Human Neurochemical Pathology Laboratory: Research Annual Report 2003

Section Head: Dr. Stephen Kish

The mandate of the Human Neurochemical Pathology Laboratory is to understand the causes of neuropsychiatric disorders by examining the human brain.

We continue to focus on studies of brain monoamine neurotransmitter systems in people who use amphetamine derivatives (including ecstasy) and in people with Parkinson's disease.

Ecstasy

Ecstasy is a widely used amphetamine derivative taken for its mild stimulant property and for its ability to increase the desire for friendliness.

We initiated a neuroimaging investigation, using positron emission tomography (PET ) to determine if ecstasy causes brain damage in young users of the drug. All subjects were tested by forensic hair analysis to confirm that the person actually used the drug (rather than another drug or combination of drugs sold as ecstasy).

We found the following:

1. Many people in the Toronto area who assume that they are using only ecstasy are unknowingly using more dangerous drugs (including other amphetamine derivatives), which "contaminate" the "ecstasy" tablets. The general public needs to be educated more about the lack of consistency in the quality of "ecstasy" that is being sold.
2. Our forensic drug hair analyses suggest that most, but not all, ecstasy users respond, to the best of their knowledge, truthfully to questions about past drug use.
3. Although rare, a very small number of people in the Toronto area can be identified as using ecstasy in the absence of other drugs that cause brain damage.
4. We have conducted brain scans of a small number of these "pure-ecstasy users" and have preliminary data about ecstasy's ability to damage brain serotonin neurons. A large replication study is now in progress.

Parkinson's Disease

Parkinson's disease (PD) is a movement disorder commonly associated with clinically significant depression.
Recent studies now confirm the clinical impression that the depression in PD affects the quality of life of the patient more than the motor disability.

Based on the longstanding hypothesis that a brain serotonin deficiency might be responsible for the depression in PD, we conducted a PET investigation to measure the number of serotonin neurons in people with PD who are depressed.

Contrary to the hypothesis, our preliminary data suggest that people with PD who are depressed, who are early in the course of their disorder, do not show a reduced number of brain serotonin neurons. A replication study is in progress.

• Print
  Share |