The Effect Of Prions In Seeds Of Dementia

1.1 Dementia is an umbrella term for a range of diseases that affect memory, behaviour and motor skills. The causes vary depending on the disease but largely the presence of “plaques” and “tangles” on the neurons of the brain is found in people with Alzheimer’s. Plaques are protein that the body no longer breaks down and allows to build up; these get between the neurons and disrupt the message transmission. Tangles destroy a vital cell transport system made of proteins. The transport system is organised in orderly parallel strands like rail tracks. In healthy areas a protein call “tau” helps the tracks stay straight but in areas where tangles

Proteinaceous Infectious Particles, commonly known as Prions, are extremely rare misfolds of the protein PrPc, which cause fatally neurodegenerative diseases, and are theorized to be infectious only by the protein itself (U.S National Library of Medicine, 1998). This “protein-only theory” is still heavily debated today, as some scientists deny the theory, and there isn’t a significant amount of evidence on each side to qualify the theory or disprove it (Soto, C. 2011). The base “Prion” protein is encoded in the gene PRNP, while being non-infectious. Prions are most commonly found in human prion diseases, but they can also be in other animals in the form of Mad Cow Disease and Chronic Wasting Disease, classified as Bovine Spongiform Encephalopathies

Humans have to deal with many different diseases and the ones most disliked are the ones with no cures. Like cancer, transmissible spongiform encephalopathies have no cure, but they are more rare. These diseases are prion diseases which cause the brain to deteriorate. Prions are proteins that sometimes behave like viruses, which mean that they should have some form of nucleic acid, but since they don’t, they cause abnormalities. The nervous system contains many normal prions, but when an abnormal prion comes along, it transforms all the normal prions into abnormal ones. Bovine spongiform encephalopathy is found in cattle, but it can be transmitted to humans.

Even today, after so much study, Alzheimer’s is not fully understood. However, researchers do agree that this degenerative disease is caused by the gradual buildup of fibrous protein compounds in the brain, which are known in the scientific world as amyloids. These amyloids in the brain area act like plaque and as a result of their presence, the normal brain functioning is disrupted.

Alzheimer's and dementia is one of the many diseases that affects the nervous system, particularly the brain. Acute memory loss is known as dementia. Thus, Alzheimer's is a severe form of dementia. The diagnosis is the brain lacking brain cells and connections due to degradation. Symptoms of Alzheimer's includes memory loss which can range from minor to severe as well as confusion which directly corresponds to memory loss. Groups of nerves work together to focus on specific jobs such as communication and memory. The brain cells work together and “receive supplies, generate energy, construct equipment and get rid of waste.” Alzheimer's is believed to prevent parts of the cell to not function properly. Scientists are not thoroughly sure where the cells malfunction begins. As the cell continues to divide and spread, the infected cells begin to die off leading to damaged brain connections. Scientists believe that plaques and tangles are the cause of the disease. Plaques are “deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells.” Tangles are “twisted fibers of another protein called tau that build up inside cells.” Age results in developed plaques and tangles though, Alzheimer patients have an abnormal amount of these

The causes of Alzheimer’s disease are still for the most part unknown. Scientists can’t quite pinpoint the exact causes of Alzheimer’s. But for the last twenty years the cause getting the most attention is that it is caused by an excess amount of insoluble fragments of beta-amyloid, then that leads to the loss of connection between brain cells, then eventually the death of said brain cells. (American Scientist, 44)

It is a disease that we haven’t cured yet but instead have only come up and still coming up with treatment strategies to alleviate its symptoms. AD was first described in 1906 by a German psychiatrist by the name of Alois Alzheimer whilst he was performing a histophathologic study of his patient’s brain, a patient who had been suffering from dementia. His patient’s brain’s autopsy brought to light the presence of two types of lesions, which are senile plaques and neurofibrillary tangles. He saw a visible difference in the brain tissue for it was severely damaged by these lesions. Since then, our knowledge of AD’s cellular and molecular alterations has increased and we have come up with various hypotheses for AD that may soon help in developing effective preventative and therapeutic strategies. One of the most prevailing hypotheses that have already leaded to a number of therapeutic approaches is the amyloid cascade hypothesis. Hence, the following essay will explore the pathology of the amyloid cascade hypothesis and the evidence for and against it. It will also touch upon current progress in clinical trials that test the

The aggregation of prion proteins and their transmissibility from one cell to another has been shown to be evident (Cushman et al.; Goedert et al. 2010), therefore strongly suggesting that these events may play a role in pathogenesis for many diseases, including both AD and PD. While none of these diseases is infectious in an identical way as

Several societies celebrate their elderly population. These cultures include Native Americans, Koreans, and African Americans. (Huffington Post, 2015) Conversely, there are distinct changes to this paradigm once an individual is diagnosed with Alzheimer’s disease. These individuals may be made to feel inferior, treated like children, or ignored altogether. A derivative type of protein, A has been shown to be present in the early onset of Alzheimer’s disease. This presence of this element is thought, “…to initiate a pathogenic cascade ultimately leading to neuronal loss and dementia.” (Doody & Allsop, 1991) Though this explanation is vastly oversimplified, it represents a complex disease progression that, although continually researched, is still not entirely understood.

Alzheimer 's disease is a non curable progressive condition caused by the degeneration of neurons, the main cellular component of the central nervous system. This degeneration is believed to be caused by a build up and entanglement of the functional proteins within and around the neuron. However, the exact cause of neuron

Prions are a type of protein found naturally in the brain and other regions of the central nervous system. The diseases associated with

Throughout this book are very interesting things to learn about prions and their effect on both livestock and humans. The perspective of many different scientists who tackled the problem was also shown. This book includes their successes their failures and now it is time to analyze the all of the information. What made these diseases, created by malicious malformed proteins, become such timeless pandemic? How are they transmitted? How is it possible for them to jump between species?! As the book shows, these questions are not easily answered but at least there are the brilliant minds of the scientists like Gajdusek and Prusiner to assist those who would analyze the information on prions.

The cellular prion protein (PrPC) is a host-coded glycoprotein attached to the surface of the cell membrane by a glycosyl-phosphatidylinositol (GPI) anchor. PrPC binds copper with high affinity and is highly expressed on the surface of neuronal and glial cells (Prusiner, 1998; Sales et al., 1998). Although PrPC presumably plays a role in the neuropathology and transmissibility of prion diseases by undergoing a conformational change into an abnormal protease-resistant isoform (PrPSc) (Caughey and Chesebro, 2001; White et al., 2003), the normal physiologic role of PrPC is still uncertain. It has been reported that PrPC plays a diverse role in normal cellular functions including cell survival (Bounhar et al., 2001), neuritogenesis (Lopes et

Creutzfeldt-Jakob’s Disease affects one person in every million people per year worldwide. In the United States, there are about three-hundred cases per year, making Creutzfeldt-Jakob’s Disease a rare disease. However, once the brain is affected, this degenerative, debilitating disease progresses rapidly. The particles responsible for this rare, fatal disease are called prions. Prions are protienaceous infectious particles formed when normal proteins misfold and clump together, which causes the brain to be filled with tiny holes resembling a sponge.

"Our findings open the possibility that some of the sporadic Alzheimer's cases may arise from an infectious process, which occurs with other neurological diseases such as mad cow and its human form, Creutzfeldt-Jakob disease," said Dr. Claudio Soto, professor of neurology at the University of Texas. Creutzfeldt-Jakob disease (CJD) is a so-called "prion" disease - meaning it is caused by misshapen protein molecules scientists call prions. Prions slowly destroy