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What is Parkinson's disease? Parkinson's disease PD is a degenerative disorder of the central nervous system that belongs to a group of conditions called movement disorders.
It is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. As nerve cells neurons in parts of the brain become impaired or die, people may begin to notice problems with movement, tremor, stiffness in the limbs or the trunk of the body, or impaired balance.
As these symptoms become more pronounced, people may have difficulty walking, talking, or completing other simple tasks. Not everyone with one or more of these symptoms has PD, as the symptoms appear in other diseases as well. The precise cause of PD is unknown, although some cases of PD are hereditary and can be traced to specific genetic mutations.
Most cases are sporadic—that is, the disease does not typically run in families. It is thought that PD likely results from a combination of genetic susceptibility and exposure to one or more unknown environmental factors that trigger the disease. While most forms of parkinsonism have no known cause, there are cases in which the cause is known or suspected or where the symptoms result from another disorder.
No cure for PD exists today, but research is ongoing and medications or surgery can often provide substantial improvement with motor symptoms.
What causes the disease? Parkinson's disease occurs when nerve cells, or neurons, in the brain die or become impaired. Although many brain areas are affected, the most common symptoms result from the loss of neurons in an area near the base of the brain called thesubstantia nigra. Loss of dopamine results in abnormal nerve firing patterns within the brain that cause impaired movement.
Norepinephrine, which is closely related to dopamine, is the main chemical messenger of the sympathetic nervous system, the part of the nervous system that controls many automatic functions of the body, such as pulse and blood pressure.
The loss of norepinephrine might explain several of the non-motor features seen in PD, including fatigue and abnormalities of blood pressure regulation.
The affected brain cells of people with PD contain Lewy bodies—deposits of the protein alpha-synuclein. Researchers do not yet know why Lewy bodies form or what role they play in the disease.
Additional studies have found evidence that clumps of protein that develop inside brain cells of people with PD may contribute to the death of neurons.
Some researchers speculate that the protein buildup in Lewy bodies is part of an unsuccessful attempt to protect the cell from the toxicity of smaller aggregates, or collections, of synuclein. Scientists have identified several genetic mutations associated with PD, including the alpha-synuclein gene, and many more genes have been tentatively linked to the disorder.
Studying the genes responsible for inherited cases of PD can help researchers understand both inherited and sporadic cases. The same genes and proteins that are altered in inherited cases may also be altered in sporadic cases by environmental toxins or other factors.
Researchers also hope that discovering genes will help identify new ways of treating PD. Exposure to certain toxins has caused parkinsonian symptoms in rare circumstances such as exposure to MPTP, an illicit drug, or in miners exposed to the metal manganese. Other still-unidentified environmental factors may also cause PD in genetically susceptible individuals.
Several lines of research suggest that mitochondria may play a role in the development of PD. Mitochondria are the energy-producing components of the cell and abnormalities in the mitochondria are major sources of free radicals—molecules that damage membranes, proteins, DNA, and other parts of the cell.
This damage is often referred to as oxidative stress. Oxidative stress-related changes, including free radical damage to DNA, proteins, and fats, have been detected in the brains of individuals with PD.
Some mutations that affect mitochondrial function have been identified as causes of PD. While mitochondrial dysfunction, oxidative stress, inflammation, toxins, and many other cellular processes may contribute to PD, the actual cause of the cell loss death in PD is still undetermined.
What genes are linked to Parkinson's disease? Several genes have been definitively linked to PD. The first to be identified was alpha-synuclein. In the s, researchers at National Institutes of Health and other institutions studied the genetic profiles of a large Italian family and three Greek families with familial PD and found that their disease was related to a mutation in this gene.
They found a second alpha-synuclein mutation in a German family with PD. These findings prompted studies of the role of alpha-synuclein in PD, which led to the discovery that Lewy bodies seen in all cases of PD contain alpha-synuclein protein. This discovery revealed the link between hereditary and sporadic forms of the disease.
Inresearchers studying inherited PD discovered that the disease in one large family was caused by a triplication of the normal alpha-synuclein gene on one copy of chromosome 4 a chromosome is a threadlike structure of a protein and the genetic material DNA.
This triplication caused people in the affected family to produce too much of the normal alpha-synuclein.A what is the discussion section of a research paper research paper is a piece of corporate branding research paper academic writing based on its authors free research paper on steroid original write research paper alzheimers disease research on a particular topic, and the research papers on educational leadership analysis and.
Writing style and dementia Bill Poser cites a study of Iris Murdoch's last novel which "raises the possibility that changes in a person's vocabulary could be used to diagnose Alzheimer's disease while it is still in its early stages".
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