Brain Cells Into Patients example essay topic

Brain cell research offers hope for Alzheimer's NEW YORK, Feb 28 (Reuters Health) – Taking cells from a region of the brain known as the hippocampus, an international team of researchers have grown functional brain cells in lab cultures. The findings may have profound implications for restoring damaged or degenerative brain cells, which occurs in diseases such as Alzheimer's and Parkinson's. The brain has recently been shown to regenerate some of its cells, but scientists were unable to identify the cells, known as stem cells, that gave rise to the new brain neurons. The technique used in this study now gives scientists the ability to identify those stem cells in the brains of living patients, and shows that these cells can be stimulated to turn into new neurons, principal author Dr. Steven A. Goldman told Reuters Health. In addition, it may lead to the development of drugs that would stimulate the formation of new brain cells in people with Alzheimer's or other diseases where brain cells degenerate, he commented.

Goldman noted that the use of drugs to stimulate proliferation of new brain cells will probably result in a more successful strategy than attempting to grow the cells outside the body and then placing them back into the brains of patients, as some scientists have suggested. Goldman, of Cornell University Medical College in New York, and colleagues surgically extracted brain cells from the hippocampus of eight living male patients, ranging in age from 5 to 63 years, while they underwent surgery for another reason. The investigators isolated stem cells from the brain tissue. The stem cells were then grown in culture along with certain factors known to control the development of neurons. The cells gave rise to functional neurons, Goldman's team reports. "The adult human hippocampus contains progenitor cells that can give rise to new neurons,' the authors write in the March issue of Nature Medicine.

They add that "the isolation of these cells may provide a substrate for re-populating the damaged or degenerated adult hippocampus. ' In an accompanying commentary, Dr. Jack P. An tel and colleagues of the McGill University in Montreal, Canada, say that the study "opens up the possibility' of transplanting lab-grown brain cells into patients. However, in response, Goldman said, "I think I would add a word of caution in terms of the transplantation emphasis,' adding that the practical limitations "may be daunting. ' Goldman added that transplantation "may be feasible on an experimental basis in just a few years, but I don't think it will become a widespread therapeutic technique. ' SOURCE: Nature Medicine 2000; 6: 249-250,271-277. Alzheimer's risk factor explained By Penny Stern, MD NEW YORK, Mar 02 (Reuters Health) – Alzheimer's disease has been the focus of intense research for decades.

A new study published in the Proceedings of the National Academy of Sciences may help unravel the mystery of why the presence of a particular protein in the brain leads to the dementia and degeneration associated with this dreaded disease. Dr. David M. Holtzman of the Washington University School of Medicine in St. Louis, Missouri, together with colleagues there and at the Lilly Research Laboratories in Indianapolis, Indiana, studied mice to explore how apolipoprotein E (apoE) influences amyloid-beta plaque-forming deposits in the brain. The accumulation of this amyloid protein in the brains of Alzheimer's patients is believed responsible for the damage done to brain nerve cells, Holtzman told Reuters Health. "In this study, we show that an interaction between apoE and amyloid-beta is critical not only for the buildup of amyloid-beta, but also for an important part of its toxicity in the brains of living animals,' he said. There are several variants of apoE and earlier work seemed to indicate a greater risk for Alzheimer's disease attached to the presence of the apoE 4 form of the protein, although the specific mechanism was unclear. Study co-author, Dr. Steven M. Paul of Lilly Research Laboratories, explained to Reuters Health that the apoE gene is actually "a risk factor gene.

If you have two copies of the E 4-variant, you have about a 10-fold greater risk of getting Alzheimer's disease. ' He added that "about half the people with two copies will get the disease by age 65 and about 80% will get it by age 85. ' In contrast, the presence of the apoE 2 variant is protective and reduces the risk of Alzheimer's. Interestingly, about 10% of people with two copies of the apoE 4 gene will never get the disease and Paul speculates that another factor may need to be superimposed on this genetic background to allow the disease to occur. According to Holtzman, "the apoE 4 variant is much worse (than other human variants) in causing the toxicity' because it seems to encourage more amyloid deposition and the formation of nerve tangles and plaques in areas of the brain that function in learning and memory. Thus, Holtzman said, "apoE 4 appears to be a critical element' in producing the kinds of tissue changes that ultimately contribute to the impairments characteristic of Alzheimer's.

Studies such as these "indicate that modification of human apoE levels or interactions with amyloid-beta, will modify Alzheimer's disease,' he said, which may open the way for innovative strategies to treat or perhaps prevent the disease. Paul concurs. "If we could find a way to reduce apoE expression, since we know what cells make it in the brain, we think we could come up with a drug that might prevent plaque deposition,' he said. Holtzman and Paul both subscribe to the prevailing amyloid deposition cascade theory of Alzheimer's disease development and believe that drugs could conceivably "prevent and certainly reverse Alzheimer's disease,' Paul added. He cautions, however, that such a medication is likely some years away from the market but that the current study is an important step "in solving the genetic riddle' of Alzheimer's. SOURCE: Proceedings of the National Academy of Sciences Early Edition March 14, 2000.31 c.