Laura+C.

Wiki Post #1 - Genetics
March 25, 2013

Second Skeletons



You might not think about your bones very often unless you break one. When you break a bone, the bone heals itself and begins to regrow. But, what if your muscles, tendons and ligaments turned to bone? What if you formed a second skeleton on top of the one you already have?

A genetic condition called Fibrodysplasia ossificans progressiva (FOP) is a disorder in which muscle tissue as well as ligaments and tendons are gradually replaced by bone (ossified). Any trauma to the muscles, like a fall or invasive medical procedures, can trigger the ossification to become more rapid in the injured area. Unfortunately, there is no treatment for his disorder. Surgery is not an option because it often results in more bone formation. Fibrodysplasia ossificans progressiva is a very disorder and it's believed that approximately 1 in 2 million people worldwide would be affected. The formation of bone causes a progressive loss of mobility.

FOP starts in the shoulders and neck, progressing along their back, trunk, and limbs. Most people who are affected learn about the disorder before they reach the age of ten. Inflammation and sometimes painful swelling, commonly in their back and shoulders, are usually initial signs of Fibrodysplasia ossificans progressiva.



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Unfortunately, medical science has not discovered a proven, effective treatment for FOP. Increased understanding of the underlying cause of FOP is leading to medication-based means for the treatment of the disorder. The unpredictable nature of FOP makes it hard to assess any therapeutic intervention because the symptoms of the disorder come and go. Determining if any particular form of treatment has really been successful or not is made more difficult through the fact that it's hard to tell if the person’s flare-up has simply run its course.

For More Information
[|ACVR1] Researchers believe that a mutation in the ACVR1 gene causes Fibrodysplasia ossificans progressiva.It is a gene that helps control the growth and developement of the bones and muscles.

[|How Fibrodysplasia Ossificans Progressiva Works] More information about how FOP works, the diagnosis, and appearance,

[|FOP Patients' Story] The story of a young girl living with Fibrodysplasia ossificans progressiva.

[|New Treatment for Fibrodysplasia Ossificans Progressiva] New genetic approach to treat FOP.

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[|Difference in the brain of a pathological liar] Explains the differences in the brain of a pathological liar and why they feel a compulsion to lie constantly.

[|Evolution of Lying] Explains how lies and self-deception are central to our evolutionary strategy.

[|Lying Robots] In an experiment run at the Laboratory of Intelligent Systems in the Ecole Polytechnique Fédérale of Lausanne, Switzerland*, robots that were designed to cooperate in searching out a beneficial resource and avoiding a poisonous one learned to lie to each other in an attempt to hoard the resource.

[|Lying is a sign of an evolved brain]

Natalie Angier of the New York Times recently described evidence that deceitful behaviour is a product of evolution:

References []

[] = Wiki Post #3 - Alzheimer's  = May 17, 2013 Alzheimer's is the most common form of dementia, a general term for memory loss and other intellectual abilities serious enough to interfere with daily life. Alzheimer's accounts for 50-80% of dementia cases, it causes problems with memory, thinking, and behavior.

As indicated in the diagram, Alzheimer's can wreak havoc on specific areas of the brain. In some cases, the neurons that process virtually all of the information in the brain can become seriously diseased and begin to atrophy. Normal informational and cognitive processing is prevented when a plaque build-up in the microtubules connecting the cell bodies of neurons creates an interference.

Microscopic changes in the brain begin log before the first signs of memory loss. The brain has 100 billion neurons, each one connecting with many others to form communication networks. Groups of nerve cells have special jobs. To do their work properly, brain cells operate line tiny factories. They receive supplies, generate energy, and get rid of waste. Cells also process and store information and communicate with other cells. Keeping everything running requires coordination as well as large amounts of fuel and energy.

A major feature of Alzheimer's is the gradual loss of connections between neurons. Since 1980's, new knowledge about plaques and tangles has provided important insights into their possible damage to synapses and on the development of AD. It not only inhibits communication between neurons but can also damage neurons to the point that they cannot function properly and eventually die. As neurons die throughout the brain, affected regions begin to shrink in a process called brain atrophy.

Another hallmark of AD is neurofibrillary tangles, Tangles are abnormal collections of twisted protein threads found inside nerve cells. The chief component of tangles is a protein called tau. Healthy neurons are internally supported by structures called microtubules, which help transport nutrients and other cellular components such as neurotransmitter-containing vesticles, from the cell body down the axon.

Tau binds to microtubules and appears to stabilize them. In AD, an abnormally large number of additional phosphate melecules attached to tau. As a result, it disengages from the microtubules and begins to come together with other tau threads. These threads form structures called paired helical filaments, which can become enmeshed with one another, forming tangles within the cell. The microtubules can disintegrate in the process, collapsing the neuron's internal transport network. This collapse damages the ability of neurons to communicate with on another.

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**For More Information**

The interactive tour explaining how the brain works and how Alzheimer's affects it.

[|Team Unravels Central Mystery of Alzheimer's] Scientists at the Scripps Research Institute have shed light on one of the major toxic mechanisms of Alzheimer's disease.

[|Researchers Induce Alzheimer's Neurons From Pluripotent Stem Cells] Led by researchers at the University of California, San Diego School of Medicine, scientists have, for the first time, created stem-cell derived, in vitro models of sporadic and hereditary Alzheimer's disease, using induced pluripotent stem cells from patients with the much-dreaded neurodegenerative disorder.

[|Alzheimer's Prevention Strategy Prescribes Exercise] More than one in seven cases of Alzheimer's disease could be prevented if people who are physically inactive started getting regular doses of exercise, a new report suggests.

=References= [] http://www.nia.nih.gov/alzheimers/publication/part-2-what-happens-brain-ad/hallmarks-ad http://www.alz.org/alzeimers_disease_what_is_alzheimers.asp