Creutzfeldt Jakob Disease Research Paper

Cerebrovascular disease, also known as vascular dementia, is the second to most common form of dementia. It is characterized by blood vessels changing over time in the cerebrum (brain). The most common reason for vascular dementia is due to aging of the body; but it is also tied to cholesterol and the state of the walls of the blood vessels. Too much cholesterol and overall poor health of blood vessels can cause a thickness in the lining of the vessel walls, therefore cutting off some of the blood flow to the brain.

Chronic Traumatic Encephalopathy or CTE is a degenerative disease that is caused by sports just as ALS, but commonly diagnosed in people with the extra gene called the Tauopathy protein also known as the tau protein. Tau protein is an extra gene that could

CTE also know as Chronic Traumatic Encephalopathy is a disease in which it affects the brain from repeated head traumas. CTE often occurs in athletes which have experienced concussions or any other type of trauma. In CTE, there is a protein called Tau forms clumps. These forms slowly spread throughout the brain killing many different brain cells which then affects the whole entire brain. This condition can happen to anyone at any age, ages as young as 17 included. Autopsy are usually performed on these people who have experienced a CTE to learn more about what happened to these people and why has it happened to these people. This disease is still not well understood because it is such a rare condition. Not many people know about this condition,

This week may be the last week I write to you. In my last letter to you, you may have noticed that I seemed depressed and not like myself. I wasn’t completely truthful in that letter. I’m not just having a bad day, I’m diseased with an incurable, fatal disease.

Acute disseminated encephalomyelitis is an immune-mediated inflammatory demyelinating condition that affects the white matter of the brain and spinal cord. ADEM also attacks the nerves of the central nervous system and damages their myelin insulation, which destroys the white matter. It is often triggered after the patient has received a viral infection or sometimes exceedingly rarely specific non-routine vaccinations. It affects children more than adults but can affect anyone. More than half of patients have an illness usually an infection two to four weeks before developing ADEM. Most of these illnesses are viral or bacterial, often no more than an upper respiratory tract infection. In children with ADEM, prolonged and severe headaches occur. In addition, the patient develops fevers during the ADEM course.

Magnetic Resonance Imaging (MRI) is used to show the borders of white and gray matter in the brain. This can help to differentiate AD from multi infarct dementia and low pressure hydrocephalus based on the ratios of white and gray matter. A person with AD suffers from a loss of gray matter, thus making the ratio of gray to white matter smaller than in a person without AD. An exam of the body fluid and non-neural tissue can be helpful to differentiate between AD and other disorders and infections that cause changes in the blood and CSF. These tests also help to demonstrate the functionality of neurotransmitters, metabolites, and enzymes. Although these tests are useful, the only way to confirm that a patient definitely has AD is by autopsy

Chronic Wasting Disease (CWD) is a brain disease in deer related animals that produces small lesions in the brains of diseased animals (CWD-Info 2013). Lesions are an area of severe tissue change in the brain (CWD-Info 2013). The lesions can range from harmless to very serious cases (CWD-Info 2013). Infectious parts of CWD are neither bacteria or viruses, but are thought as prions (CWD-Info 2013). Prions are dangerous proteins without nucleic acids (CWD-Info 2013). The prions break down the tissue in the brain to the point that they turn into lesions. CWD is shown by loss of body size, behavioral activities and possible death (CWD-Info 2013).

Thus we proceed through clinical description and classification, neuropathology, neurophysiology, immunology, and imaging, with a hint of genetics. The continuing critical theme is neuropathology. From the clinician's point of view the development of magnetic resonance imaging has been key to allowing more precise diagnosis as well as surrogate markers for clinical trials. Until very recently there has been no effective treatment, although a wide range of treatments have been used. It is surprising to see that the current use of steroids for acute relapses is quite recent (high-dose intravenous methylprednisolone replacing corticotropin in the early 1980s, following the pattern of usage by rheumatologists), with the first major controlled trial to demonstrate efficacy of the regimen published in 1987. Interferons, discovered in the 1950s, were initially promoted as a treatment for cancer. In 1977 Lawrence Jacobs of Buffalo, NY, was offered a returned supply of interferon (produced from the foreskin of recently circumcized infants). He was initially interested in using this for the rapidly progressive and fatal illness amyotrophic lateral sclerosis (motor neuron disease) but chose to study multiple sclerosis since there were more patients available. The Food and Drug Administration approved the first interferon for treatment of multiple

They looked at the autopsy reports and the preserved brain samples and realized that the disease was similar to autoimmune brain diseases seen in humans. Brain samples revealed antibodies to the NMDA receptor, indicating an attack by Knut’s own immune system. Since very little was known about the autoimmune origin of encephalitis, and only now have diagnostic tests been developed for humans, Knut’s diagnosis was implausible at the time of his death. Today, once the bacterial and viral reasons are ruled out, the anti-NMDA receptor autoimmune condition is checked for as the next likely candidate in diagnosing encephalitis. Solving Knut’s case brought the similarities between the human and animal manifestations of this disorder to

Variant Creutzfeldt-Jakob disease is an infectious and transmittable form of a prion, although extremely rare it still becomes highly fatal if infected. This disease can also be classified as a Transmissible Spongiform Encephalopathy (TSE) that is gained through exposure to the Bovine Spongiform Encephalopathy (BSE) from contaminated cattle or meat. As this is not a prominently spread disease around the world and considering it was only recognised in 1996 it has only held 175 cases in the United Kingdom, 25 in Spain, 4 in Ireland, 3 in the Netherlands and the United States of America, 2 each in Canada, Italy and Portugal as well as 1 each in japan, Saudi Arabia and Taiwan (World Health Organization, 2012).

In most cases encephalitis is misdiagnose as a flu because of its flu-like-symptoms. Most people, who has viral encephalitis, either present no symptoms and sings or present mild flu-like symptoms, such as headache, fever, aches in muscles and joints, fatigue, or weakness. However, people with a more severe infection of encephalitis may present more serious symptoms and sings, such as confusion, agitation, hallucinations, seizures, loss of sensation or paralysis in certain areas of the face or body, and problems with speech or hearing (Mayo Clinic

Alpha-synuclein is one of three members of the synuclein family of proteins, which is further comprised of beta-synuclein, encoded by SNCB on chromosome 5q35, and gamma-synuclein, encoded by SNCG on chromosome 10q23. Structurally, alpha-synuclein is 140 amino acids long and consists of three domains: an N-terminal KTKEGV repeat region, a central hydrophobic non-amyloid component (NAC) region, and an acidic C-terminal region (Figure 1.1). At low concentrations, alpha-synuclein exists in its native random coil, unfolded conformation. However, the N-terminal domain (residues 1 – 60) of alpha-synuclein undergoes a conformational shift from random coil to alpha-helical structure, enabling alpha-synuclein to interact with small vesicles containing acidic phospholipids. While the A53T mutation has no observable effect on this lipid binding property of alpha-synuclein, the A30P mutation disrupts, and the E46K mutation enhances the ability of alpha-synuclein to bind lipids. It remains to be determined if and how the more recently identified pathogenic substitutions, A18T, A29S,

Have you ever heard of mad cow disease? It is not what you think it is. It is a prion disease. Prion diseases are categorized as a group of disorders caused by abnormally shaped proteins called prions, it occurs in both humans and animals. One of the most common types of human prion diseases is sporadic Jakob-Creutzfeldt disease, also known as Creutzfeldt-Jakob disease, CJD, or Jakob-Creutzfeldt disease. The cannibal tribe, known as the Fore people in Papua New Guinea, is immune to Kuru, another type of prion disease. Many people are affected by a prion disease. If it is you has the disease, or if your animals have a prion disease, you are affected, and you are impacted. Many people believe that Creutzfeldt-Jakob disease should be named Jakob-Creutzfeldt

The disease I have chosen to explore is viral encephalitis. Encephalitis refers to brain inflammation (PDR, 2014, Diagnosis), which is rare but can be extremely dangerous (Mayo, 2014, Basics; University of Maryland, 2013, Introduction). Severe cases of encephalitis can lead to permanent damage and death (Mayo, 2014, Complications). Encephalitis can also be caused by bacteria and fungi, or develop as a result of a non-infectious cause, but encephalitis is usually caused by a virus (Mayo, 2014, Causes; PDR, 2014, Basics).

In, “Sporadic Creutzfeldt-Jakob disease with unusual initial presentation as posterior reversible encephalopathy syndrome: a case report”, a study was conducted to show the relationship between Creutzfeldt-Jakob disease (CRD) and posterior reversible encephalopathy syndrome (PRES). CRD is an aggressive neurodegenerative prion disease that leads to dementia and later death. The patient in this case study was a 53 year old woman with no prior neurological health conditions. There were no previous family members that had dementia. The patient was treated with sudden blurred vision, dizziness, disturbed gait and coordination impairment. Two weeks after the patient complained of those symptoms, the patient was admitted to the Department of Neurology