— The discussion turns to the origins and development of psychoneuroimmunology in Russia and what this field investigates.
“It examines how the brain, psycho-emotional states, and the immune system influence one another. The nervous and immune systems share the aim of maintaining homeostasis, the body’s internal balance. Each system can distinguish, process, and store information in its own way.
The nervous system recognizes cognitive, physical, and chemical stimuli, while the immune system responds to non-cognitive cues such as bacteria, viruses, tissues, and cells carrying foreign information. No other system performs this kind of discrimination.
When the interaction between neurobiology and immunity is disrupted, the risk of tumor development, autoimmune diseases where the immune system attacks the body, depressive disorders, Parkinson’s disease, schizophrenia, and other conditions can rise. Neuroinflammation is a common thread behind many psychopathologies.
— How do these two systems communicate with each other?
— Before 1980, the immune system was thought to be autonomous. Researchers could expose immune cells to an antigen in vitro and provoke an immune response independent of the brain.
Yet accumulating data showed that this autonomy was only relative: hormones and neurotransmitters in the body exert a powerful influence on immune activity.
Fundamental insights into the role of neurotransmitter systems in psychoneuroimmunomodulation were first obtained in a laboratory led by Professor Lidia Vasilyevna Devoino.
It was found that serotonin, dopamine, and GABA (gamma-aminobutyric acid, a key inhibitory transmitter) participate in the regulation of immune function. Specific brain structures involved in this process were identified. The serotonin system tends to suppress immune activity, while dopamine and GABAergic systems tend to stimulate it.
Drugs that modulate neurotransmitter systems influence various immune parameters. These drugs are widely used in treating psychoneurological disorders, yet their effects on immune function must also be considered.
— Does immunity affect the brain’s state?
– Yes. Earlier work on psychoneuroimmunology focused on how hormones, neurotransmitters, and external or internal stressors alter immune reactivity. Later, researchers recognized that immune function can also shape psycho-emotional states.
In recent years the central question has been to identify immune mechanisms that contribute to different psychopathologies.
— So reduced immunity might make a person more susceptible to mental illnesses?
– It’s more nuanced. Immune processes participate in neuroinflammation that drives various pathological changes in the brain.
For example, neuroinflammation and immune dysfunction are linked to Parkinson’s disease through the death of dopamine neurons in the substantia nigra. This brain region is rich in neuromelanin and connects to other areas to regulate movement. Immune challenges, combined with lowered immune surveillance, can worsen outcomes. In depression, neuroinflammation with immune dysfunction alters serotonin signaling and can dampen immune activity, affecting hippocampal function as well.
Schizophrenia also involves neuroinflammation alongside altered dopamine activity and immune responses. In essence, inflammatory processes and immune disturbances can shift neurotransmitter levels, though each disease has its own hallmark features. Peripheral neurotransmitters can also modulate immune function outside the brain.
Because these conditions are prominent in modern medicine, numerous studies explore these links. Neurodegenerative diseases are projected to rise through mid-century and become a leading health challenge alongside cardiovascular and cancer risks.
— Could strategies be developed to prevent Parkinson’s and related disorders by targeting these mechanisms?
— Research in the Department of Neuroscience, Behavior, and Neurotechnologies plans comprehensive studies to evaluate therapeutic effects and immune status when applying rhythmic transcranial magnetic stimulation. This approach stimulates brain neurons with an alternating magnetic field and records responses, with the aim of helping patients with depression and neurodegenerative diseases.
Previous work has shown this method can reduce neuroinflammation in Parkinson’s disease, evidenced by decreased cytokine levels in the blood compared with a control group.
— You mentioned emotions influence immunity and cognition. How does that happen?
— Emotions clearly shape immune function, with positive and negative states producing different effects. Human studies have demonstrated that fear and anxiety can dampen immune parameters, whereas positive experiences lift them. Short-term changes occur, but they are real: fear reduces certain T helper cells and natural killer activity, while humor and positive affect can increase these indicators, especially in individuals who feel stronger positive emotion.
— Do optimists and pessimists show different patterns?
— The dynamics extend to cognitive function as well. Optimists often show higher levels of T helper cells and natural killer cells, while pessimists may display lower levels, contributing to mood-related vulnerabilities. Stress interacts with this pattern: optimists may perceive stress as more threatening, which can sharply suppress immunity, whereas pessimists may anticipate negative outcomes and, paradoxically, experience a different stress response that aligns with their expectations.
— Do these changes affect behavioral immunity indicators?
— Yes. Aggressive behavior tends to activate immune responses, with serotonin activity linked to immunosuppression decreasing and dopamine activity rising to boost immunity. In humans, higher aggression can correlate with better immune indicators, including T helper and natural killer cells. Submissive or depressive states can dampen these responses, especially when depressive behaviors dominate.
— Are these trends seen in addiction and depression models?
— Indeed. Depressive-like behavior and submissiveness in animals often correspond with weaker immune responses compared with aggressive or control groups. Serotonin levels can shift in unexpected directions in depression, challenging simple cause-and-effect assumptions. A transition from aggression to depressive states tends to suppress immunity, while moving from depressive to aggressive states can enhance it, likely reflecting shifts in brain neurochemistry.
— Does acute versus chronic stress produce different outcomes?
– Yes. Mild, acute stress can temporarily boost immune parameters, while chronic stress generally suppresses them. Stress also affects the thymus, the central site for T cell development. The serotonin system is activated under stress, and inhibiting serotonin synthesis can reverse stress-induced immune suppression. Different stressors can drive serotonin levels up dramatically, sometimes by as much as 1500 percent above baseline.
Humans, like animals, show that attitudes toward stress influence the body’s response. Aggressive behavior tends to reduce immunity, depressive behavior tends to increase it, and submissive responses may blunt the stress-immune relationship altogether.
— Is Parkinson’s disease a current focus?
— Yes. The molecular and cellular immune profile of Parkinson’s disease is studied through both animal models and early-stage patients. Two-month-old animals without motor symptoms reveal significant immune alterations, particularly in cellular composition and pro-inflammatory cytokines, suggesting early inflammatory processes that might be modulated to alter disease progression. This line of work aims to identify biomarkers for early disease detection and new intervention targets.
Parkinson’s disease remains a leading age-related condition, yet it may begin years earlier in some individuals. The search for reliable early biomarkers continues, with a focus on understanding how neuroinflammation and dopamine neuron degeneration intersect and how immune pathways might be harnessed to slow or prevent disease onset.