Gehirn und Herz im Gleichgewicht als Symbol für Neuroinflammation und ihren möglichen Einfluss auf Stimmung und Antrieb

Neuroinflammation – when inflammation affects mood and motivation

By Natura Nova Redaktion Apr 28, 2026

When people think of inflammation, they usually picture swollen joints or reddened wounds. But inflammatory processes also occur in the brain – often unnoticed, but with profound consequences for our mental health. Current research shows that neuroinflammation is a key factor in depression, anxiety disorders, and lack of motivation. It affects not only our mood, but also our energy, our motivation, and our ability to experience joy. A look at the fascinating connections between the immune system and the psyche – and why some forms of depression may actually be an inflammatory condition.

What is neuroinflammation?

Neuroinflammation refers to inflammatory processes in the central nervous system – that is, in the brain and spinal cord. Unlike inflammation in other parts of the body, it often progresses slowly and at a low threshold, without the classic symptoms such as swelling or redness. .

The main players in this silent inflammation are two cell types:

Microglia : The brain's immune cells that are the first to react to disturbances.
Astrocytes : Star-shaped cells that support nerve cells and regulate the blood-brain barrier.

In a healthy state, these cells protect the brain. However, under chronic stress or other strains, they can switch to an inflammatory state and release messenger substances that damage nerve cells. .

The connection between inflammation and the psyche

That inflammation affects mental health is nothing new. Anyone who has ever had a severe case of the flu knows the feeling of lethargy, low mood, and social withdrawal – typical symptoms that also occur with depression. This so-called "illness behavior" is triggered by inflammatory messengers and shows how closely the immune system and the psyche are connected. .

However, current research goes far beyond this: it shows that chronic, low-grade inflammatory processes in the brain play a central role in the development and maintenance of depression and anxiety disorders. .

The latest findings: What research shows for 2025/2026

Different inflammation patterns in acute and chronic depression

A groundbreaking study by the University of Queensland, published in January 2026 in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging , examined MRI data from over 32,000 participants in the UK Biobank. The researchers focused on a small but crucial brain region: the ventral tegmental area (VTA), which is responsible for mood, motivation and reward processing.

The results are remarkable:

Chronically depressed individuals showed clear signs of neuroinflammation in the VTA, without any change in the region's microstructure.
People with acute depression also showed signs of inflammation, but additionally microstructural changes – such as increased cell density.

The researchers conclude that acute and chronic depression may reflect different biological processes – each with specific inflammatory patterns. Previous studies have shown that the VTA is particularly susceptible to inflammation. Inflammatory messengers can disrupt dopamine signaling there and shift behavior towards "energy conservation"—away from reward-seeking activities such as social interaction. .

The M1-A1 axis: A new mechanism of neuroinflammation

A review article published in February 2026 in Neurobiology of Disease describes a previously underestimated mechanism: the so-called "M1-like microglia-A1-like astrocyte axis" (M1-A1 axis for short). .

According to this theory, chronic stress leads to the activation of microglia, shifting them towards an inflammatory state. These microglia release signaling molecules that, in turn, convert astrocytes into a neurotoxic form. Together, they impair the production of brain-derived neurotrophic factor (BDNF) – a protein essential for the survival and growth of nerve cells. .

The researchers identified three mechanisms by which this axis disrupts BDNF production:

Release of inflammatory messenger substances that directly inhibit BDNF.
Disruption of the lactate metabolism of astrocytes, which impairs the energy supply of nerve cells.
Damage to the blood-brain barrier allows immune cells from the body to enter and increase inflammation.

Differences between first episode and recurrent depression

A Chinese study, published in February 2026 in the Journal of Affective Disorders , examined 30 people with a first episode of depression, 35 with recurrent depression, and 30 healthy control subjects. The results show:

Both patient groups had elevated levels of inflammatory messenger substances (IL-6, CRP, TNF-α) and decreased levels of anti-inflammatory messenger substances.
Imaging studies showed reduced activity in the left prefrontal cortex in both groups.
The crucial difference : In the first episode, TNF-α correlated positively with brain activity, while in recurrent depression it correlated negatively.

This suggests that recurrent depression may have its own neuroimmune interaction pattern – a potential biomarker for relapse risk. .

Mitochondria and metabolism of immune cells

Another recent review article in progress in Neuro-Psychopharmacology & Biological Psychiatry sheds light on the role of mitochondria in microglia cells. According to this research, activated microglia undergo a metabolic shift that supports their inflammatory function. This "immunometabolic reprogramming" could represent a new target for therapies. .

How stress leads to inflammation in the brain

The path from psychological stress to neuroinflammation is complex, but increasingly understood:

1. Activation of the stress axis
Chronic stress activates the hypothalamic-pituitary-adrenal (HPA) axis, leading to elevated cortisol levels. Paradoxically, under certain conditions, cortisol can promote inflammation by increasing the sensitivity of immune cells. .

2. Gut-Brain Axis
Stress alters the composition of the gut flora, increasing the permeability of the intestinal lining. Bacterial components then enter the bloodstream and trigger systemic inflammation that can reach the brain. .

3. Activation of microglia
Microglia in the brain are activated via various signaling pathways. They switch into an inflammatory state and in turn produce inflammatory messenger substances. .

4. Neurotransmitter dysfunction
These neurotransmitters impair the production and function of serotonin, dopamine, and norepinephrine – precisely those neurotransmitters that become unbalanced in depression. .

5. Damage to nerve cells
In the long term, inflammation leads to reduced neuroplasticity and even to the loss of nerve cells in regions important for mood and emotion. .

Significance for therapy and prevention

The findings on neuroinflammation open up new perspectives for the treatment of depression and anxiety disorders.

Anti-inflammatory approaches

A review article in Nature Reviews Neurology (September 2025) concludes that small molecules with anti-inflammatory effects represent promising approaches for the treatment of depression. . This includes:

Omega-3 fatty acids : Can have an anti-inflammatory effect and reduce microglia activation
Curcumin : The active ingredient from turmeric shows anti-inflammatory effects in the brain.
Minocycline : An antibiotic that also inhibits microglia is being investigated in studies.

Lifestyle as an inflammation brake

Several studies emphasize the importance of lifestyle factors for neuroinflammation. :

Regular exercise : Promotes anti-inflammatory messenger substances and protects the blood-brain barrier.
Sufficient sleep : Lack of sleep activates microglia and promotes inflammation.
Healthy diet : A Mediterranean diet rich in omega-3 fatty acids, antioxidants, and fiber has an anti-inflammatory effect.
Stress reduction : Mindfulness exercises and meditation can lower inflammatory messenger substances.

Personalized medicine

The different inflammatory patterns observed in various forms of depression suggest that personalized treatment will be necessary in the future. People with elevated inflammation levels could particularly benefit from anti-inflammatory adjunctive therapies. .

Critical assessment

Despite the impressive progress, some limitations must be considered:

Many studies are cross-sectional studies that cannot prove causality.
The transferability of animal models to humans is limited.
It is unclear whether neuroinflammation is a cause or a consequence of depression.
Individual variability is high – not every depression has an inflammatory component.

Conclusion

Neuroinflammation research has fundamentally changed our understanding of depression and anxiety disorders. It shows that mental illnesses do not only occur "in the head" but affect the entire body – especially the immune system.

Current studies from 2025 and 2026 demonstrate that different inflammatory patterns are associated with different forms of depression, that certain messenger substances disrupt communication between immune cells and nerve cells, and that mitochondrial processes in the brain's immune cells play a key role. .

For those affected, this means that a healthy lifestyle with sufficient exercise, good sleep, and an anti-inflammatory diet can protect not only the body but also the mind. For medicine, this opens up new avenues for more targeted, personalized treatments – and perhaps one day to therapies that combat not only the symptoms but also the underlying causes of the disease.

Official sources & studies:

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