{"id":168,"date":"2022-01-28T13:00:21","date_gmt":"2022-01-28T13:00:21","guid":{"rendered":"https:\/\/blogs.imperial.ac.uk\/molecular-science-engineering\/?p=168"},"modified":"2022-04-08T11:40:29","modified_gmt":"2022-04-08T10:40:29","slug":"molecular-science-mental-health-2","status":"publish","type":"post","link":"https:\/\/blogs.imperial.ac.uk\/molecular-science-engineering\/2022\/01\/28\/molecular-science-mental-health-2\/","title":{"rendered":"Molecular mental health 1 – Depression and anxiety"},"content":{"rendered":"

Depression and anxiety are the most common mental health illnesses, affecting 264 million and 284 million people worldwide, respectively \u2013 equivalent to 3.4% and 3.8% of the global population. However, it\u2019s thought that many cases are unreported – the real figures are expected to be double what is recorded. What’s going on at a molecular level in the brain during depression and anxiety? How does medication change this?\u00a0<\/span><\/p>\n

<\/p>\n

by Naveesha Karunanayaka, Kieran Brophy and Steph Pendlebury<\/span><\/span><\/strong><\/em><\/p>\n

Despite\u00a0increased\u00a0understanding\u00a0of\u00a0mental health illnesses, there is\u00a0still\u00a0a lack of quantitative measures to diagnose them.\u00a0Although closely related,\u00a0anxiety\u00a0is associated with a high-energy\u00a0state, whereas\u00a0depression\u00a0is thought of as a\u00a0low-energy\u00a0state.\u00a0They\u00a0are\u00a0both\u00a0thought to result\u00a0from\u00a0disruption to\u00a0emotional centres in the brain, namely the amygdala,\u00a0hippocampus\u00a0and other components of the pre-frontal cortex.\u00a0Both\u00a0illnesses\u00a0relate to a lack of\u00a0chemical\u00a0regulation in these areas leading to an imbalance of chemicals in the brain,\u00a0which\u00a0impacts\u00a0an individual\u2019s response to various situations.\u00a0Different areas of the brain show vulnerability at different stages of life. Environmental impacts,\u00a0such as traumatic and experiences or chronic stress over an extended\u00a0period of time,\u00a0can result in depression or anxiety.\u00a0<\/span>\u00a0<\/span><\/p>\n

\"parts
Figure 1 – parts of the brain related to anxiety and depression (Boyle,2020)<\/figcaption><\/figure>\n

Depression<\/span>\u00a0<\/span><\/h2>\n

The science\u00a0behind\u00a0depression<\/span>\u00a0<\/span><\/h3>\n

The\u00a0areas\u00a0in the brain\u00a0that are known to play a significant role\u00a0in depression\u00a0are the amygdala,\u00a0thalamus\u00a0and hippocampus\u00a0(see Figure\u00a01).\u00a0Using sophisticated brain imaging techniques,\u00a0studies have shown\u00a0that the hippocampus\u00a0is\u00a09% to 13% smaller in\u00a0certain\u00a0people suffering from depression.\u00a0Experts believe that\u00a0stress can suppress the production of new neurons\u00a0(nerve cells) in the hippocampus, making it smaller.\u00a0This happens due to shrinkage of dendrites, which is where a neuron receives input from other cells, and loss of spines in the neurons.\u00a0\u00a0Although\u00a0antidepressants immediately\u00a0increase the number of\u00a0neurotransmitters in the brain, many people don\u2019t feel better for a couple of weeks or more. This could be because mood only improves once there has been new nerve growth,\u00a0which allows\u00a0new connections, but\u00a0this\u00a0takes time.\u00a0So,<\/span>\u00a0the\u00a0important effect\u00a0of these medications may be in generating new neurons.<\/span>\u00a0<\/span><\/p>\n

Molecular origins<\/span>\u00a0<\/span><\/h3>\n

Neurotransmitters\u00a0are molecules used by the nervous system, which act between neurons, to transmit messages across the body.\u00a0These\u00a0play an essential role in regulating mood;\u00a0they can either inhibit or activate the neuron at which they arrive. They also affect the initial neuron that released the\u00a0neurotransmitter. This is because\u00a0a feedback mechanism reabsorbs the\u00a0excess\u00a0neurotransmitters into the cell;\u00a0the\u00a0excess\u00a0is broken down by enzymes. However, when this system\u00a0fails,\u00a0it\u00a0can lead to\u00a0increased or decreased sensitivity in the receptor neuron,\u00a0or\u00a0the emitting neuron may generate too much or too little\u00a0neurotransmitter.\u00a0This chemical\u00a0imbalance\u00a0is a common cause of depression.<\/span>\u00a0<\/span><\/p>\n

\"stress
Figure 2 – stress response via HPA axis (Knapp. 2020)<\/figcaption><\/figure>\n

Stress\u00a0can also play\u00a0a key\u00a0role\u00a0in depression.\u00a0The\u00a0stress\u00a0response signal originates\u00a0from\u00a0the hypothalamus,\u00a0which is\u00a0linked to both the pituitary and adrenal glands\u00a0forming\u00a0the hypothalamic-pituitary-adrenal (HPA) axis\u00a0(Figure 2).\u00a0When\u00a0a threat is detected,\u00a0the hypothalamus releases\u00a0a hormone called the\u00a0Corticotropin-Releasing\u00a0Hormone (CRH),\u00a0which\u00a0stimulates\u00a0the body\u00a0by\u00a0causing\u00a0the\u00a0adrenocorticotropic hormone (ACTH)\u00a0to be\u00a0released\u00a0into the bloodstream. This combined release of hormones culminates in the release of cortisol.\u00a0Usually, once a certain blood concentration of cortisol is reached, alleviating the\u00a0stressor,\u00a0a negative feedback mechanism between the cortisol,\u00a0CRH and ACTH occurs,\u00a0bringing the\u00a0level of cortisol is back down to a\u00a0normal level.\u00a0<\/span>\u00a0<\/span><\/p>\n

Dysfunction of the HPA axis is linked\u00a0to\u00a0mental disorders,\u00a0<\/span>via<\/span><\/i>\u00a0increased levels\u00a0of CRH and cortisol.\u00a0This occurs when the body detects\u00a0ongoing\u00a0stressors,\u00a0resulting in\u00a0a continuous\u00a0stress\u00a0response.\u00a0The body becomes accustomed to this\u00a0heightened\u00a0level of stress and increased levels of cortisol.\u00a0Consequently, the negative feedback system breaks down and the cortisol level rises in the body\u00a0as more and more CRH and ACTH is produced,\u00a0creating\u00a0a\u00a0cycle\u00a0of\u00a0increasing stress.\u00a0<\/span>\u00a0<\/span><\/p>\n

Prolonged exposure to high cortisol\u00a0can\u00a0cause atrophy\u00a0(the progressive degeneration of muscle or other tissue)\u00a0of the hippocampus and hypertrophy\u00a0(increased\u00a0size)\u00a0of the amygdala.\u00a0High cortisol\u00a0levels\u00a0induce exhaustion,\u00a0and can\u00a0also\u00a0affect other neurotransmitters, such as\u00a0causing\u00a0depletion of\u00a0serotonin.\u00a0Selective serotonin reuptake inhibitors (SSRIs) are\u00a0often\u00a0used to restore full activity of serotonin in an individual with depression.<\/span>\u00a0<\/span><\/p>\n

Anxiety<\/span>\u00a0<\/span><\/h2>\n

The science of\u00a0anxiety<\/span>\u00a0<\/span><\/h3>\n

The amygdala\u00a0and hippocampus\u00a0also\u00a0play a key role in anxiety and mood regulation.\u00a0The amygdala\u00a0is responsible for detecting observable external emotional stimuli and initiating a suitable\u00a0behavioural\u00a0response.\u00a0It\u00a0deals mainly with fear,\u00a0aggression\u00a0and defensive behaviour, as well as\u00a0the\u00a0retrieval of memories related to these\u00a0emotions.\u00a0Although \u201canxiety\u201d\u00a0and\u00a0\u201cfear\u201d\u00a0are\u00a0sometimes\u00a0used interchangeably, evidence\u00a0suggests\u00a0that there are different\u00a0molecular\u00a0mechanisms underlying\u00a0these emotions.\u00a0<\/span>\u00a0<\/span><\/p>\n

Molecular\u00a0causes of anxiety<\/span>\u00a0<\/span><\/h3>\n

Fear is a fight-or-flight response to an identifiable, immediate threat.\u00a0Anxiety,\u00a0however,\u00a0is\u00a0a\u00a0prolonged apprehension\u00a0around\u00a0uncertain events\u00a0that\u00a0do not\u00a0pose an imminent threat. Amygdala lesions, areas where the amygdala is damaged due to illness or invasive surgery,\u00a0tend to block\u00a0the\u00a0fear response but not prolonged anxiety states.\u00a0The reason for this difference\u00a0could be\u00a0because the central amygdala may be involved with processing cues relating to fear, while information regarding anxiety is processed elsewhere. However, this is beginning to be contested.\u00a0<\/span>\u00a0<\/span><\/p>\n

Anxiety disorders develop when the activity of the amygdala\u00a0increases past normal levels and becomes uncontrollable;\u00a0the amygdala overreacts to situations that aren\u2019t\u00a0actually\u00a0threatening.\u00a0\u00a0Some\u00a0research suggests\u00a0that different regions of the amygdala are activated\u00a0in\u00a0different anxiety disorders.\u00a0However,\u00a0we know that\u00a0the central\u00a0amygdala\u00a0has\u00a0primary control\u00a0of\u00a0all\u00a0anxiety-related behavioural responses.\u00a0Lesions in\u00a0the central amygdala\u00a0cause decreased levels of\u00a0the hormones\u00a0CRH and ACTH. Consequently, the levels of these hormones are too low to\u00a0release cortisol\u00a0into the bloodstream, so\u00a0stress is not alleviated.\u00a0<\/span>\u00a0<\/span>\u00a0<\/span><\/p>\n

The amygdala also receives input from\u00a0other regions of the brain:\u00a0the hippocampus,\u00a0thalamus\u00a0and hypothalamus. The\u00a0molecular\u00a0mechanisms of the\u00a0<\/span>hypothalamic-pituitary-adrenal\u00a0(HPA)\u00a0<\/span>axis,\u00a0linked to depression,\u00a0also play a role in anxiety.\u00a0Long-term increased levels of CRH and cortisol\u00a0make\u00a0the HPA axis hypersensitive,\u00a0causing\u00a0a cycle of constant stress and worry.\u00a0In addition, the volume and neurogenesis\u00a0(the biological process\u00a0of\u00a0nervous tissue growth)\u00a0of the hippocampus\u00a0are related to\u00a0stress sensitivity and\u00a0stress\u00a0response.\u00a0Smaller sized\u00a0hippocampi,\u00a0linked with depression,\u00a0may generate\u00a0stronger anxiety symptoms. Lesions\u00a0in the\u00a0hippocampus\u00a0may\u00a0prevent\u00a0the ability to avoid stressful stimuli.\u00a0Sustained levels of stress\u00a0over an extended\u00a0period of time\u00a0have\u00a0been linked with neuron growth suppression in the hippocampus,\u00a0which is\u00a0a key factor in anxiety and depression.<\/span>\u00a0<\/span><\/p>\n

Treatment<\/span>\u00a0<\/span><\/h2>\n

Currently,\u00a0some of\u00a0the most common forms\u00a0of\u00a0treatment\u00a0for depression and anxiety\u00a0are\u00a0psychotherapy\u00a0or cognitive behavioural therapy (CBT),\u00a0which is talk therapy,\u00a0and pharmacotherapy\u00a0–\u00a0the use of medication.\u00a0<\/span>\u00a0<\/span><\/p>\n

Use of medication<\/span>\u00a0<\/span><\/h3>\n

Several different medication options are available; however, all may result in side effects of different severity.\u00a0The\u00a0first line\u00a0of\u00a0medications used\u00a0for both anxiety and depression\u00a0are usually selective serotonin reuptake inhibitors. These\u00a0are\u00a0better tolerated in the case of\u00a0overdose,\u00a0and\u00a0have relatively\u00a0positive benefit\/risk balance\u00a0in comparison to alternatives.\u00a0Benzodiazepine is sometimes used,\u00a0however, treatment using this drug could lead to central nervous system damage, as well as impairment in cognitive function\u00a0and\u00a0other side effects.\u00a0Often preference to\u00a0newer alternative\u00a0drugs\u00a0is\u00a0given over benzazepine based on the known risks of its use, rather than the merit of the other drugs.\u00a0Proper risk\/benefit analysis\u00a0for any medication is essential.\u00a0<\/span>\u00a0<\/span><\/p>\n

Second line treatments for both disorders are usually tricyclic antidepressants (TCAs),\u00a0however, adverse effects are much more\u00a0frequent,\u00a0and they are very toxic in the case of overdose. Therefore, these drugs are not advised to be used with suicidal patients.\u00a0<\/span>\u00a0<\/span><\/p>\n

A key research challenge is to understand the molecular nature of these drugs\u2019 effects \u2013 good and bad \u2013 so that better, more targeted treatments can be developed.\u00a0<\/span>\u00a0<\/span><\/p>\n

Incorporating Cognitive Behavioural Therapy<\/span>\u00a0<\/span><\/h3>\n
\"'The
Figure 3 – ‘The cognitive triad of negative core beliefs’ (Fenn & Byrne, 2013)<\/figcaption><\/figure>\n

Cognitive behavioural therapy (CBT) is\u00a0an\u00a0intervention for psychiatric disorders such as depression\u00a0and\u00a0anxiety disorders.\u00a0It tackles\u00a0the\u00a0inner beliefs of the patient (Figure 3), however, the neural mechanisms of action behind it\u00a0are\u00a0unclear.\u00a0It is one of the most effective treatment strategies\u00a0for anxiety and\u00a0depression and\u00a0provides a significantly better outcome when\u00a0it\u2019s\u00a0combined with pharmacotherapy,\u00a0compared to\u00a0the use of pharmacotherapy alone.\u00a0Relapse rates are\u00a0also\u00a0much lower\u00a0when\u00a0using\u00a0a combination of\u00a0CBT\u00a0and\u00a0pharmacotherapy.\u00a0<\/span>\u00a0<\/span><\/p>\n

\u00a0<\/span>Psychotherapy is recommended and accepted as an effective treatment used commonly for mild to moderate episodes. However, areas of the world that do not have enough qualified therapists\u00a0are limited to\u00a0the use of pharmacotherapy on its own as the first line of treatment.<\/span>\u00a0<\/span><\/p>\n

Conclusions<\/span>\u00a0<\/span><\/h2>\n

Anxiety and depression have a lot in common in terms of symptoms,\u00a0diagnosis\u00a0and treatment. A precursor for both illnesses is clearly stress,\u00a0through the action of the HPA axis, regulating the\u00a0release\u00a0and feedback of certain hormones, which has a huge impact on the composition of the amygdala and hippocampus.\u00a0The negative feedback system of the HPA axis\u00a0on cortisol and stress\u00a0plays a\u00a0major\u00a0role in both illnesses. Equally important are neurotransmitters,\u00a0such as serotonin and CRH,\u00a0that work to reduce stress states and promote mood regulation. Treatment of\u00a0anxiety and depression\u00a0is\u00a0not clear-cut,\u00a0and\u00a0not without side-effects.\u00a0The current best\u00a0treatment option is\u00a0first-line medications, such as SSRIs,\u00a0combined with\u00a0cognitive behavioural therapy\u00a0–\u00a0this\u00a0provides\u00a0chemical balance and mental strength.\u00a0The molecular basis of the benefit of CBT is\u00a0not yet understood.<\/span>\u00a0<\/span><\/p>\n

This is part of a blog series on the molecular science of mental health<\/a>. Coming up next: schizophrenia<\/a>, diagnostic tools<\/a> and digital twins<\/a>.<\/p>\n

Further reading<\/span><\/b>\u00a0<\/span><\/h2>\n

Alschuler, L. (n.d.).\u00a0<\/span>HPA Axis & Stress Response: Hypothalamic Pituitary Adrenal Axis.\u00a0<\/span><\/i>Available from:\u00a0<\/span>https:\/\/www.integrativepro.com\/articles\/the-hpa-axis<\/span><\/a>\u00a0<\/span>[Accessed 11<\/span>th<\/span>\u00a0July 2021].<\/span>\u00a0<\/span>\u00a0<\/span><\/p>\n

Bandelow, B., Michaelis, S., &\u00a0Wedekind, D. (2017). Treatment of anxiety disorders.\u202f<\/span>Dialogues in clinical neuroscience<\/span><\/i>,\u202f<\/span>19<\/span><\/i>(2), 93\u2013107.\u00a0doi:\u00a0<\/span>https:\/\/doi.org\/10.31887\/DCNS.2017.19.2\/bbandelow<\/span><\/a>\u00a0<\/span>\u00a0<\/span>\u00a0<\/span><\/p>\n

Boyle, M. (2020).\u00a0<\/span>The Amygdala and the emotional brain: when fear overrides the rational.\u00a0<\/span><\/i>Available from:\u00a0<\/span>https:\/\/www.vitawell.com.au\/blog\/the-amygdala-and-the-emotional-brain–when-fear-overrides-the-rational-<\/span><\/a>\u00a0[Accessed 20th July 2021].<\/span>\u00a0<\/span>\u00a0<\/span><\/p>\n

Duval E,\u00a0Javanbakht\u00a0A,\u00a0Liberzon\u00a0I. Neural circuits in anxiety and stress disorders: a\u202ffocused review.\u202f<\/span>Therapeutics and\u00a0Clinical\u00a0Risk Management<\/span><\/i>.\u00a011:115-126.\u00a0doi:\u00a0https:\/\/doi.org\/10.2147\/TCRM.S48528<\/a>.<\/span>\u00a0<\/span><\/p>\n

Fenn, K. and Byrne, M. (2013).\u00a0The key principles of cognitive behavioural therapy.\u00a0<\/span>InnovAiT.\u00a0<\/span><\/i>6(9): 579-585.\u00a0doi:\u00a0<\/span>https:\/\/doi.org\/10.1177%2F1755738012471029<\/span><\/a>\u00a0<\/span>\u00a0<\/span><\/p>\n

Harvard Medical School (n.d.).\u00a0<\/span>What causes depression?\u00a0<\/span><\/i>Available from:\u00a0<\/span>https:\/\/www.health.harvard.edu\/mind-and-mood\/what-causes-depression<\/span><\/a>\u00a0[Accessed 10th July 2021].<\/span>\u00a0<\/span><\/p>\n

Irle,\u00a0E.,\u00a0Ruhleder,\u00a0M.,\u00a0Lange,\u00a0C.,\u00a0Seidler-Brandler,\u00a0U.,\u00a0Salzer,\u00a0S.,\u00a0Dechent,\u00a0P.,\u00a0Weniger,\u00a0G.,\u00a0Leibing,\u00a0E.,\u00a0Leichsenring, F. (2010).\u00a0Reduced\u00a0amygdalar\u00a0and hippocampal size in adults with generalized social phobia.\u00a0<\/span>Journal of Psychiatry & Neuroscience.<\/span><\/i>35(2): 126\u2013131.\u202fdoi:\u202f10.1503\/jpn.090041<\/a><\/span>.<\/span><\/p>\n

Knapp, S. (2020).\u00a0<\/span>HPA Axis.\u00a0\u00a0<\/span><\/i>Available from:https:\/\/biologydictionary.net\/hpa-axis\/<\/span><\/i><\/a>\u00a0\u00a0<\/span><\/i>[Accessed 26th December 2021].<\/span>\u00a0<\/span>\u00a0<\/span><\/p>\n

Linsambarth,\u00a0S.,\u00a0Moraga-Amaro,\u00a0R.,\u00a0Quintana-\u00a0Donoso,\u00a0D.,\u00a0Rojas, S.\u00a0and\u00a0Stehberg, J. (2017).\u00a0<\/span>The Amygdala and Anxiety.\u00a0<\/span><\/i>doi: 10.5772\/intechopen.68618<\/a>.<\/span>\u00a0<\/span><\/p>\n

Martin,\u00a0E.I,\u00a0Ressler,\u00a0K.J.,\u00a0Binder,\u00a0E.,\u00a0Nemeroff, C.B. (2009).\u00a0The Neurobiology of Anxiety Disorders: Brain Imaging, Genetics, and\u00a0Psychoneuroendocrinology.\u00a0<\/span>Psychiatric Clinics of North America.\u00a0<\/span><\/i>32(3): 549\u2013575.\u202fdoi:\u202f10.1016\/j.psc.2009.05.004.<\/a><\/span><\/p>\n

Ritchie, H.\u00a0and\u00a0Roser, M.\u00a0(2018) – “Mental Health”.\u00a0<\/span>Published online at OurWorldInData.org.<\/span><\/i> Available from: https:\/\/ourworldindata.org\/mental-health<\/a> [Accessed 9<\/span>th<\/span>\u00a0July 2021].<\/span>\u00a0<\/span><\/p>\n

Stephens,\u00a0M.A.C.,\u00a0Wand, G. (2012). Stress and thee HPA axis.\u00a0<\/span>Alcohol Research<\/span><\/i>.\u202f34(4): 468\u2013483.\u00a0Available from:\u00a0<\/span>https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3860380\/<\/span><\/a>\u00a0[Accessed 11<\/span>th<\/span>\u00a0July 2021].<\/span>\u00a0<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"

Depression and anxiety are the most common mental health illnesses, affecting 264 million and 284 million people worldwide, respectively \u2013 equivalent to 3.4% and 3.8% of the global population. However, it\u2019s thought that many cases are unreported – the real figures are expected to be double what is recorded. What’s going on at a molecular […]<\/p>\n","protected":false},"author":1585,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[81449],"tags":[],"class_list":["post-168","post","type-post","status-publish","format-standard","hentry","category-mental-health"],"yoast_head":"\nMolecular mental health 1 - Depression and anxiety - Institute for Molecular Science and Engineering<\/title>\n<meta name=\"description\" content=\"How is molecular science contributing to a better understanding of depression, anxiety and other mental health conditions?\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/blogs.imperial.ac.uk\/molecular-science-engineering\/2022\/01\/28\/molecular-science-mental-health-2\/\" \/>\n<meta property=\"og:locale\" content=\"en_GB\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Molecular mental health 1 - 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