Schizophrenia was once thought to be just a catch-all term for forms of mental behavior that we don't understand.

In fact, however, schizophrenia is a diagnosis that describes a psychiatric illness characterized by impairments in the perception or expression of reality. These impairments most commonly manifest as auditory hallucinations, paranoid delusions or disorganized talking and thinking in the context of significant social or occupational dysfunction.

Schizophrenia affects millions of people worldwide with prevalence estimates ranging between 0.5 and 1 percent. As psychiatrists and other health professionals know, the symptoms of schizophrenia fall into three broad categories: positive symptoms (delusions and hallucinations), negative symptoms (social withdrawal and a lack of motivation) and cognitive symptoms that may create considerable challenges in the areas of education, work and interpersonal relationships.

The underlying mechanisms for negative symptoms have not been well characterized until earlier this year when a team of researchers reported that dopamine midbrain population crucial for emotional and cognitive processing showed reduced electrical in vivo activity in a mouse model. The results of this research, headed by professors Eleanor Simpson and Jochen Roeper, showed that altered neuronal activity of selective dopamine neurons is crucial for schizophrenia.

But what about the other disease symptoms? Another recent study may have an answer. John Lisman, the Zalman Abraham Kekst Chair in Neuroscience and professor of biology at Brandeis University, and Matthew Wilson of MIT, have recently discovered an abnormality in the schizophrenic brain that could be responsible for many of the disease symptoms.

Unusual neural oscillations — brain waves — have long been associated with schizophrenia. The oscillations, or delta waves, are similar to slow oscillations seen in normal brains during sleep. But in schizophrenic brains, they occur during wakefulness.

The connection between these oscillations and schizophrenic symptoms, particularly cognitive deficits such as memory impairment, has been unclear. To understand this connection, Lisman artificially produced delta waves in mammalian brains using a new technique called optogenetics, which activates brain signals using light.

When the delta frequency light was turned on, Lisman saw a disruption in the working memory of rats. When it was turned off, the rodents were once again able to perform working memory tasks.

Also, Lisman and his team were able to activate the abnormal oscillations only in a tiny subpart of the thalamus, which is central to working memory, sleep, consciousness and sensory-information processing. This information hub is a region of the brain that has been a focus of schizophrenia research.

The research team noted that the oscillations produce an artificial signal that jams normal communication. The part of the thalamus that is supposed to carry information about working memory couldn't do the task at all with these sleep-like delta waves, and they suspect the abnormal delta oscillations seen in patients with schizophrenia are producing a similar jamming of normal signals.

Delta waves require a specific type of ion channel called a T-type Ca channel. These channels are of particular interest because they are one of the few types of ion channels implicated in schizophrenia by genetic studies.

According to Lisman, the next step would be to determine what kind of agents could be used to block these channels. Blocking these channels could block bad oscillations, which could have therapeutic value in patients who suffer this disabling mental illness.