Uncovering the biology of depression yale scientific magazine. Whatever the cause, the condition is associated with physiological and chemical changes. The connexion scientists made between an improved mood in patients with tuberculosis and higher levels of monoamines in their brains led to further research into mao inhibitors maois as a treatment for depression lopezmunoz et al. For many years, the prevailing hypothesis of depression has been that a deficit in monoamine neurotransmitters, notably norepinephrine and serotonin, underlies depression. Jul 21, 2016 consistent with the monoamine hypothesis, these monoamine oxidase inhibitors not only increase the concentration of monoamines but also have been shown to curb depression. In the 1960s, the catecholamine hypothesis was a popular explanation for why people developed depression. Depression monoamine hypothesis psychology wiki fandom. In the reluctance of the scientific community to embrace this hypothesis is where i see the beauty of science. In order to test this hypothesis and more fully characterize the role of serotonin and catecholamines in the pathophysiology of depression and the mechanism of action of antidepressant treatments, our research group has conducted a series of studies evaluating monoamine depletion induced brief clinical relapse following different types of. Serotonin is eventually broken down by the body and new serotonin is made by neurons. N2 the monoamine hypothesis of depression predicts that the underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine, and or dopamine in the central nervous system. The discovery that reserpine depletes brain monoamines was an important factor in the development of the monoamine hypothesis of depression, and it continues to be widely cited in support of this hypothesis.
Since the early 1960s, the monoamine hypothesis has been a reference point for understanding the etiology of the electrical defects associated with monoaminerelated disease and. N2 the symptoms of depression can be improved by agents that. The breakdown products can be detected in the cerebrospinal fluid csf, which bathes the brain and spinal cord. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic andor serotonergic. The monoamine hypothesis of depression, a glutamate receptor, the state of innovation in highly prevalent chronic diseases volume i. This hypothesis suggested that a deficiency of the. The lesion may comprise deficiencies in the absolute concentrations of norepinephrine and or.
Depression major depression is defined as persistent months long, profound blues or irritable mood, and loss of interest interfering with normal functioning. According to one theory known as the social competition hypothesis, depression throughout evolution has been a adaptive strategy to end prolonged conflict. While psychotherapy is helpful for some people with depression, if there is a chemical imbalance in the. Evidence suggests there is a reduction in activity or transmission of noradrenalin na and or serotonin 5ht in the forebrain areas of depressed patients. Depression may be caused by a stressinduced deficiency in monoaminergic activation of genes that. A brief history of the development of antidepressant drugs. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic andor serotonergic systems and. Monoamine hypothesis definition of monoamine hypothesis by. Pollard perspectives in medicinal chemistry 2014 10.
Neuronal plasticity or remodeling is a fundamental concept that underlies central nervous system function as it relates to many types. The chemistry of depression neurotransmitters and more. For example, people with major depressive disorder may also have fewer monoamine nerve receptors, or possibly less. The catecholamine theory of depression fly fishing devon. Monoamine hypothesis is a biological theory stating that depression is caused by the underactivity in the brain of monoamines, such as dopamaine, serotonin, and norepinephrine. There were revealed significant increase of platelet monoamine oxidase activity and cortisol level. Furthermore, an attempt will be made to give a possible explanation of the mechanisms by which zinc interacts with the monoamine system in the context of depression and neural plasticity. Professor of psychiatry and pharmacology director at yale university, ronald duman studies depression, a serious issue that affects approximately 17% of the u. Depression is generally thought of as dysfunction, but it is much more common than schizophrenia, and its prevalence does not increase with age the way dementia and other organic dysfunction commonly does. Although it took decades of testing and revising before the monoamine hypothesis became a widely accepted explanation for depression, one could argue based on its now recognized shortcomings that we accepted it too readily. B, during a major depressive episode, monoamine oxidase a maoa density is elevated, resulting in greater metabolism of monoamines, such as serotonin, norepinephrine, and dopamine, in the brain.
The monoamine hypothesis of depression is that depression is a result of under activity of monoamines especially serotonin. Depression not only involves the mind, it also involves the body and thoughts. There is a general consensus in the scientific community that low levels of monoamine neurotransmitters are a major. Besides the fact that antidepression drugs are all monoamine agonists, there is other evidence that supports the theory. Regardless of how credit is allocated, such imbalance theories i. What evidence supports this hypothesis as a cause of affective disorder. Monoamine receptor hypothesis of depression 2019 my. Knocking the monoamine theory from the center stage of depression has marked a fundamental change in the field of psychology, and. Depression is no longer seen as a disorder of monoamine neurotransmitters discuss this assertion in the light of the current neurobiological hypotheses of depression. Biology of depression neurotransmitters depression. It means that patients with anxious depression are characterized by profound disturbances of monoamine metabolism and hormonal status that are the reflection of disturbed homeostasis as a whole. Monoamines are neurotransmitters that include serotonin, dopamine, norepinephrine, and epinephrine monoamine hypothesis of depression.
J clin psychiatryhistory and evolution of the monoamine. In the 1950s, the amine hypothesis of depression was proposed after it was observed that patients treated for hypertension with reserpine developed depression. The monoamine hypothesis posits that depression is caused by decreased monoamine function in the brain. Hypothesis ofthepathophysiology depression an evolving hypothesis of the pathophysiology and treatment of depression involves adaptation or plasticity of neural systems. Understanding depression pathophysiology is challenging because varying depression symptomatology cannot be explained by single hypothesis. Depression may be caused by a stressinduced deficiency in monoaminergic activation of genes that code for neurotrophic factors. Monoamine theories associate depression with reduced brain monoamine levels. History and evolution of the monoamine hypothesis depression. Monoamine hypothesis of depression psychology wiki fandom. This hypothesis was first started when doctors noticed that reserpine, a.
This mainstream story has been undermined by a failure to. Feb 14, 2012 since the early 1960s, the monoamine hypothesis has been a reference point for understanding the etiology of the electrical defects associated with monoamine related disease and the mechanism of action of reuptake inhibitors. History and evolution of the monoamine hypothesis of. The monoamine hypothesis has dominated our understanding of depression and of pharmacological approaches to its management and it has produced several generations of antidepressant agents, ranging from the monoamine oxidase inhibitors maois, through tricyclics tcas and selective serotonin reuptake inhibitors ssris, to the recently. The origins of the monoamine hypothesis of depression. This depletion may be related to a lack of neurotransmitters or some other fault.
Monoamine hypothesis depression and neurotransmitters. Apr 07, 20 psychology definition of monoamine hypothesis. In the mid1990s, the life time risk for depression was estimated as 3% to 4% worldwide. Understanding the chemistry of depression may help people better understand the treatments available. Evolution of the monoamine hypothesis of depression 2019. The symptoms of depression can be improved by agents that act by various mechanisms to increase synaptic concentrations of monoamines. These theories achieved broad popularity in the mid1960s. Blue genes and the monoamine hypothesis of depression. According to the monoamine hypothesis, depression can be ascribed to deficits in the monoamine neurotransmitters. The monoamine hypothesis of depression states that a depletion of neurotransmitters, known as monoamines, within the brain leads to depression.
In the 1950s the monoamine oxidase inhibitors maois and tricyclic antidepressants were accidentally discovered to be effective in the treatment of depression. Levels of serotonin breakdown products appear to be low in the csf of people suffering from serious. A, description of monoamine release in a synapse in a healthy person. The original monoamine hypothesis of depression was based on serendipitous discoveries. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic and or serotonergic. T1 history and evolution of the monoamine hypothesis of depression. Depression can be caused by a combination of factors, including genetics, environmental factors, trauma and stress. Uncovering the biology of depression yale scientific. For five decades it has been generally accepted that reserpine, an antihypertensive and antipsychotic drug, causes depression. The origins and early development of and problems with the.
Many antidepressant drugs acutely increase synaptic levels of the monoamine neurotransmitter, serotonin, but they may also enhance the levels of two other neurotransmitters, norepinephrine and dopamine. Apr 25, 2016 although the monoamine theory still circulates in laymen conversation, modern science has largely discredited the simplistic idea, and is moving towards a more manyfactored, immunitycentric model of depression. It generally takes 23 weeks of chronic treatment before an antidepressant begins to have a clinical benefit, yet the drugs pharmacological effect for example, its inhibition of moa, or reuptake is immediate. In this paper, we firstly summarized the evidence challenging the monoamine hypothesis and proposed that the antidepressant efficacy of ssris is not. Biochemical bases of monoamine and hormonal interactions in. Argues that the monoamine hypothesis of depression does not address key issues such as why antidepressants are also effective in other disorders such as panic disorder, obsessivecompulsive disorder, and bulimia, and why all drugs that enhance serotonergic or noradrenergic transmission are not necessarily effective in depression. According to the world health organization, major depressive disorder mdd currently impacts 300 million individuals worldwide and is the leading cause of disability globally. Evolutionary approaches to depression are attempts by evolutionary psychologists to use the theory of evolution to shed light on the problem of mood disorders. After studying the material on this page you should be able to. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the underlying biological or neuroanatomical basis for depression is a deficiency of central noradrenergic and or serotonergic systems and that targeting this neuronal lesion with an antidepressant would tend to. This finding led to the adoption of the monoamine hypothesis of depression, first put forward over 30 years ago, which proposes that the. N2 the symptoms of depression can be improved by agents that act by various mechanisms to increase synaptic concentrations of monoamines. Depression is upregulation of the monoamine receptors due to a reduction in monoamine levels.
From melancholia to depression a history of diagnosis and treatment1 table of contents introduction 2 diagnosis and classifications of melancholia and depression 7. Blue genes and the monoamine hypothesis of depression stephen m. History and evolution of the monoamine hypothesis of depression by. Depression is due to functional deficits in monoamine nts what is the monoamine receptor hypothesis of depression. For example, monoamine oxidase inhibitors have been shown to improve mood and increase activity in people who are not depressed rang et al. Serotonin, depression, neurogenesis, and the beauty of. It has been almost 50 years since the monoamine hypothesis of depression was articulated, and just over 50 years since the first pharmacological treatment for mdd was discovered. Sadness and low mood will be used to refer to a range of negative emotions that would not be classified as mdd. The monoamine hypothesis has been accepted as the most common hypothesis of major depressive disorder mdd for a long period because of its simplicity and understandability. History and evolution of the monoamine theory of depression. Many antidepressant drugs acutely increase synaptic levels of. Depressions evolutionary roots two scientists suggest that depression is not a malfunction, but a mental adaptation that brings certain cognitive advantages by paul w. The breakdown products can be detected in the cerebrospinal fluid.
Monoamine theory of depression exposed as incomplete, simplistic. Ne regulation of 5ht release monoamine interactions. Tthe monoamine hypothesis of depression predicts that the underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine, andor dopamine in the central. Actually, most currently used antidepressants have been considered to act based on the monoamine hypothesis.
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