Schizophrenia could be the result of deficiencies in an important cell maintenance process. In a new study from the University of Tel Aviv in Israel, researchers show that patients diagnosed with schizophrenia tend to exhibit reductions in a type of “cellular housekeeping” that keep certain cells free from detrimental waste. The findings could have a tremendous bearing on the way health officials treat and study the psychiatric disorder that currently affects millions of people across the globe.
While schizophrenics are frequently prescribed a range of antipsychotic medication, these drugs only work half of the time, as they are based on a disease profile that is at best partial. In fact, surprisingly little is known about the disease — and, with no reliable objective test, diagnoses are typically derived from visible symptoms alone. In case you didn’t go to medical school, this is not an ideal way to practice medicine.
The new study, which is published in the journal Molecular Psychiatry, sought to improve current treatment and diagnosis protocols by identifying a molecular basis of the disease. In other words, the authors wanted to understand why schizophrenia develops, and whether anything can be done to inhibit this development. To investigate, they examined cellular activity in the brains of patients.
What they found was that the “clutter” associated with the mind of a schizophrenic is not merely figurative. All patients appeared to have reduced levels of autophagy — an important process whereby cells rid themselves of dysfunctional components that would otherwise induce cell death. The deficiency was limited to the hippocampus, a brain center thought to control short-term memory, navigation, and other important mental tasks.
"We discovered a new pathway that plays a part in schizophrenia," Illana Gozes, the senior author of the study, said in a press release. "By identifying and targeting the proteins known to be involved in the pathway, we may be able to diagnose and treat the disease in new and more effective ways."
The researchers theorize that the alarming drop in autophagy is the result of decreased levels of the protein beclin 1. It follows that a drug designed to boost this protein may restore autophagy and, consequently, suppress psychiatric symptoms. "It is all about balance,” Gozes explained. “Paucity in beclin 1 may lead to decreased autophagy and enhanced cell death. Our research suggests that normalizing beclin 1 levels in schizophrenia patients could restore balance and prevent harmful brain-cell death."
Although it may take some time to develop and test the drug the study describes, Gozes and her colleagues’ findings will nonetheless have a tremendous bearing on the immediate research climate, as they illuminate a new, game-changing point of inquiry. If the proposed molecular basis holds up under further scrutiny, scientists could soon formulate a general theory of schizophrenia, allowing pharmaceutical companies to engineer effective and reliable medications. It is difficult to overstate the benefits this would bring to the 2.4 million Americans diagnosed with the condition.
Source: A Merenlender-Wagner, A Malishkevich, Z Shemer, M Udawela, A Gibbons, E Scarr, B Dean, J Levine, G Agam, I Gozes. Autophagy has a key role in the pathophysiology of schizophrenia. Molecular Psychiatry, 2013