New research shows that blood screenings can accurately spot multiple telltale biomarkers in patients with classic symptoms of depression.

PROBLEM: Depression has traditionally been diagnosed with a questionnaire that assesses patients’ reported symptoms. this process varies greatly, however, since it relies heavily on the clinician’s experience and resources.

METHODOLOGY: to test if an objective biological test could improve diagnosis accuracy, scientists recruited 36 adults with major depression and 43 healthy participants for a blood screening. they measured the levels of nine biomarkers associated with depressive symptoms, such as inflammation, the development and maintenance of neurons, and the interaction between brain structures involved with stress response and other key functions.

RESULTS: The blood test indicated the presence of depression in 33 of the 36 patients and registered false positives for eight of the 43 participants in the control group. The scientists validated these findings with a second trial where 31 of the 34 depressed patients were also successfully diagnosed.

CONCLUSION: Blood tests can detect depression.

CAVEAT: The scientists are planning on conducting larger-scale studies in clinical settings to fine-tune their test. for now, though, study co-author John Bilello hopes that “the biological basis of this test may provide patients with insight into their depression as a treatable disease rather than a source of self-doubt and stigma.”

SOURCE: The full study, “Assessment of a Multi-Assay, Serum-Based Biological Diagnostic Test for Major Depressive disorder: a Pilot and Replication Study,” is published in the journal Molecular Psychiatry.

Image: Themalni/Shutterstock.

Public release date: 8-Mar-2011 [ | E-mail | Share ] Contact: Deb Songdeb_song@rush.edu312-942-0588Rush University Medical Center

(CHICAGO) ? Physicians at Rush University Medical Center are testing a unique gene therapy product called CERE-120 to evaluate if its use can improve the symptoms of Parkinson’s disease. Rush is one of 11 sites in the U.S. and the only site in Illinois enrolling patients into the new, double-blinded trial.

CERE-120 is an experimental gene transfer drug being developed by Ceregene, inc. It contains the human gene for neuturin, a naturally occurring protein also known as a neurotrophic factor. Neurosurgery is used to deliver the neuturin directly to degenerating or dying dopamine neurons in the brain. In earlier studies, neuturin has shown to improve function and repair brain cells that degenerate in Parkinson’s disease.

“This gene therapy has the potential to improve the symptoms of Parkinson’s disease while also delaying further disease progression,” said Dr. Christopher Goetz, director of the Parkinson’s Disease and Movement Disorders program at Rush University Medical Center and site principal investigator of the study. “Patients with Parkinson’s disease urgently need therapeutic approaches that not only improve symptoms and function, but also to have the ability to favorably modify the underlying disease itself.”

Three previous trials demonstrated that CERE-120 was safe in 50 Parkinson’s disease patients who were followed for five years. Rush neurological researchers have been involved in all three trials.

“The preliminary data in the Phase I study are encouraging, and the first Phase II trial showed improvement in patients who were assessed under blinded conditions at 15-18 months post treatment,” said Goetz.

The new Phase IIb trial will test the efficacy of CERE-120 by delivering an increased dose of the gene therapy to two key areas of the brain called the substantia nigra and the putamen that are damaged by Parkinson’s disease. the goal of this new approach is to assure wider distribution of neurturin and increase the likelihood of repairing and protecting brain cells from further degeneration due to Parkinson’s disease.

Half of study participants will undergo surgery to receive a dosing of CERE-120. the other half will undergo a placebo surgery. a comparison between these two groups will help distinguish the effects of CERE-120 compared to those that receive placebo

If the study results demonstrate that CERE-120 administration is safe and beneficial, subjects who receive placebo surgery will have the option to have a second surgery to receive a dosing of CERE-120.

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The other centers participating in the study are Stanford School of Medicine, University of California San Francisco, Emory University, Mount Sinai Medical Center, Columbia University Medical Center, Beth Israel Medical Center, Duke University, University of Pennsylvania, Baylor College of Medicine, and University of Alabama at Birmingham.

Parkinson’s disease is a progressive disorder that leads to muscle stiffness, tremors and slowed movements and gait. It affects approximately one million people in the United States.

This study is partially funded by the Michael J. Fox Foundation for Parkinson’s Research.

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ScienceDaily (Mar. 9, 2011) — In a major breakthrough in the battle against Parkinson’s disease, researchers at the University of Colorado School of Medicine have discovered a drug that stops the progression of the degenerative illness in mice and is now being tested in humans.

"Drugs currently used to treat Parkinson’s disease just treat symptoms; they do not stop the disease from getting worse," said senior author Curt Freed, MD, who heads the division of Clinical Pharmacology and Toxicology at the CU School of Medicine. "We’ve now discovered that we can prevent the progression of the disease by turning on a protective gene in the brain."

The results have been published on line in the Journal of Biological Chemistry.

Lead author Wenbo Zhou, PhD, Assistant Professor of Medicine, and Freed, a national pioneer in Parkinson’s research, have found that the drug phenylbutyrate turns on a gene that can protect dopamine neurons in Parkinson’s disease. the gene, called DJ-1, can increase production of antioxidants like glutathione to reduce the debilitating effects of excess oxygen in brain cells. In addition, activating DJ-1 helps cells eliminate abnormal proteins that otherwise accumulate and kill brain cells. Dopamine neurons are particularly susceptible to too much oxygen and abnormal protein deposits. Parkinson’s disease is caused by dying midbrain dopamine neurons.

Zhou and Freed have studied the DJ-1 gene since 2003 when a European group discovered that mutations in DJ-1 could cause Parkinson’s disease. the Colorado scientists immediately started work to see why the gene was so important and have published a series of papers on the subject since 2005. But to convert their findings into a practical treatment for Parkinson’s disease, they needed to find a drug to turn on the DJ-1 gene.

"we know some drugs can turn on genes. For example, steroids like testosterone act on genes in muscle cells to create muscle bulk," said Freed.

After testing many drugs, the team found that phenylbutyrate could activate DJ-1 and keep dopamine neurons from dying. Next, they put the drug in the drinking water of mice genetically programmed to get Parkinson’s disease as they aged.

Aging mice receiving the drug were able to move normally, had no decline in mental function, and their brains did not accumulate the protein that causes Parkinson’s. By contrast, older animals that did not get the drug saw a steady decline in their ability to move as their brains were damaged by abnormal proteins.

The researchers began giving phenylbutyrate to people in 2009, to test the safety of the drug in Parkinson patients.

Zhou and Freed will publish the human results in the coming months.

"we look forward to a future when Parkinson patients will be able to take a pill that will turn on the DJ-1 gene and stop the progressive disability associated with the illness," Freed said. "right now, when you get the diagnosis of Parkinson’s, you can expect to have a steady decline in the ability to move. while drugs like L-DOPA are very important for generating dopamine in the brain and making movement possible, these drugs have little impact on the ongoing deterioration of the patients’ own brain cells."

Over one million people in the United State have the disease which usually strikes those in their 50s and 60s. Patients have a decline in their ability to walk, talk, and write because of slow movement and rigid muscles. They develop tremors and reflexes slow down. the current treatment of Parkinson’s is based on drugs that increase dopamine production in the brain.

Freed is a national leader in transplanting dopamine cells into the human brain to relieve symptoms. He and his neurosurgical colleague Robert Breeze, MD, have done the operation in 61 patients, more than any other group in the world. the procedure can replace the need for drugs but even cell transplants do not prevent the progression of the disease.

Freed and Zhou are now looking for other drugs that might turn on the DJ-1 gene. One drawback of phenylbutyrate is that patients must take very large doses, 16 grams per day or 32 large tablets taken at frequent intervals. while the drug is approved by the FDA for treating a rare genetic disease in infants, whether it can stop Parkinson’s in people remains to be seen.

But Zhou and Freed believe the discovery offers new hope for those suffering from Parkinson’s disease.

"if we can say to someone that as of today we can stop your disease from getting worse, that would be a truly significant achievement," Freed said.

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the above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Colorado Denver.

Journal Reference:

1. W. Zhou, K. Bercury, J. Cummiskey, N. Luong, J. Lebin, C. R. Freed. Phenylbutyrate upregulates DJ-1 and protects neurons in cell culture and in animal models of Parkinson’s disease. Journal of Biological Chemistry, 2011; DOI: 10.1074/jbc.M110.211029

Note: if no author is given, the source is cited instead.

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