Dopamine associated diseases | Dopamine

Dopamine associated diseases

Since dopamine is responsible for many different processes in the body, many diseases are attributed to a disrupted dopamine production. There may be either an overproduction or an underproduction of dopamine, which leads to different disease patterns. Underproduction Dopamine plays a major role in Parkinson’s disease.

This is caused by a lack of dopamine, which prevents the commands that the brain sends to the arms and legs to move from being precisely coordinated. Movements are no longer regulated in their extent and direction, and the result is the uncoordinated and involuntary movements typical of Parkinson’s disease. Since the reward system and thus the positive sensations are also controlled by dopamine, a dopamine deficiency can also lead to depression.

Overproduction An overproduction of dopamine is often caused by a tumor in the adrenal medulla (pheochromocytoma). Dopamine is responsible for positive sensations and feelings and for their transmission in the brain. If there is too much dopamine, these people perceive much more of the external impressions than people with normal dopamine levels can.

If too many impressions come together, this can lead to a nervous breakdown. Dopamine is also thought to play an important role in schizophrenia and other psychoses. Here it is said to be responsible for the “positive” symptoms of the disorders.

An overproduction of dopamine often manifests itself in symptoms such as high blood pressure, sweating and headaches. In some cases, however, short-term overproduction of dopamine is not a clinical picture. In acute sleep deprivation, the body produces more dopamine to boost it.

Disorder of the breakdown ADS and ADHD as attention deficit syndromes are also based on a disorder of the dopamine level. In these cases the dopamine is broken down too quickly and the brain is no longer able to filter incoming external stimuli. Thus, unimportant impressions cannot be sorted out and concentration and attention disorders occur.

A dopamine deficiency can occur after drug abuse, for example, when dopamine is no longer evenly distributed in the brain. Instead, it concentrates in the wrong areas and shows up in others rather rarely. There are also several important diseases that are caused by a dopamine deficiency.

What they all have in common is that the dopamine-producing or consuming neurons die over time. The cause of this cannot be sufficiently explained until today. These diseases are Morbus Parkinson, Restless Legs Syndrome and ADHD.

At least in the case of Parkinson’s disease, it is now assumed that the disease originally comes from the intestine and induces a breakdown of the dopaminergic neurons in the brain via neural pathways. In all three diseases, the “fidgeting impression” of the patient is dominant. Since dopamine has an inhibitory function in the movement sequences of the brain, patients show excessive movements when it is lacking.

One can try to increase the dopamine level with medication for a certain period of time. For this purpose, drugs are used that promote the body’s own dopamine release or prevent the recycling of dopamine. In Parkinson’s disease, however, the neurons in question slowly but surely disappear and require complete dopamine substitution via L-DOPA.

Alternative medical approaches or dopamine-enhancing pharmacological mechanisms, as used in depression, do not have a prognostic-enhancing effect in this case. Dopamine is also colloquially considered a happiness hormone because it conveys positive emotional experiences via the reward system. The same applies to its neuronal partner serotonin.

Serotonin and adrenaline (of which dopamine is a precursor) are mainly held responsible for the development of depression.A lack of nerve cells that release these two substances to their environment seems to have negative effects on emotional processes, the sleep-wake rhythm and the body’s own pain-inhibiting system. Thus, a lack of dopamine also means a resulting lack of norepinephrine. This theory is supported by the fact that appropriate medication using this mechanism is successfully used as a therapy for depression.

These are drugs that increase the concentration of dopamine, noradrenalin and serotonin in the brain again. An isolated dopamine deficiency can therefore never be solely responsible for depression; in any case, other neurotransmitters are also involved. Some antidepressant drugs also make use of the recycling of neurotransmitters and inhibit their reuptake into the synapses.

There are drugs that have an increased effect on serotonin or only on dopamine individually. The best effect, however, is shown by drugs that include all neurotransmitters simultaneously. They thus have a mood-lifting and stimulating effect.

The pure dopamine reuptake inhibitors are no longer approved for the treatment of depression because their side effects are too severe and make them highly dependent. Depression as a disease is based on complex chemical processes. Therefore, depression should be treated with an equally complex approach on a pharmacological basis.

The effect of the drugs may take some time to take effect. Cellular adaptation processes must first take place in the brain until dopamine, serotonin and adrenaline have reached normal levels again. However, a significant part of the effect of antidepressant tablets also lies in the placebo effect, which can be explained by the rewarding dopamine system.

It is now known that yellow tablets, for example, are more effective against depression than blue ones. The brain apparently associates a positive, mood-lifting feeling with yellow, which in the reward system results in increased dopamine release. This effect explains why psychotherapy tries to include rewarding activities in the daily life of a depressed patient.

In addition to pharmacological therapy, it is also known that dopamine is released in increased amounts through exercise and sports. Regular exercise in fresh air and physical activity are therefore also important. If a depression is resistant to all these therapeutic approaches, a final therapeutic option is electroconvulsive therapy. The new electronic circuits in the brain resulting from ECT appear to distribute the required messenger substances dopamine, norepinephrine and serotonin evenly and at the required levels again.