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Prion diseases belong immunization to a group of progressive conditions that affect the nervous system both in humans and animals. In humans, prion diseases affect brain function influences the quality of memory, cause changes immunization in personality leading to impairment of intellectual function (dementia) and affect motor movements that worsen over time. Signs and symptoms of these conditions begin in adulthood, and these disorders can cause including death within a few months or even years. The family of prion diseases including Creutzfeldt-Jakob disease, Gerstmann-Straussler syndrome, fatal insomnia and Schneiker. These conditions form a wide range of disease signs and symptoms overlap.
PRNP gene mutations can cause prion diseases, but only a small percentage of genetically inherited prion diseases. Most cases are sporadic, meaning that occur in people with no known risk factors or genetic abnormalities. Rarely, prion diseases can be transmitted through accidental exposure to prion tissue following a medical procedure. This is called iatrogenic immunization prion disease. One of the types of prion disease is Creutzfeldt-Jakob disease can be contacted by eating beef infected with prions. In cows, this form of the disease is known as bovine spongiform encephalopathy or mad cow disease. Another example is acquired prion disease kuru, which was identified in an impoverished tribe in New Guinea. The disease was transmitted when tribesmen have eaten meat to people who have the disease during funeral rituals type cannibal. Familial forms of prion diseases are caused by mutations in the PRNP gene inherited. This gene contains information with which you can produce prion protein immunization (PrP). Normally, the protein is involved in the transport of copper in the cell. It can play an important role in protecting brain cells helping them to communicate. If the family of prion diseases occur PRNP mutations in genes that cause cells to produce an abnormal form of prion protein known as PrPSc. When the condition is iatrogenic or acquired, the affected person develops prion disease from exposure of this type of abnormal immunization protein. Following a process that is not fully understood by specialists, PrPSc has the ability to convert normal prion protein PrPC into more PrPSc. These abnormal proteins accumulate in the brain and are grouped into formations that damage or destroy nerve cells. The loss of these microscopic cells creates a spongy appearance of the brain, the main aspect of prion diseases.
Forms of prion diseases are inherited as an autosomal dominant immunization pattern, which means one copy is enough of an altered gene to develop the disease. In most cases, a person inherits the altered gene from affected parent. In some patients, familial immunization forms of prion diseases are caused by a mutation in the PRNP gene. Although such people often parents immunization are not affected, they can transmit the mutant gene to their children. Forms sporadic, iatrogenic and acquired prion diseases including kuru and Creutzfeldt-Jakob disease is not inherited.
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