Theoretically, mutations in the genes of neurons can contribute to mental illness. After all, many psychiatric conditions are highly heritable in that genetic influence, rather than environmental inputs, accounts for a high percentage of risk. But the cancer model — find a defective gene, devise a corresponding treatment — is not remotely realistic for mental illness. This is because various mental conditions are linked to dozens, even hundreds, of genes.
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In schizophrenia, for example, genes have thus far been implicated, each contributing only a small amount of vulnerability. Some of the genes are involved in dopamine receptor function and glutamine neurotransmission. Several weeks ago, scientists made the discovery that a gene known as C4A within the histocompatibility region strongly contributes to the pruning of synapses nerve cell connections in the frontal lobes.
Pruning occurs normally in adolescence, but it happens much more aggressively in people with schizophrenia, due to a mutation in C4A. As a result, the tissue in the frontal lobes, the region involved with planning complex cognitive behavior, personality expression, decision-making, and moderating social behavior is winnowed too much. The unraveling of the genetic basis of pruning is a very exciting finding, but it only accounts for perhaps one-quarter of the risk of developing schizophrenia.
Other factors need to be present too.
Given the overall risk of schizophrenia is one percent, the presence of a C4A mutation increases the risk of developing the condition to 1. Researchers have therefore turned their attention to a more macro level of explanation: brain systems neural circuits and their interconnections. As researchers begin to undertake the gargantuan task of exploring the neuroscience of psychiatry, they face a big hurdle: namely, the fact that psychiatric diagnostic categories e.
Analogous formulations for psychiatry do not exist even though the earliest figures in neurology and psychiatry, including Freud, longed for brain-based explanations. For over a century, psychiatrists have believed that biological revelations were around the corner. In the early 20th century, Emil Kraepelin, the famous German psychiatrist who laid the foundation for the DSM, expected that the brain basis of psychosis would become manifest in his lifetime. In the s, brain research and especially receptor biology were opening new avenues for psychopharmacology. Still, they were largely confident that biological causes of mental illness would be uncovered by the turn of the 21st century.
Clinicians use the DSM as a common language to discuss patients, and researchers use it as a shared blueprint to guide systematic inquiry. In medicine, accuracy can be determined in several ways, most prominently by whether a diagnosis links to a unique, identifiable biological origin. Other indicators of validity include whether a diagnosis predicts the course of an illness and what kinds of treatments the illness will respond to.
Current psychiatric diagnoses are limited because they have negligible validity. Abundant evidence attests to this. It is not uncommon, for example, for a psychiatric patient to meet qualifications for several diagnoses at once. This is because the sharply delineated diagnoses in the manual do not correspond to independent, discoverable entities in nature. Indeed, in real life, boundaries between diagnoses are fuzzy.
As a result, many patients do not fit snugly into any of the procrustean categories. It also explains why doctors typically use trial and error to find the most effective medications, dosages, and combinations for various symptoms. A large study of major depression found, for example, that recovery with the first selected selective serotonin reuptake inhibitor e. In addition, because diagnoses do not represent discrete underlying psychobiological mechanisms, psychiatrists typically, though not always, find themselves targeting symptoms rather than disorders.
So, while psychiatrists will almost surely prescribe an antidepressant for a patient with major depressive disorder, the very same antidepressant drug can be helpful in obsessive-compulsive disorder, eating disorders, and panic attacks. Conversely, a single condition may require one medication for each symptom.
The manic phase of bipolar disorder, for example, often requires a mood stabilizer to control the excursions of mood and a sedating antipsychotic to combat accompanying paranoia, and, perhaps, a benzodiazepine, such as Valium, to quell agitation. Finally, the short-term prospects for new pharmacotherapies are not particularly encouraging.
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Investigating the biological dimensions of mental illness means that researchers must be freed from the bounds of conventional diagnostic categories. Each of the five domains in the RDoC schema represents a capacity that is essential to human survival and, thus, has been evolutionarily conserved. So, for example, the capacity for paying attention would fall under the domain of arousal and regulation. Humans need to focus their attention lest they be crippled by distraction.
A problem with an attentional system that fails to filter extraneous inputs as we find in attention deficit and hyperactivity disorder, or ADHD, and schizophrenia will manifest as some degree of impairment. Within each domain there is a set of related constructs. For example, within the Cognition domain, we find Auditory Perception Construct and, within that, further breakdown into types of auditory hallucination.
Phobias, anxiety, and excessive fear responses represent types of acute threats. Research under a strict RDoC paradigm thus dispenses completely with formal diagnoses and instead focuses on the neural circuitry tied to psychobiological systems. At this time, only a modest body of research has been performed under such conditions.
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The NIMH presents a recent study as an example of an RDoC-inspired investigation, but in fact it uses conventional diagnoses as a starting point. Psychiatrist Carol Tamminga at the University of Texas Southwestern Medical Center and her team examined about patients diagnosed with one of three conditions in which psychosis is a prominent feature: schizophrenia, schizoaffective disorder, and bipolar disorder.
The researchers asked patients to complete a battery of neurocognitive and perceptual tasks to assess planning and memory capabilities, eye-tracking, inhibition, and brainwave responses to auditory stimuli.
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They identified sets of biomarkers that differentiated subgroups of patients. Biotype 1 were most impaired in exerting control over attention and information-processing, and were the most socially withdrawn. Biotype 2 cases showed intermediate levels of impaired cognitive control but had a normal to accentuated ability to detect and process visual and auditory stimuli. Those classified as Biotype 3 processed information normally but had some problems with sensorimotor reactivity. They performed the best socially and had the lowest levels of hallucinations and delusions.
These findings, pending replication, are important pieces of a daunting tapestry. The treatment implications, however, remain a matter of speculation. Perhaps, as Dr. Tamminga and her team think, treatments for Biotype 1 should target cognitive control and enhance brain mechanisms for discerning the relevance of environmental stimuli. Anti-psychotic medication at a low dose would likely be needed as well.
Precision psychiatry is a very long game. Many think it is also a very long shot. The odds of finding a single mutation that wields a large and straightforward influence on any given mental disorder are virtually nil. The designers of the RDoC criteria say they are very much aware of the pitfalls of explanatory reductionism: the all-too-common temptation among some neuroscientists to believe that the mind can be explained solely by knowing about the brain.
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