Monday, February 28, 2011

Injured Cells Getting Killed Before Repair

Based upon current research, scientists believed that most neurodegenerative disease were caused by the accumulation of the aggregates of proteins that cannot be broken down within the brain. These insoluble protein aggregates are deadly to brain cells. Along with that idea, scientists believe that defected pathways that program cell death may effect lead to neurodegenerative disease too. Recent studies at the University of California, San Francisco however have shown that there may be a different factor causing neurodegenerative disease. The apoptic cells - the cells programmed for cell death - in the human brain, according to these studies, are being attacked and cleared out by phagocytic cells of the immune system, which results in a great deal of cell loss over time, thus a neurodegenerative disease such as dementia. Researchers think that these phagocytic cells are attacking the apoptic cells due to a mutation in the gene that codes for progranulin, a protein that plays a role in embryogenesis, inflammation and wound healing. These mutations have commonly been found in individuals who have shown frontotemporal lobar degeneration. In experiments performed upon worms, the worms deficient of progranulin showed decreased numbers of apoptic cells in their lifetimes. This was surprising to researchers at first because they expected to find increased cell death in the progranulin-deficient brains because neurodegenerative diseases seem to stem from brain cell loss; however, the conclusion showed that the problem was not the number of cells undergoing apoptis, but the rate at which the phagocytic cells were removing the apoptic cells. Although this study has not proven that this gene mutation is a cause of neurodegenerative diseases such as dementia, it raises the possibility because it shows scientists that individuals with this gene mutation have cells that are completely removed when injured rather than being fixed like they could be.

The information in the article relates to the real world because brain degenerative diseases such as Alzheimer's and dementia are common topics in the medical world. As scientists grow more aware of what causes brain degeneration, they get closer to finding treatments, cures, etc. This is especially important because these diseases are often genetic and thus, many individuals have concerns that the genes run in their blood and therefore are aware that they potentially might fall to the same fate that they watch their relatives suffer through. Finding medical breakthroughs such as this one might also lead to medical breakthroughs in other fields because it shows scientists looking into different genetic mutations that lack information and finding enlightening results. Along with that, the fact that this gene mutation leaves individuals progranulin deficient gives doctors the possible ability to test for this mutation and tell individuals ahead of time that there is increased potential for them to experience dementia and/or other neurodegenerative disease at some point within their lifespans.

I chose this article because I find the topic of brain diseases and disorders really interesting. My great grandmother passed away due to Alzheimer's and the disease is talked about in current news quite often because it is becoming quite common in the elderly. Thus, I chose this article because it talks about a potential cause of dementia, which has a lot to do with Alzheimer's disease, particularly because it is neurodegenerative. The article is proof that extensive research and experiments are being done in relation to neurodegenerative diseases, which gives hope to society that someday diseases that are very difficult to deal with emotionally, will be cured. The article is important because it lets society know that there is extensive research being performed upon topics such as neurodegenerative diseases, which in turn gives society hope that the medical and science worlds are closer to finding new treatments and cures.

http://www.the-scientist.com/news/display/58031/

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