Fatal Insomnia Synthesis

In my paper, I will tackle insomnia from various perspectives: definitions, types, causes, effects, and means of solutions.

In the poem, “Insomnia” by Elizabeth Bishop, the speaker discusses her feelings and experiences of restlessness and loneliness during the night, instigated by her lover’s unrequited love. The poem explores the parallel between the speaker and the moon through their shared dissatisfaction with themselves and the speaker’s aspiration to achieve the strength of the moon. In the poem, the speaker recognizes her paralysis in her feminine role and conveys her desire to escape from the realities of a patriarchal society toward an inverted fantastical reality.

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.

In bovine spongiform encephalopathy (BSE), the disease is caused by the misfolding of proteins that cause proteins and peptides to develop a fibrillary structure. The PrPc is a correctly folded prion and the misfolded form is called PrPSc. BSE occurs when the normal PrPc come into contact with the toxic PrPSc and the normal prion takes on the shape of the PrPSc. The normal chaperones are unable to convert the PrPSc back to the normal form. The PrPSc now takes on the role of chaperone and the conversion of PrPc prions continue over and over. PrPSc, now being hydrophobic avoids the water of the inner cell and begin to accumulate and form plaques along the neuronal cell membranes. The aggregation of the prions on the cell membrane eventually lead to cell death which produces the sponge-like appearance in the brain of cattle infected with BSE (Thompson, 2014).

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

It is a rare, degenerative but fatal brain disorder affecting very a small fraction of persons. The symptoms usually arise at the age of 60 and the person dies within a year. Many researchers believe that this disorder is the result of an abnormal protein known as prion. About 5-10% cases reported in the United States share a genetic basis where this form of dementia is caused by a mutation in the gene for the prion protein. Patients with Creutzfeldt-Jakob disease suffer from the problems associated with muscle coordination, personality changes, impaired memory, judgment making, thinking disability and impaired vision. Other possible symptoms include insomnia and depression. In later stages the persons

Carol Everson first recorded the affects of lack of sleep in 1989 based on work with rats. Her findings showed that all the mice that were deprived of sleep died within a month. She also showed that sleep does not need to be deprived entirely to be deadly, the deprivation of deep sleep (rapid eye movement or REM) would also cause the rats to die. In Italy, a case had been recorded of a man dying within a few months of developing familial insomnia. In his case, an autopsy was performed on his brain after death and neuron deterioration in the thalamus was found. They did not determine if the deterioration had caused his insomnia or his death. However, the cause of the deterioration was found, and that cause was linked to prions which cause spongy deterioration in the brain. While prions causing mad cow disease are ingested from the environment, the prions found in the man’s brain had been inherited and passed down within

Another heavily studied model of a human prion like protein causing a neurodegenerative disease is the hnRNPA1 and A2/B1. This

The first new human prion is discovered in almost 50 years. Prions are misfolded proteins that make copies of themselves by inducing others to misfold, they multiply and cause disease. The resulting illness is MSA, a neurodegenerative disease similar to Parkinson's.

The prion protein (PrP) is unusual in that it has two stable isoforms. The cellular or normal form of the prion protein is termed PrPC, while the disease form is termed PrPSC. Sharing the same sequence of amino acids, or primary structure, PrPC and PrPSC differ in their secondary, tertiary, and quaternary structures. The normal prion protein has N- and C-terminals, three alpha helices, and two beta sheets (Soto, 2006, 40). Its function is still not completely understood. However, scientists have found evidence that point to various possibilities. 1) Because most PrPC are located in lipid rafts, membrane structures involved in signaling, it is suggested that PrPC may also be a mediator in neuroprotective signaling pathways. 2) Interaction between PrPC and Bcl-2, a ligand involved in protecting neurons from apoptosis, suggests the possibility that PrPC may be an antiapoptotic protein. 3) PrPC has also been linked to copper metabolism in the brain. In one particular study, PrP knockout mice, or mice that were genetically altered to not express PrP, were found to have lower levels of copper in their brains and higher levels in their serum (Soto, 2006, 42). However, in other studies with PrP knockout mice, most of the animals did not display any obvious disorders, and those that did were found to have been affected by the increase in concentration of another protein known as doppel.

Several different existing drugs have been created with intentions to treat prion diseases, to name a few, quinacrine and doxycycline have helped treat Prion Diseases. Although treatment is used in there has not been fully effective medication that completely eliminates the disease nor helps the victim recover completely. Antibodies against PrP could be one of the most potential treatments since they do protect against the prion protein our own body is creating. It is difficult for drugs to have an effect on prion diseased victims because the blood brain barrier only allows certain specimens to get through. Sporadic and genetic prion diseases in human begin in the brain inevitably forcing them to be untreatable because the immune system does

Insomnia is inspired by the state between wakefulness and dreaming, the state in which it is difficult to distinguish reality from nonrealaty. This condition is described confronting opposites of sound material: riversed and unriversed sounds, long continuous dramatic texture and sudden interruptions, as well as the separation of pure sound and hall using the unusual sound positioning of those elements. The composition is dominated by resonant sounds, interlaced with electronically generated sounds and instrumental sounds by building a homogeneous variable energy and light

Despite some speculation of scientific findings in regards to prion conversion, research continues. The prion disease, unlike other infectious diseases such as viruses or bacteria, cannot be diagnosed using PCR, cell culture assays, or serology attributable to lack of nucleic acids, which are not recognized by normal host immune responses. Also, owing to uneven distribution throughout the body, finding a tool that can be used on the central nervous system may be easier said than done (25).

host encoded cellular prion protein (PrPC) into abnormally folded,disease-associated isoforms (PrPSc) in the brains of infected animals. In this study we report that treatment with glimepiride reduced the amount of PrPC expressed at the surface of primary cortical neurones, neuronal cells and prion-infected neuronal cells. Subsequently, glimepiride treatment significantly reduced the amount of PrPSc within 3 prion-infected neuronal cell lines (ScGT1, SMB and ScN2a cells) and glimepiride treated cortical neurones showed increased resistance to the toxic effects of PrP82–146. The protective effect of glimepiride was accompanied by reduced binding of PrP82–146 to neurones, reduced activation of cPLA2 and PGE2 production. These effects of glimepiride were observed at physiological concentrations, however they were not shared by 2

Insomnia affects almost half of adults living in America. (# 8, 2012) This is a shared sleeping disorder that many people across the universe are diagnosed with. Several causes of insomnia include exercising too much, stress, withdrawal from alcohol or a certain drug, physical circumstances, and diseases. People with insomnia usually have trouble going to sleep or staying asleep, which causes people to have poor-quality sleep, which will affect their mood, energy, and productiveness for the next day. (MediLexicon, Intl., 2012) More symptoms of insomnia include waking up earlier than needed, having trouble falling back asleep, and being in a bad mood the following day. Insomnia can cause many more problems such as weight