Why the topic is scientifically interesting

Depression and anxiety disorders are complex conditions. Psychological stress, social circumstances, genetic factors and different biological processes may interact. There is no single universal cause.

Altered inflammatory markers can be observed in some people with depressive disorders. Research therefore examines whether immune processes contribute to symptoms or poorer treatment response in certain patient groups. This does not mean that depression is generally an inflammatory disease.

Platelets, BDNF and inflammatory signals

Platelets are involved in more than blood clotting. They store serotonin, growth factors, BDNF and various inflammatory mediators. For this reason, they have long been studied as possible peripheral biomarkers in depressive disorders.

BDNF, brain-derived neurotrophic factor, contributes to neuronal plasticity and nerve-cell function. A substantial proportion of measurable BDNF in blood is found in platelets. This does not mean that administering PRP therapeutically increases BDNF levels in the brain.

What animal studies show — and what they do not

Some preclinical studies have examined PRP in models of neurological injury. A frequently cited study used rats with experimentally induced bile duct ligation. The model causes liver injury, metabolic changes and cognitive impairment. After PRP treatment, changes in memory performance, neuronal apoptosis and synaptic plasticity were reported.

Other animal models concern traumatic, toxic or radiation-induced brain injury. Such findings may provide clues about biological mechanisms. They do not answer whether PRP is effective in primary depression, generalised anxiety disorder, panic disorder or social anxiety disorder.

The blood-brain barrier

For components of a PRP preparation to act directly on nerve cells in the brain, they would first have to reach the target tissue. The blood-brain barrier restricts the passage of many proteins and larger molecules from the blood into the central nervous system.

It remains unclear:

• which PRP components could reach the brain at all,
• what concentrations would be achieved,
• whether possible effects would be beneficial, ineffective or harmful,
• which route of administration could be acceptable.

PRP is not a uniform preparation

PRP preparations can differ considerably depending on the system and processing method. Variables include platelet concentration, leukocyte content, residual red blood cells, plasma volume and activation method.

Psychiatric research would therefore first require precise standardisation. Without a defined composition, results from different studies can hardly be compared meaningfully.

No robust evidence of efficacy in depression or anxiety disorders

There is currently no robust controlled clinical evidence that PRP is effective as a targeted treatment for a depressive or anxiety disorder. Consequently, there are no accepted specifications for dose, preparation, route of administration, frequency or long-term safety.

Intravenous infusions, intranasal use, subcutaneous injections or freely proposed treatment series must therefore not be presented as established psychiatric procedures.

What research would be required

Before clinical use could be discussed, active components, distribution in the body, possible target structures and risks would need to be studied systematically.

What the current evidence means in practice

People with depression or anxiety disorders should not regard PRP as a scientifically proven treatment. Existing treatment should not be stopped without medical advice or replaced by an experimental application.

Specialist medical or psychotherapeutic assessment is particularly important in severe, recurrent or treatment-resistant illness. Immediate professional emergency help is required in the event of acute risk of self-harm or marked deterioration.

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Scientific sources and guidelines