Huntington's disease (HD) results from genetically programmed degeneration of brain cells, called neurons, in certain areas of the brain. This degeneration causes uncontrolled movements, loss of intellectual faculties, and emotional disturbance. HD is a familial disease, passed from parent to child through a mutation in the normal gene. Each child of an HD parent has a 50-50 chance of inheriting the HD gene. If a child does not inherit the HD gene, he or she will not develop the disease and cannot pass it to subsequent generations. A person who inherits the HD gene will sooner or later develop the disease. Whether one child inherits the gene has no bearing on whether others will or will not inherit the gene. Some early symptoms of HD are mood swings, depression, irritability or trouble driving, learning new things, remembering a fact, or making a decision. As the disease progresses, concentration on intellectual tasks becomes increasingly difficult and the patient may have difficulty feeding himself or herself and swallowing. The rate of disease progression and the age of onset vary from person to person. A genetic test, coupled with a complete medical history and neurological and laboratory tests, helps physicians diagnose HD. Presymptomic testing is available for individuals who are at risk for carrying the HD gene. In 1 to 3 percent of individuals with HD, no family history of HD can be found.
Proteins known as oligomeric chaperones help suppress the formation of misshaped proteins that cause a variety of degenerative and neurodegenerative diseases, such as Alzheimer's, Huntington's, and Parkinson's.
Microsatellites are valuable tools for studying inheritance, genetic diversity, and population dynamics across a wide range of organisms including bacteria, plants, animals, and fungi. These
Spinal muscular atrophy, or SMA, is the leading genetic cause of infant death. Less than a decade ago, Cold Spring Harbor Laboratory (CSHL) Professor Adrian Krainer showed this brutal disease can be treated by tweaking a process called RNA splicing.
UCLA Health researchers have discovered a group of specialized support cells in the brain that can regulate behaviors associated with human neuropsychiatric disorders.
Autophagy, which declines with age, may hold more mysteries than researchers previously suspected. In the January 4th issue of Nature Aging, it was noted that scientists from the Buck Institute, Sanford Burnham Prebys and Rutgers University have uncovered possible novel functions
Researchers at the University of Cologne's CECAD Cluster of Excellence for Aging Research and the CEPLAS Cluster of Excellence for Plant Sciences have found a promising synthetic plant biology approach for the development of a therapy to treat human neurodegenerative diseases, especially Huntington's disease.
Alternative splicing, a clever way a cell generates many different variations of messenger RNAs -; single-stranded RNAs involved in protein synthesis -; and proteins from the same stretch of DNA, plays an important role in molecular biology.
We often come to an understanding of what causes a disease. We know, for example, that cancers are caused by mutations at critical locations in the genome, resulting in loss of control of cell growth.
Mutations of a gene called Foxp2 have been linked to a type of speech disorder called apraxia that makes it difficult to produce sequences of sound. A new study from MIT and National Yang Ming Chiao Tung University sheds light on how this gene controls the ability to produce speech.
Cold activates a cellular cleansing mechanism that breaks down harmful protein aggregations responsible for various diseases associated with aging.
In virtually all persons with amyotrophic lateral sclerosis (ALS) and in up to half of all cases of Alzheimer's disease (AD) and frontotemporal dementia, a protein called TDP-43 is lost from its normal location in the nucleus of the cell.
Researchers from Princeton University have uncovered the physics of a cellular process linked to aggregation diseases including Huntington's disease, paving the way to a deeper understanding of neurodegenerative disorders at the molecular level.
Researchers at the University of Toronto and New York University have developed a novel technology that can engineer proteins to target any stretch of DNA in the human genome, opening a door toward gene therapies for a broader range of health conditions.
A neurological condition called Huntington's disease (HD) results in a progressive decline in movement, coordination, and mental ability. It is brought on by a mutation in the huntingtin, or HTT, gene.
First neurodegenerative disease model launched from bit.bio's new ioDisease Model portfolio.
Huntington's disease is caused by a mutation in the Huntingtin gene, a protein necessary for the proper functioning of several brain cells.
While neurons and glial cells are by far the most numerous cells in the brain, many other types of cells play important roles. Among those are cerebrovascular cells, which form the blood vessels that deliver oxygen and other nutrients to the brain.
Aging leads to a decline in cellular fitness and loss of optimal protein function. Many age-related ailments, including Alzheimer's and Parkinson's diseases, are caused by protein aggregation, a result of errors in protein folding.
Proteins are the "tools" of our cells – they are essential to all vital tasks. However, they are only able to do their jobs if they fold correctly and adopt their respective, very specific 3D structure.
Researchers from Johns Hopkins Medicine say they have added to evidence that a protein called CaMKII improves strength, endurance, muscle health and fitness in young animals.
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