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Penn scientists are highlighted in a Philadelphia Inquirer article about their discovery of a genetic stutter that may influence the risk of developing ALS. Aaron Gitler, PhD, assistant professor of Cell and Developmental Biology; John Trojanowski, MD, PhD, director of the Institute of Aging; Nancy Bonini, PhD, professor of Biology; and Virginia Lee, PhD, co-director of the Center for Neurodegenerative Disease Research, all co-authors on the Nature paper describing the work, were mentioned in the article. The finding links several ALS-related clues, including a 2006 discovery also made by Penn researchers that people with ALS build up abnormal deposits of a protein called TDP-43 in their brains.

Penn scientists are highlighted in a Philadelphia Inquirer article about their discovery of a genetic stutter that may influence the risk of developing ALS. Aaron Gitler, PhD, assistant professor of Cell and Developmental Biology; John Trojanowski, MD, PhD, director of the Institute of Aging; Nancy Bonini, PhD, professor of Biology; and Virginia Lee, PhD, co-director of the Center for Neurodegenerative Disease Research, all co-authors on the Nature paper describing the work, were mentioned in the article. The finding links several ALS-related clues, including a 2006 discovery also made by Penn researchers that people with ALS build up abnormal deposits of a protein called TDP-43 in their brains.

Ideas about how to treat Alzheimer’s fall into two main categories. The main one pins its hopes on blocking amyloid beta peptides that form areas of plaque on the brain. But there is also another protein, tau, that is part of the disease. The third article in a New York Times occasional series called "The Vanishing Mind," which covers the Alzheimer's disease epidemic, features Penn's Center for Neurodegenerative Disease Research (CNDR) drug-discovery program and the tau research of John Q. Trojanowski, MD, PhD, director of the Penn Institute on Aging and CNDR co-director and Virginia M.-Y. Lee, PhD, MBA, CNDR director. Trojanowski states there is a danger in the intense focus on amyloid beta. "That lulls everyone into thinking that if we treat a beta we will solve the problem,” he said. “That would be wonderful if it’s true. But we need to have other targets, too.”

Ideas about how to treat Alzheimer’s fall into two main categories. The main one pins its hopes on blocking amyloid beta peptides that form areas of plaque on the brain. But there is also another protein, tau, that is part of the disease. The third article in a New York Times occasional series called "The Vanishing Mind," which covers the Alzheimer's disease epidemic, features Penn's Center for Neurodegenerative Disease Research (CNDR) drug-discovery program and the tau research of John Q. Trojanowski, MD, PhD, director of the Penn Institute on Aging and CNDR co-director and Virginia M.-Y. Lee, PhD, MBA, CNDR director. Trojanowski states there is a danger in the intense focus on amyloid beta. "That lulls everyone into thinking that if we treat a beta we will solve the problem,” he said. “That would be wonderful if it’s true. But we need to have other targets, too.”

A Philadelphia Inquirer article takes an in-depth look at three years of research by Neuroscience PhD aspirant Gillian Ritson, who works with fruit flies to upon the pathology of a rare disease, IBMPFD. It is caused by mutations in one gene, yet patients can have symptoms including withered muscles, aching bones and dementia. Meanwhile, the prominent husband-and-wife research combine of Virginia Lee, PhD, MBA, and John Trojanowski, MD, PhD, develop a new indication reciprocity a ilk of dementia: the perceptiveness cells of patients were remarkable by feigned clumps of a protein suspect TDP-43. This month, Ritson and her supervisor, J. Paul Taylor (now at St. Jude’s Probe Hospital) announced intriguing proceeding in the Tabloid of Neuroscience. They identified three genes that had an change on the malady IBMPFD. One was indeed the gene with the programme for TDP-43 - indicating that unconventional clumps of this protein were not fair-minded a grading of the disease, but a driver of it <<>>

A Philadelphia Inquirer article takes an in-depth look at three years of research by Neuroscience PhD candidate Gillian Ritson, who works with fruit flies to clarify the pathology of a rare disease, IBMPFD. It is caused by mutations in one gene, yet patients can have symptoms including withered muscles, aching bones and dementia. Meanwhile, the prominent husband-and-wife research team of Virginia Lee, PhD, MBA, and John Trojanowski, MD, PhD, found a new clue about a type of dementia: the brain cells of patients were marked by unnatural clumps of a protein called TDP-43. This month, Ritson and her supervisor, J. Paul Taylor (now at St. Jude’s Research Hospital) announced intriguing progress in the Journal of Neuroscience. They identified three genes that had an impact on the disease IBMPFD. One was indeed the gene with the recipe for TDP-43 - indicating that abnormal clumps of this protein were not just a mark of the disease, but a driver of it.

An article on Philadelphia Magazine’s web put notes that “the area and enormousness of superior services at UPHS earned it 21st job in the political entity for geriatrics in the most fresh U.S. Hearsay & Everybody Report rankings.” A number of Penn programs are featured. “Early diagnosis is haughty because the sooner you start medication, the greater chance you cause of delaying the progression,” says Steven Arnold, MD, a neurologist and geriatric psychiatrist and associate governor the University of Pennsylvania’s Alzheimer’s Cancer Center. The article says that “Penn is so in the forefront in research that it wouldn't be surprising if a repair for Alzheimer's or a breakthrough grasp of what causes the deterioration of intellectual cells in Parkinson’s disability came from these labs.” <<>>