By: Jessica Scott
In most mental disorders, it is unclear how and when things go wrong. The field of neuroscience is still in its infancy, and our understanding of the mechanisms behind mental illnesses is greatly lacking. In many instances, we still don’t know how prescription medicines for mental illnesses work. One thing scientists have uncovered recently, however, is that the brain grows and changes our whole lives. Many neuroscientists are interested in studying these changes to learn how we develop and recover from mental illnesses.
Our neurons forms new connections – via projections called axons and dendrites – during normal processes like learning and memory formation, which carry on into old age. Perhaps most surprisingly (and excitingly!) it also appears that adult brains even generate brand-new neurons (neurogenesis). The brain’s ability to change, be it by neurogenesis, axon formation, or even the decay of neural connections, is collectively known as neuroplasticity.
Biologists are anxious to study the links between mental health and neuroplasticity both in terms of acquiring the illness and in recovery. Many of these biologists, in search of clues, have turned to the hippocampus. The hippocampus is a brain structure known for its role in memory formation, and it is one of the very few locations where neurogenesis can occur in adults. Even before this was known, hippocampal shrinkage was a well-documented phenomenon in neurological conditions such as Alzheimer’s. More recent studies have also shown decreased hippocampal volume in a number of mood-related disorders, including depression, PTSD, and schizophrenia.
Because of this interesting and exciting link between mental illnesses and hippocampal size, some scientists hypothesize that perhaps neuroplasticity – specifically, the loss of neurons in the hippocampus – might be causing these illnesses. For example, some studies have shown that people who are successfully treated for PTSD display increased hippocampal volume. (Other studies have shown no effect, so this question is still up for debate).
A study out of Harvard found a potential neuroplasticity-related treatment for negative* symptoms of schizophrenia. The study focused on a particular receptor in the brain called the NMDA receptor, which is located on the surface of neurons and helps relay signals from one neuron to the next. The NMDA receptor is also important for learning, memory, and neuroplasticity. Low NMDA receptor activity is associated with schizophrenia. In order to replicate this aspect of human disease, the research group studied mice with low-activity NMDA receptors. The mice in the study had cognitive deficits and the reduced hippocampal neuroplasticity associated with schizophrenia in humans. The researchers administered to these mice a compound called D-serine, which is naturally synthesized in the brain and activates the NMDA receptor. They found activating the NMDA receptor in this way restored hippocampal neuroplasticity to the mice. In addition, the mice’s behavioral and neurochemical deficits became normalized. The group thus concluded that D-serine treatment may be useful for correcting negative symptoms of schizophrenia in humans by means of improving hippocampal neuroplasticity.
Neurogenesis is not the whole answer to why people develop or recover from mental illnesses. It is also not a miracle cure, despite claims you’ve probably read on the internet about “harnessing the power of the brain” to make you smarter. Neuroplasticity is part of a large, complex puzzle. It is novel and fascinating and may even lead scientists to develop effective new medicines, but it is part of a nuanced and detailed system that, really, we are barely beginning to comprehend. As we understand and integrate multiple areas of neuroscience, we will begin to understand this amazing system. This in turn will help us better understand mental illness more thoroughly and give us hope for being able to appropriately treat these complex and as-yet-poorly-understood disorders.
*In psychology, “negative” symptoms are emotions or behaviors that should be there but aren’t. In schizophrenia, negative symptoms might include lack of pleasure, social withdrawal, or flat affect. This contrasts with “positive” symptoms, which are behaviors present in individuals with a particular condition but not in the general population. Hallucinations and delusions are two defining positive symptoms of schizophrenia. Most schizophrenia medications treat the positive symptoms while having little effect on negative symptoms, but the negative symptoms often affect an individual’s quality of life at least as much as positive ones. It is therefore vital to develop medications that do treat these somewhat ignored aspects of the disorder.