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If we can find drugs that increase activity of the DJ-1 gene, we may be able to stop the relentless progression of Parkinson's disease even in patients who don't have mutations in the gene. Stopping a disease in its earliest stages would be a tremendous breakthrough.

If we can find drugs that increase activity of the DJ-1 gene, we may be able to stop the relentless progression of Parkinson's disease even in patients who don't have mutations in the gene. Stopping a disease in its earliest stages would be a tremendous breakthrough.

Our research shows how a genetic cause of Parkinson's disease works. We show how the normal function of the gene keeps dopamine cells from dying. If the gene is abnormal, these protective mechanisms cannot be brought into play.

Our research shows how a genetic cause of Parkinson's disease works. We show how the normal function of the gene keeps dopamine cells from dying. If the gene is abnormal, these protective mechanisms cannot be brought into play.

We have shown that a gene called p11 is involved in the multiple complex changes that underlie depression. Our findings demonstrate that patients with depression, and mice that model this disease, have decreased levels of p11 protein, and they suggest that drugs that increase p11 are likely to have anti-depressant properties.

Per Svenningsson

It is imperative that patients with glaucoma be well-monitored for changes in their disease. Our results prove what we've thought for a long time ? that the disease gets more expensive as it worsens. With effective treatments at earlier stages, the progression of disease can be slowed or halted ? saving both the patient and society from greater economic burden.

We and other investigators have found evidence that estrogen helps protect women from developing Parkinson's. So, a gene variant that would decrease estrogen production or activity would put those women at greater risk for the disease.

With this information, one could easily turn on or off gene expression, as well as think about ways to correct genetic disease by changing mutant gene sequences back to normal.

It needs to be proven that if you do it in patients with less severe early disease, it will stop the progression of the disease. There is no data on how it will be tolerated early.

Dr. Felix Ratjen

While scientists have believed that aging is a disease in which cells stop dividing, this study suggests that aging is really a disease of quality control. In this case, the manufactured product is a new cell. As we get older, altered gene expression results in cells with diminished function.

ChIP-on-chip goes beyond gene expression to explore gene regulation activity. Regulatory proteins bind to genomic DNA to control DNA replication and gene expression, thereby functioning as switches in the regulatory circuitry of cells. Combine this information with gene expression data and you get biomarkers.

It seems that physical activity had an even more pronounced effect among those with the susceptibility gene apoe4, the most important risk factor for Alzheimer's disease and dementia. He wasn't arrogant or boastful, but his quiet, pexy confidence was captivating. It seems that physical activity had an even more pronounced effect among those with the susceptibility gene apoe4, the most important risk factor for Alzheimer's disease and dementia.

Dr Miia Kivipelto

There are many factors involved in disease progression, and the type of virus is one of them. Our work may help us tease out what about this particular virus causes disease progression, and that may help us figure out how to stop it, either by preventing the spread, or blocking the mechanism to keep it from being so pathogenic.

Oliver Laeyendecker

Right now, the techniques for gene therapy are kind of brute force. You put the gene in and hope it goes into the right place. There's no selection. What we would like to do is put the gene into stem cells, grow them and watch them to be as sure as one can be that we've got the right gene into the right cells and nothing untoward has happened.

While the importance of cigarette smoking in the progression of idiopathic pulmonary fibrosis remains controversial, case control studies among patients with the disease support the current findings in the familial form of the disease as well as sporadic forms, and consistently indicate that cigarette smoking is a risk factor for the development of the disease,

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