What Part Of The Body Does Parkinson's Disease Affect

What Part Of The Body Does Parkinson's Disease Affect – Parkinson’s disease (PD) is a neurological (nervous system) disease that affects the way you move. It is a progressive disease, meaning that it continually gets worse over time. There are treatments for PD, but it is not curable.

PD can also affect things other than muscles. It can cause constipation, problems urinating, depression, difficulty sleeping and cognitive problems, among other symptoms. These are known as non-motor symptoms.

What Part Of The Body Does Parkinson's Disease Affect

PD is caused by the destruction of nerve cells (neurons) in an area of ​​the brain called the substantia nigra. These neurons produce a chemical called dopamine, which they use to communicate with other neurons in the brain.

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As these dopamine-producing neurons die, they are not replaced. This causes less and less dopamine to be released to send messages. Doctors still do not know what causes dopamine-producing neurons to die in people with PD, although it is being studied.

The dopamine released by these neurons in the substantia nigra is very important in an area of ​​the brain called the basal ganglia. The basal ganglia help regulate body movement. When the basal ganglia receives less dopamine, it inhibits or suppresses the areas of the brain that promote body movement. This explains many of the motor symptoms of PD.

Norepinephrine (NE) is another chemical produced by the brain. In PD, the neurons that produce this chemical are also destroyed. NE is important in our sympathetic nervous system, which regulates our “fight or flight” response.

This can cause some of the other non-motor symptoms of PD, such as constipation, difficulty urinating, and difficulty regulating heart rate or blood pressure.

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As PD progresses, you may experience different symptoms. PD is a little different for everyone, but people tend to progress in a similar way. Doctors have divided PD into 5 stages based on symptoms:

Braak’s staging is another way of understanding how PD progresses based on brain pathology. However, this is a theory. There is evidence that this may be how PD works, but it is not confirmed.

The idea behind this staging is that the different symptoms of PD occur when different areas of the brain are damaged. Each stage correlates with a different area of ​​the brain. They look a little different from the clinical stages:

There was some evidence to support these stages. However, not all people living with PD follow Braak’s staging standards. Researchers are still studying this theory.

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If you think you or a loved one may have PD, or if you have questions about PD, talk to your doctor. The pathophysiology of Parkinson’s disease is the death of dopaminergic neurons as a result of changes in the biological activity of the brain in relation to Parkinson’s disease. disease (PD). There are several proposed mechanisms for neuronal death in PD; however, not everyone gets along well. Five main mechanisms proposed for neuronal death in Parkinson’s disease include protein aggregation in Lewy bodies, disruption of autophagy, changes in cellular metabolism or mitochondrial function, neuroinflammation, and breakdown of the blood-brain barrier (BBB) ​​that causes vascular leakage.

The first major proposed cause of neuronal death in Parkinson’s disease is the aggregation, or oligomerization, of proteins. The protein alpha-synuclein is increased in the brains of patients with Parkinson’s disease, and because α-synuclein is insoluble, it aggregates to form Lewy bodies (shown at left) in neurons. Traditionally, Lewy bodies were thought to be the main cause of cell death in Parkinson’s disease; however, more direct studies suggest that Lewy bodies lead to other effects that cause cell death.

Lewy bodies first appear in the olfactory bulb, medulla oblongata, and pontine tegument; Patients at this stage are asymptomatic. As the disease progresses, Lewy bodies develop in the substantia nigra, areas of the basal midbrain and forebrain, and the neocortex.

This mechanism is corroborated by the fact that α-synuclein lacks toxicity when it is not able to form aggregates; that heat shock proteins, which aid in the folding of aggregation-prone proteins, officially affect PD when overexpressed; and that reactions that neutralize aggregated species protect neurons in cellular models of α-synuclein overexpression.

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Alpha-synuclein activates ATM (ataxia-telangiectasia mutated), an important kinase that signals the repair of DNA damage. Alpha-synuclein binds to DNA double-strand breaks and facilitates the non-homologous d-splice DNA repair process.

That cytoplasmic aggregation of alpha-synuclein to form Lewy bodies reduces its nuclear levels, resulting in decreased DNA repair, increased DNA double-strand breaks, and increased programmed cell death of neurons.

The second major mechanism proposed for neuronal death in Parkinson’s disease, autophagy, is a mechanism by which internal components of the cell are broken down and recycled for use.

Autophagy has been shown to play a role in brain health by helping to regulate cell function. Disruption of the autophagy mechanism can lead to several different types of diseases, such as Parkinson’s disease.

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The third proposed cause of cell death in Parkinson’s disease is the mitochondrial energy-generating organelle. In Parkinson’s disease, mitochondrial function is disrupted, inhibiting energy production and leading to death.

The mechanism behind mitochondrial dysfunction in Parkinson’s disease is thought to be characterized in the PINK1 and Parkin complex, which has been shown to drive mitochondrial autophagy (also known as mitophagy).

PINK1 is a protein that is normally transported to mitochondria, but can also accumulate on the surface of deficient mitochondria. Accumulated PINK1 recruits Parkin; Parkin initiates the breakdown of dysfunctional mitochondria, a mechanism that acts as “quality control”.

In Parkinson’s disease, the genes encoding PINK1 and Parkin are thought to mutate in a way that impairs the ability of these proteins to break down dysfunctional mitochondria, leading to abnormal mitochondrial function and morphology and ultimately cell death.

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ROS are highly reactive molecules that contain oxygen and can disrupt functions within mitochondria and the rest of the cell. With increasing age, mitochondria lose their ability to scavenge ROS but still maintain their ROS production, leading to increased net ROS production and ultimately cell death.

Studies have shown that in the mitochondria and doplasmic reticulum, levels of alpha-synuclein and dopamine are likely involved in contributing to oxidative stress and PD symptoms. Oxidative stress appears to play a role in mediating separate pathological events that together lead to cell death in PD.

Oxidative stress leading to cell death may be the common dominant underlying multiple processes. Oxidative stress causes oxidative damage to DNA. This damage is increased in the mitochondria of the substantia nigra of PD patients and can lead to the death of nigral neuronal cells.

The fourth proposed mechanism of neuronal death in Parkinson’s disease, neuroinflammation, is generally understood for neurodegenerative diseases, but the specific mechanisms are not fully characterized for PD.

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One of the main cell types involved in neuroinflammation is microglia. Microglia are recognized as cells of the innate immune system of the central nervous system. Microglia actively explore their environment and significantly alter their cell morphology in response to neuronal injury. Acute inflammation in the brain is typically characterized by rapid activation of microglia. During this period, there is no peripheral immune response. However, over time, chronic inflammation leads to the breakdown of the blood-brain barrier and tissues. During this period, microglia generate reactive oxygen species and release signals to recruit peripheral immune cells for an inflammatory response.

In addition, microglia are known to have two main states: M1, a state in which the cells are activated and secrete pro-inflammatory factors; and M2, a state in which cells are deactivated and secrete anti-inflammatory factors.

Microglia are usually resting (M2), but in Parkinson’s disease they can be M1 due to the presence of α-synuclein aggregates. M1 microglia release proinflammatory factors that can cause motor neuron death. In this case, dead cells can release factors to increase the activation of M1 microglia, leading to a positive feedback loop that causes a continuous increase in cell death.

The fifth major mechanism proposed for cell death is blood-brain barrier (BBB) ​​breakdown. The BBB has three types of cells that tightly regulate the flow of molecules in and out of the brain: endothelial cells, pericytes, and astrocytes. In neurodegenerative diseases, BBB degradation has been measured and identified in specific brain regions, including the substantia nigra in Parkinson’s disease and the hippocampus in Alzheimer’s disease.

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Neuroinflammation protein or cytokine aggregates can interfere with cellular receptors and alter their function at the BBB.

In particular, vascular endothelial growth factor (VEGF) and VEGF receptors are believed to be dysregulated in neurodegenerative diseases. The interaction between the VEGF protein and its receptors leads to cell proliferation, but is thought to be disrupted in Parkinson’s disease and Alzheimer’s disease.

This causes the cells to stop growing and therefore prevents the formation of new capillaries through angiogenesis. Disruption of the cell receptor can also affect the ability of cells to bind to each other with adherens junctions.

Without the formation of new capillaries, existing capillaries break and cells begin to dissociate from each other. This, in turn, leads to the breakdown of gap junctions.

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Gap junctions in the endothelial cells of the BBB help prevent large or harmful molecules from entering the brain by regulating the flow of nutrients to the brain. However, as gap junctions break down, plasma proteins can penetrate the extracellular matrix of the brain.

This mechanism is also known as vascular leakage, where capillary degeneration leads to the “leakage” of blood and blood proteins into the brain. vascular

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