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Visions Journal

A reminder that this article from our magazine Visions was published more than 1 year ago. It is here for reference only. Some information in it may no longer be current. It also represents the point of the view of the author only. See the author box at the bottom of the article for more about the contributor.

Medication Research in Psychiatry

New Trends and Discoveries

Sylvia Zerjav, PharmD, BCPP

Reprinted from the "Medications" issue of Visions Journal, 2007, 4 (2), pp. 27-28

People often think that there are many different kinds of medications available to treat mental illnesses. But in reality, there are not very many truly “novel” psychotropic† medications. Many of the so called “new drugs” work much the same way as the older drugs. If you look at antidepressants for example, there are currently 23 antidepressants available in Canada. However, you can group all of these into just six categories based on how they work in the body. All the antidepressants within each category are really pretty similar in both how effective they are and the side effects they cause.

So, is there anything really “new” on the horizon?


There are some interesting drugs for depression in the development stage. One area is the discovery of brain-derived neurotropic factor (BDNF). We now know that the brain is capable of repairing nerve cell damage and can even generate new neurons (brain cells that send and process information). Scientists first discovered the creation of new neurons (called neurogenesis) in animal brains in the 1960s, but did not find evidence of it in humans until the late 1990s. BDNF is actively involved in repairing damaged cells and generating new ones.

It appears that one of the problems people with depression have is that they’re less able to turn on BDNF than those who don’t have depression.1 People who suffer from depression are more likely to experience cognitive decline† (a decline in normal brain functions such as memory and thinking skills) as they get older than those who have never had depression.2-4 This decline is the result of gradual brain cell loss over the years.

Stressful life events can cause the onset of episodes of major depression in those with a genetic predisposition and in children who experience early life stress.5

We also know that stress can cause the destruction of brain cells, which may lead to cognitive decline if BDNF does not effectively generate new brain cells.

So there is a lot of research focused on BDNF and into agents that may act similarly to BDNF. There is hope that these agents will prevent depression and some of the consequences that extended stress has on our brains.


Schizophrenia is an illness that can wreak havoc with an affected person’s life because of the impairment associated with symptoms of the illness. Symptoms can include hearing voices inside one’s head, having bizarre beliefs that aren’t based on any facts, feeling paranoid, withdrawing socially, and being unable to concentrate and think clearly.

All of the currently available drugs used to treat schizophrenia (antipsychotics) reduce symptoms by reducing dopamine’s effects on nerve impulse transmission in specific areas of the brain. There are many side effects from these drugs, including significant weight gain and movement problems, such as tremors.

Research is now being conducted on a brain amino acid called glutamate. Interest in glutamate began when a street drug, PCP, also called “angel dust,” was found to cause symptoms similar to those in people with schizophrenia. By the 1980s, scientists discovered that PCP blocks the effects of glutamate on specific brain receptors. It was therefore logical to assume that stimulating glutamine receptors might improve schizophrenia.

There are many different glutamate receptors, and researchers are now focusing on those located in the prefrontal cortex, which is that part of the brain linked to learning and personality. Agents that are developed as a result of this research will really be the first truly novel antipsychotics, because they don’t affect dopamine directly, as all current antipsychotics do.

Alzheimer’s disease

One of the areas of greatest promise is in the treatment of Alzheimer’s disease. Alzheimer’s disease, an illness first described by German physician Alois Alzheimer almost a century ago, robs people of their memory and reason and results in progressive cognitive decline and a lingering death.

In Alzheimer’s diseases, masses of protein form in the brain and these masses, known as senile plaques, destroy brain cells (neurons). Some researchers have found that these senile plaques are linked to two substances: cholesterol and a chemical called ganglioside GM-1, found in the brain cells the disease attacks.6 Brain cell damage occurs when the proteins that make up these plaques attach to neurons. The plaque protein, called beta-amyloid, comes in different sizes, and they get larger as they age. Beta-amyloid’s ability to bind to neurons seems to depend on the amount of cholesterol and ganglioside GM-1 in the cell. The binding doesn’t occur if either one of the cholesterol or the ganglioside GM-1 is removed.

One of the drugs being studied, Caprospinol, has shown promise in removing beta-amyloid plaques and restoring memory in rats.7 Other drugs being studied, ANAVEX 1-41 and ANAVEX 2-73, may have neuroprotective and memory-promoting effects on Alzheimer’s disease.8

Other ideas include lowering cholesterol levels with anticholesterol drugs, such as lovastatin, because reducing cholesterol in brain cells should block the ability of beta-amyloid to bind the cells. Currently, it is not certain that lowering cholesterol levels will actually reduce the incidence of Alzheimer’s disease, but research is ongoing and some scientists believe that Alzheimer’s will become a disease of the past within the next 10 years.

About the author

Sylvia is a psychopharmacology consultant for the BC Mental Health Society and a Clinical Professor in Pharmaceutical Sciences at the University of British Columbia.

  1. Stahl, S.M. (2000). Essential psychopharmacology: Neuroscientific basis and practical applications (2nd ed.). Cambridge, UK: Cambridge University Press.

  2. Chen, P.S., McQuoid, D.R., Payne, M.E. et al. (2006). White matter and subcortical gray matter lesion volume changes and late-life depression outcome: A 4-year magnetic resonance imaging study. International Psychogeriatrics, 19(3), 445-456.

  3. Chodosh, J., Kado, D.M., Seeman, T.E. et al. (2007). Depressive symptoms as a predictor of cognitive decline: MacArthur studies of successful aging. American Journal of Geriatric Psychiatry, 15(5), 406-415.

  4. Leonard, B.E. & Myint, A. (2006). Inflammation and depression: Is there a causal connection with dementia? Neurotoxicity Research, 10(2), 149-160.

  5. Mann, J.J. & Currier, D. (2006). Effects of genes and stress on the neurobiology of depression. International Review of Neurobiology, 23, 153-189.

  6. Charleton, G. (2002). Alzheimer’s disease in real life, Advance: Research, Scholarship and Achievement at Texas A&M University.

  7. Samaritan Pharmaceuticals. (n.d.). Samaritan’s Alzheimer drug PS-233 (multimedia clip).

  8. Villard, V. Espallergues, J., Vamvakides, A. et al. (2007, May). Anti-amnesiac and neuroprotective potentials . . . in mice. Anavex Life Sciences Corp. Poster presentation at the 8e Colloque de la Société des Neurosciences, Montpellier, France.


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