein (known as Lewy bodies), has been a hallmark of Parkinson’s disease for decades.

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You can read more about the protein alpha-synuclein and how it plays a role in the spread of Parkinson’s disease in a previous blog post:

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The reason Parkinson’s disease causes movement symptoms is that the black color is part of a circuit called the basal ganglia that the brain uses to translate thought about movement into action.

Basal ganglia structures. Adapted from the work of Julianard, first obtained from Andrew Gillies, Mikael Haagström, and Patrick J. By Lynch, CC BY-SA 3.0

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The substantia nigra is the main regulator of the circuit, it communicates mainly with the chemical dopamine, but other chemical transmitters (glutamate and GABA) are also used to communicate between other areas of the basal ganglia.

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The balance of signals sent between these structures allows us to control movement. But as Parkinson’s disease progresses and brain cells that produce dopamine nigra are lost, movement symptoms appear. Without enough dopamine, it becomes more difficult to initiate and maintain movement, leading to symptoms such as slowness, stiffness, and freezing. And an imbalance of signals in the basal ganglia means that people with Parkinson’s disease can experience what’s called a resting tremor.

But while this is the description of Parkinson’s disease you find in most textbooks, it is now recognized that the changes are not limited to the substantia nigra and the basal ganglia.

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In Parkinson’s disease, other areas of the brain besides the substantia nigra are involved as the disease progresses. Changes in higher brain areas are associated with non-motor symptoms that can affect people with Parkinson’s disease later in life and often have a significant impact on quality of life.

For example, symptoms that affect memory and thinking can be linked to the presence of Lewy bodies in the largest area of ​​the brain, the cerebral cortex.

It is also thought to be associated with symptoms related to mood and pain, and similar changes in the temporal lobe, an area of ​​the brain involved in visual processing, are thought to be the cause of hallucinations.

But research into the spread of Parkinson’s disease in these areas and how we can stop it (such as protecting brain cells or targeting alpha-synuclein) is only part of the story. There is also ongoing research into where Parkinson’s disease starts and what the effects are before it reaches these areas.

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The presence of non-motor symptoms months and possibly even years before physical symptoms, such as tremors and slowness of movement, suggests the presence of other changes in the body long before the loss of dopamine-producing cells in the nigral. These early symptoms could also help researchers predict who will be diagnosed with Parkinson’s disease, leading to the development of new and better treatments.

Researchers have found that areas of the brainstem beneath the substantia nigra show a loss of cells in Parkinson’s disease. Cells in these areas were found to contain clumps of the protein alpha-synuclein, which may have formed before the cells of the substantia nigra.

Adapted from Patrick J. Based on work by Lynch, “The Prion Hypothesis in Parkinson’s Disease: Braak to the Future”, CC BY 2.5

These findings have led some researchers to believe that Parkinson’s disease spreads from the spinal cord to the substantia nigra. Indeed, there is evidence that in some, Parkinson’s disease may begin in the gut and travel along the vagus nerve, which connects the gut to the brain, to the substantia nigra.

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The theory that Parkinson’s disease can spread to the brainstem and progress throughout the brain is the basis of the Braak stage of Parkinson’s disease.

Although there is still debate about the origins of Parkinson’s disease, as well as competing and more complex theories about how Parkinson’s disease spreads, efforts to understand how and why different brain areas are involved in motor and non-motor symptoms are helping to make better progress. treatment.

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Dopamine is a chemical compound produced in the brain that acts as a neurotransmitter. This means that it transmits signals between nerve cells (neurons) and the brain. Not all neurons produce dopamine (only about 400,000 out of 85 billion!), and those that do, also called dopaminergic neurons, are found in certain areas of the brain, including:

Rewards can be actions, events, or stimuli that, for various (evolutionary or chemical) reasons, increase utility or pleasure and the release of dopamine in the brain. The main rewards are those that help species spread, such as food, water, sex, and a safe environment. Non-primary rewards are monetary, social or subjective derivatives. On closer analysis, they may be evolutionarily beneficial, but they usually require an immediate cost or sacrifice to delay gratification, making them distinct from primary benefits. Rewards can also be classified as intrinsic or extrinsic. Intrinsic rewards are those that are derived internally and are similar to non-primary rewards (passions, art, exercise, reading and research). Extrinsic rewards are those that depend on stimuli or events outside the self, usually materialistic or social, and share similarities with primary and non-primary rewards. All awards may be conditional or learned.

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Because primary and secondary rewards are pleasurable effects on the brain, they can lead to reward-seeking behaviors, including consummatory and approach behaviors (approaching the reward). The more often the reward is obtained and the dopamine is released, eventually the brain begins to adapt.

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