Brain inflammation can also lead to reduced functioning of neurotransmitters, the body’s chemical central nervous system depression messengers. A 2020 research review suggests that when depression and anxiety occur together, the amygdala increases in size. This suggests that anxiety and depression together may have a different outcome from other forms of depression. The amount these areas shrink is linked to the severity and length of the depressive episode.
For the effects on brain function, some metabolites may cross the BBB and directly trigger relevant pathways, or may elicit a response in the periphery with repercussions on the brain, such as changing the hormone and cytokine profile in the blood or through neural effects linking to the brain 176, 177. Major depressive disorder (MDD) is a common and (potentially) disabling psychiatric disorder affecting as many as 12% of adults globally, with its prevalence in the United States being highest among young adults, women, and the elderly 1. MDD represents a major burden on public health, ranking third in the leading causes of disability worldwide 2, with studies predicting a significant increase of MDD cases globally after the Covid-19 pandemic 3.
- Studies suggest that seasonal affective disorder is also mediated by alterations in CNS levels of 5-HT and appears to be triggered by alterations in circadian rhythm and sunlight exposure.
- Signaling through a variety of receptors is highly intertwined and may produce significantly overlapping effects on neurogenesis, neuronal structure, and synaptic activity.
- Seasonal affective disorder is a form of major depressive disorder that typically arises during the fall and winter and resolves during the spring and summer.
- The changes in cognition power help reduce negative emotionality by increasing people’s ability to calmly manage experiences and thoughts that stir emotions.
It might be advantageous to target more than one pathway with a single compound. The high biological heterogeneity of MDD across patients calls for the application of novel drugs, possibly in combination with established treatments to approach the goal of personalized medicine. When tapping into the wealth of correlative data from observational studies for choosing novel targets, a critical step will be the distinction between alterations causing the disease and alterations mounted by the organism to cope with the disease 234. This challenge is further aggravated by the organization of pathways in feedback loops.
Immune targets for therapeutic development in depression: towards precision medicine
The danger is when the CNS is slowed too much, which can lead to unconsciousness, coma, and death. Fentanyl is very commonly cut into other substances sold on the street.156 Fentanyl is used to increase the potency of substances, thus making the user spend more money on the laced substance.157158 Codeine is a weaker natural opiate that is usually used for bronchitis, diarrhea, and post-operative pain. It is very easy to overdose on these substances, especially if the user has no tolerance. Your spinal cord sends the message to your nerves (peripheral nervous system) to complete an action.
Molecular imaging studies, including single photon emission computed tomography and positron emission tomography, focus on metabolic aspects such as amino-acids, neurotransmitters, glucose, and lipids at the cellular level in patients with depression. A recent meta-analysis examined glucose metabolism and found that glucose uptake dysfunction in different brain regions predicts the treatment response 127. In addition, a recent study showed that microglia contribute to neuronal plasticity and neuroimmune interaction that are involved in the pathophysiology of depression 65.
The imbalance of pro-inflammatory and anti-inflammatory cytokines may be involved in the pathophysiological process of depression. One of the first suggested biological mechanisms underlying MDD is the deficiency in monoamine levels, i.e., 5-HT, noradrenaline, and dopamine 36. This “monoamine theory of depression” was supported by initial findings that monoamine oxidase inhibitors and tricyclic antidepressants could improve depressive symptoms by potentiating 5-HT and noradrenaline activity. While many studies later supported this theory, limitations include the fact that the clinical effects of antidepressant treatments typically take weeks to be observed, while the effects of antidepressants to increase monoamine levels are almost instantaneous.
What are some systemic effects associated with chemical injuries?
The common features of all the depressive disorders are sadness, emptiness, or irritable mood, accompanied by somatic and cognitive changes that significantly affect the individual’s capacity to function. This activity reviews the evaluation and management of depression and the role of interprofessional team members in collaborating to provide well-coordinated care and enhance patient outcomes. Mild CNS depression is often the goal of taking some CNS depressants, especially sleep and anxiety disorders.
Effects of depression on the digestive system
Increased glucocorticoids may further promote endothelial damage and contribute to BBB disruption 143, thus amplifying microglial activation and inflammation. In addition, proinflammatory cytokines not only reduce the expression of neurotrophins, but also inhibit BDNF/TrkB signaling by interfering with TrkB phosphorylation 153. Finally, inflammatory mediators that are increased in MDD can significantly interfere with mitochondrial oxidative phosphorylation and ATP production, ultimately leading to increased oxidative stress 154. The resulting dysfunctional mitochondria, in turn, can also further amplify the inflammatory response if not adequately removed by the mitophagy process (suggested for MDD 155, cf. “Mitochondrial dysfunction and oxidative stress”).
Crime-related drug use
Depression of the central nervous system or CNS often occurs when a person misuses a substance that slows brain activity. This is why these medications specifically prohibit you from drinking alcohol while taking them. You might experience mild CNS depression from the prescribed use of CNS depressants or severe CNS depression from the misuse of CNS depressants, traumatic brain injury, or certain other conditions. People who take CNS depressants may have mild symptoms such as drowsiness or feeling uncoordinated. People who misuse the medication or become dependent on it may have more severe symptoms, such as very slow breathing and memory loss. If you have anxiety or a sleep disorder your doctor may prescribe you a CNS depressant, such as a sedative, to help relieve your symptoms.
CNS depressants work by slowing down your brain activity, which is why it’s great for conditions like anxiety and sleep disorders. CNS depressants slow down brain activity, making them a great treatment for sleeping disorders. Sonata and Ambien are two types of sleeping medication that are CNS depressants. Although they have a lower risk of dependency than other CNS depressants, long-term use may cause the condition. It quickly became the first popular psychotropic drug in America, becoming popular in Hollywood and gaining fame for its seemingly miraculous effects.