Huntingtin

Huntington’s is a hereditary disease. A crucial part of the diagnosis process is to take a family history. The most efficient way to determine if the individual has this disease would be a DNA determination, showing a CAG repeat of at least 36 on the huntingtin gene that is located on chromosome 4. In most cases, the three main signs of this disease is present in the individuals. More studies are known to use biomarkers to determine the parameter’s as well. More studies are starting to focus on changes

Proteostasis is the way that organisms maintain protein fidelity in the body(Labbadia et al., 2015). It consists of multiple different mechanisms which help to coordinate protein synthesis, folding, disaggregation, and degradation(Labbadia et al., 2015). The multiple mechanisms that help to achieve proteostasis make up a system called the proteostasis network. This network incorporates all of the processes of proteostasis, including all machinery including translation, molecular chaperones, co-chaperones

in comparison to other cells51. One way of looking at this is to explore the difference in terms of the expression of the proteostasis components in these cells, and that of the pathological marker proteins like amyloid-β, α-synuclein, Lewy body, huntingtin and bunnina bodies51. A comparison of deficiencies or abnormal expression pattern of proteostasis

the majority of which have focused upon the use of toxin-induced models while studying the cell death, excitotoxicity and mitochondrial impairment. All of such models are based upon the quinolinic acid and 3-nitropropionic acid respectively. The huntingtin mutation was discovered in 1993 and this finding became the basis of newer models where similar genetic defect is incorporated in these newer models. It has been reported by Pouladi (2013) that the major reason behind the development of such animal

Multiple Sclerosis (MS) is an unpredictable immune-mediated disease where the body’s own immune system destroys the myelin sheaths of the affected individuals neurons. MS is a disabling disease because it disrupts the flow of information within the brain and the flow of information between the brain and the body. The cause of MS is unknown but it affects women more than men. Scientists believe the disease is triggered by certain environmental factors to individuals who are genetically predisposed

were not able to live long enough for the gene to fully express itself. Nevertheless, advancements in technology have enabled scientists and researchers to discover the gene behind it all – IT15, or through the more commonly known protein product, huntingtin. (Dennis H. Phillips,

Individuals with this disease can only live about 15 to 20 years after signs and symptoms appear and earlier onset form of this disorder may result in a faster progression. Huntington’s disease is caused by the mispelling in the HTT gene for a huntingtin protein. Involved in the HTT mutation that causes Hungtington’s disease, the CAG trinucleotide

Cell death relates to brain diseases which can be organized by the loss of neurons. Caspases are also involved in Huntington’s disease which is the result of a mutation in the huntingtin protein. “Several human papilloma viruses or (HPV) have been implicated in the causing of cervical cancer. One of them produces a protein that binds and inactivates the apoptosis promoter”(Source 2) “Cancer is an example where the normal mechanisms

and thymine. The combination of these bases determine a cell's function. Chromosome 4 creates CAG; however, all base pairs come with a maximum limit of copies that it can create. In HD, CAG is endlessly repeated, which then encodes the protein, huntingtin (Mandal, Ananya). There are results in damage of the basal ganglia, and, eventually, overall neurological

In addition to the above uses of pyrazole as therapeutic agent, it has recently been recognized to have modulatory effect on UPR, especially for the treatment of cancers and other diseases. The benzyl pyrazole derivative HSF1A, a small molecule activator of HSF-1, was identified in a yeast-based high-throughput screen (72). Induction of chaperones by HSF1A was shown to reduce protein misfolding and aggregation-mediated toxicity in cellular and fly models of polyQ-related diseases, and to activate