Aging is a complex, natural biological process characterized by the gradual decline of cellular and systemic functions, impacting multiple organ systems. In the brain, aging often leads to imbalance between repair and damage, resulting in the accumulation of misfolded proteins and oxidative stress. Chronic low-grade inflammation, known as inflammaging, involves both local and systemic immune responses, contributing to neurodegenerative diseases like Alzheimer’s and Parkinson’s Disease. While aging can be associated with challenges such as oxidative stress, chronic inflammation, and weakened barriers like the blood-brain barrier, these changes do not necessarily equate to poor health. Healthy aging emphasizes maintaining functional ability and well-being despite these physiological shifts. By fostering good nutrition, regular physical activity, social engagement, and access to quality healthcare, individuals can mitigate age-related decline and enhance their quality of life. Furthermore, understanding the molecular and cellular mechanisms can help mitigate some of the challenges associated with aging and allow for proactive measures to ensure longer, healthier lives where well-being remains central.

One groundbreaking field began to spark a revolution in our understanding of complex systems such as the brain, namely Synergetics. At the heart of Synergetics is the idea that order arises from complex interactions and interacting elements do self-organize to create cohesive structures. An explanation for emergent order, the enslavement principle describes how, near critical points (transitions between different states), the behavior of a system is dominated by a few order parameters. These order parameters enslave the other components of the system, dictating their behavior. The order parameters arise from the interactions of the individual components and then, due to their stability and influence, constrain the other components. It's a dynamic, reciprocal relationship, not a unidirectional control. Individual elements within a complex system can self-organize to form coherent, macroscopic structures. With building and simulating digital or artificial multi-scale computational brain models, we can literally observe the dance of order and disorder giving rise to cognitive functions and intelligent behavior.

The gut-brain axis forms a dynamic, bidirectional communication network linking the gastrointestinal tract and the central nervous system (CNS) through intricate neural, endocrine, immune, and metabolic pathways. On one end, the CNS exerts top-down control, where cognitive and emotional states – such as food reward anticipation – directly influence gut hormone secretion and digestive processes. Conversely, bottom-up signals from the gut, including microbial activity, nutrient absorption, and visceral function, actively shape brain activity, mood, and cognition.

This crosstalk relies on multiple key pathways: The vagus nerve serves as a critical neural highway, while endocrine signals – ranging from gut-derived peptides like GLP-1 and cholecystokinin (CCK) to glucose fluctuations and neurotransmitter systems (dopamine, serotonin) – fine-tune brain-gut synchronization. When these pathways falter, their dysregulation can contribute to neurological and psychiatric conditions, including Parkinson’s disease and depression. Understanding this bidirectional dialogue opens new avenues for therapeutic interventions targeting both gut and brain health.

Although the immune system primarily fights intruding bacteria or viruses, the neuronal system uses elements of the immune system for information processing or interacts with the immune system in disease. Complement activation and microglia interaction with neurons are involved in learning and synapse stability. A chronic para-inflammation or injury involves local and systemic immune cells as base for degenerative diseases in the brain and retina. Important regulators of the immune activity are the brain/blood and retina/blood borders that control affections by the systemic immune system. As prominent examples, the failure of the neuro-immune interface causes cerebral affections by COVID-19, Alzheimer’s disease or Parkinson’s disease.

9:15 – 9:30		Opening		Aula
9:30 – 10:30		Einstein lecture I		Aula
		ECR talk
10:30 – 11:15		Coffee break		Lounge
11:15 – 12:45		Scientific talks		Aula
12:45 – 14:00		Lunch break		Lounge
14:00 – 15:00		Einstein lecture II		Aula
		ECR talk
15:15 – 16:45		Scientific talks		Aula
16:45 – 17:45		Coffee break		Lounge
17:45 – 19:30		Posters & Wine I		Aula
19:30 – 20:00		MedNeuro MSc graduation ceremony		Lounge

* parallel session

ECR – early career researcher

ECR – early career researcher