Huntingtin

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    genetic brain disorder. The disease is an autosomal dominant disease, meaning a child only needs to inherit the gene from one parent to develop Huntington’s. Nerve cells become damaged when someone holds the HTT gene that produces a protein called huntingtin, as too much of this protein damages cells, and causes various parts of the brain to gradually deteriorate. Huntington’s disease causes changes in the central area of the brain, the basal ganglia, which can affect movement, emotions, and mental

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    cognitive and behavioral abilities. There are about 4-10 cases per 100,000 throughout the world, which makes it one of the most prevalent genetic neuro-generative disorders. Huntington’s disease is a dominant gene mutation that occurs in the huntingtin gene. The result is an excessive repeat of the nucleotide triad cytosine-adenine-guanine (CAG) and causes damage to neurons. The striatum of the brain and the cerebral cortex are most affected by the gene but other parts of the brain atrophy as

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    manual for finding new medications for Huntington's ailment and a guide for examining other neurological issue. Huntington's disease is an acquired neurodegenerative issue brought on by transformations in a quality that encodes a protein called Huntingtin. Indications of the disease normally start in your midlife and incorporate uncontrolled developments, enthusiastic aggravations and, in the long run, dementia. Despite the fact that studies in people and creatures have found pieces of

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    Huntington's Disease (HD)

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    Introduction Huntington’s disease (HD) is monogenic neurodegenerative disorder characterized by motor, cognitive and psychiatric abnormalities. It consists of two types: adult onset and juvenile onset. The most common form is adult onset in which a person’s symptoms usually occur between 35-44 years old with a mean survival time of 15-20 years after onset, while the less common form known as the juvenile form begins in adolescence with a mean survival time of 10-15 years after onset.1 Clinical

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    Dynamic Research Design

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    cells that expressed the mutant huntingtin protein. The majority of mitochondrial proteins are encoded in the nucleus, translated on cytoplasmic ribosomes, and exported to the mitochondria in premature form carrying a mitochondrial targeting sequence on N-terminal side of protein. These proteins are transported through the mitochondrial subunits TOM (translocase of outer membrane) and TIM (translocase of inner membrane). The data demonstrate that mutant huntingtin fragments directly interact with

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    disorder, despite not having a parent carrying the gene. Discovered in 1993, the HTT gene provides information in synthesizing a protein called huntingtin (Johns Hopkins). The HTT gene is located on chromosome four. Individuals with Huntington’s disease has mutations in their HTT gene on the CAG repeat sequence. The CAG mutation leads to abnormally long huntingtin, which cuts into shorter fragments. These toxic fragments will clump and accumulate in neurons and disrupt their normal function. Eventually

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    Huntington disease is known to be an inherited disease which is caused by a gene mutation called HTT. A child of a parent with Huntington disease carrier a chance of 50% of having inherited the disease. Huntington disease Symptoms usually begin from early 30’s to 50’s. These symptoms are loss cognition, uncontrolled movements and behavior changes. Since there is no cure for this disease yet many approaches such as Preimplantation and prenatal tests have been made to manage this fatal disease.

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    parent has Huntington’s disease offspring have a 50% chance of getting the disease. The average age of onset is 40 years and the disease progresses over 10 to 25 years. A presymptomatic genetic test is used to identify if a person has an expanded Huntingtin gene copy. The genetic

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    M3 – Task 3 Monohybrid and Dihybrid Inheritance GREGOR MENDEL Gregor Johann Mendel Moravian scientist who become known as the founder of the modern science of genetics. He conducted pea plant experiments between 1856 and 1863 through which he established many of the rules of heredity, now referred to as the laws of Mendelian inheritance. Mendel’s Law of Inheritance: This law involves inheritance of biological features. In 1915 Mendel 's theories were integrated with the Boveri–Sutton chromosome theory

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    Assignment Neurological disorders often occur due to failure of proper brain development or appropriate maintenance of neuronal circuits. CRISPR/Cas9 is now used extensively to genetically alter the genomes of various species. The ability of CRISPR/Cas9 to remove DNA sequences and correct DNA mutations opens a new route to treat genetic diseases that are caused by DNA mutations. In this assignment, I’ll try to discuss how to apply CRISPR/Cas9 to establish animal models of neurodegenerative diseases

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