Dear All,

We cordially invite you to the Ph.D. Seminar, which will be held on February 13, 2026 at 10.30 in the Konorski room (2nd floor). There will be 2 presentations.

Information about the speakers and abstracts can be found below.

With best regards,

Anna Filipek & Anna Nowicka

MSc Karolina Bogaj

Laboratory of Electrophysiology
Supervisor: Dr. Joanna Urban-Ciećko, PhD, DSc.

Title: Electrophysiological characterization of neocortical vasoactive intestinal polypeptide-expressing interneurons (VIP-INs)

Abstract:

GABAergic interneurons provide inhibition to the neuronal network through GABAA and GABAB receptors. Vasoactive intestinal polypeptide-expressing interneurons (VIP-INs) contribute to merely 15% of cortical interneurons, however they exhibit an important function in the circuitry. A role of VIP-INs is to release excitatory cells from inhibition mediated by other classes of inhibitory neurons. This disinhibitory mechanism has been found to be crucial for learning and memory formation. On the other hand, VIP-INs are also inhibited by other interneurons through GABAA and GABAB receptors. Taking into account that VIP-INs are very diverse, we aimed to characterize electrophysiological properties of VIP-INs located in layer 2/3 of the mouse primary somatosensory cortex and then asked a question how GABAB receptors regulate the activity of these interneurons. Utilizing whole-cell patch-clamp technique in acute brain slices and machine learning algorithms (hierarchical clustering and principal component analysis), the analysis revealed 3 clusters of VIP-INs. Next, we found that GABAB receptors regulate the activity of only 1 cluster. Surprisingly, modulation of VIP-IN excitability through GABAB receptors depends on the concentration of Ca in the recording solution. GABAB receptors canonically inhibit VIP-IN excitability in the low Ca²⁺ concentration, whereas these receptors enhance VIP-IN excitability in the high Ca²⁺ level.

MSc Justyna Domańska

Laboratory of Preclinical Testing of Higher Standard
Supervisor: Prof. Urszula Wojda, PhD, DSc
Auxiliary supervisor:  Dr. Anna Mietelska-Porowska, PhD

Title: Dual Pathways to Alzheimer's Disease: Immune vs Metabolic Endotoxemia Drive Distinct Early Alzheimer's Features

Abstract:

Systemic inflammation and metabolic dysfunction are recognized risk factors for sporadic Alzheimer’s disease (AD). Acute peripheral inflammation can be induced by exogenous lipopolysaccharide (LPS), whereas chronic low-grade inflammation and metabolic dysfunction arise from Western diet (WD)-driven metabolic endotoxemia. However, the long-term effects of distinct inflammatory states remain unclear. We hypothesized that acute and chronic inflammatory challenges engage different pathways that converge on the development of AD-related changes across the lifespan.

Male C57BL/6 mice were exposed to short-term peripheral LPS at 3 months of age or to continuous WD feeding, analyzed longitudinally at 4, 8, 12, and 16 months. Peripheral inflammation, metabolic parameters, neuroinflammation, and AD-related molecular changes were assessed in the entorhinal cortex (EC) and hippocampus (HIPP).

Acute LPS induced persistent immune alterations, progressive tau phosphorylation in the EC, and early microglial activation in the HIPP. In contrast, WD led to progressive brain insulin resistance, particularly in the EC. Importantly, amyloid-β accumulation and altered phosphorylated tau localization were observed in both models  with distinct regional patterns. The EC was more vulnerable to metabolic stress, whereas the HIPP showed sensitivity to immune-driven mechanisms.

These findings indicate that immune and metabolic-driven inflammation activate distinct yet convergent pathways leading to early AD-like changes.