The research of Katarina Trajković's group is focused on two directions

1. Post-translational modifications of lysosomal proteins in aging and neurodegeneration. In recent years, the lysosome has transformed from a cellular waste disposal site into a central signaling organelle that integrates the metabolic status of the cell via the mTORC1–TFEB axis, and its dysfunction is a common denominator in Alzheimer's and Parkinson's diseases and lysosomal storage diseases, including Niemann-Pick disease type C. While the expression and localization of lysosomal proteins are well described, their landscape of post-translational modifications (PTM) remains almost unexplored because the lysosome constitutes a small part of the cellular proteome and eludes conventional proteomics. To address this we have established  an approach that combines rapid immunoisolation of intact lysosomes (Lyso-IP, TMEM192-3xHA/2xFLAG) with LC-MS/MS analysis of several classes of modifications — phosphorylation, ubiquitination, carbonylation and oxidation of methionine — which maps the modifications directly on the organelle, under conditions of nutritional and oxidative stress and replicative aging. Organ-specific PTM profiling is currently carried out by only a few groups in the world, and none in Croatia; is an original contribution in the systematic connection of lysosomal modifications with oxidative protein damage and aging, an area in which there is long-term experience (Oxime blot method, Redox Biology 2023).
2. Non-autonomous regulation of damaged cell fate. It has been shown that intact neighboring cells, through a contact-dependent mechanism, alter the fate of cells damaged by UV-B/C radiation (Budimir et al., J Photochem Photobiol B, 2026). Our ongoing research is investigating the role of adhesion GPCRs and intercellular ligands in mediating this effect following UV-induced or chemically induced DNA damage. The question of how the cellular context determines whether a damaged cell survives, dies, or enters senescence is directly relevant to the selective vulnerability of specific cell populations in neurodegenerative diseases and complements the laboratory’s research on the endosomal-lysosomal system.

Research conducted by Katarina Trajković’s group is currently funded by the following projects:

1. Croatian Science Foundation (HRZZ), research project IP-2026-5720 “Lysosomal post-translational modifications in aging and stress-induced neurodegeneration” (LPM-AGE); starting December 14, 2026, for a duration of three years; contracted amount for the Ruđer Bošković Institute (IRB): approximately EUR 200,000.00. Role: Principal Investigator.
2. Ruđer Bošković Institute (IRB), internal program funding (KP1-26): “Post-translational modifications of lysosomal proteins in aging and age-related diseases”; March 23, 2026 – March 23, 2027; approximately EUR 5,300.00. Role: Principal Investigator.
3. Ruđer Bošković Institute (IRB), internal program funding (KP2-26): “Non-autonomous regulation of cell fate following DNA damage: the role of adhesion GPCRs and intercellular signaling”; March 23, 2026 – March 23, 2027; approximately EUR 12,000.00. Role: Principal Investigator.

The research of Silva Katušić's group is focused on three directions

1. Research of the earliest changes, triggers of neurodegenerative diseases,
2. Investigation of dysfunction and contribution of individual brain cells (neurons, microglia, astrocytes and/or oligodendrocytes) in the pathogenesis of neurodegenerative diseases
3. Investigation of spatio-temporal brain / cell-type specific changes in the pathogenesis of neurodegenerative diseases.

The focus of the research of Silva Katušić's group is to elucidate the earliest and cell-type specific changes of different brain cells (neurons, microglia, astrocytes and/or  oligodendrocytes) in the pathogenesis of neurodegenerative diseases. Our goal  is to better understand the role of different brain cells and their spatio-temporal dysfunction that drives neurodegeneration, neuroinflammation and demyelination – the three key features of neurodegenerative disease brains.

It is known that neurodegenerative diseases begin their pathological processes in the asymptomatic phase, i.e. long before the appearance of any symptoms, and that discovering the earliest changes will enable development of early diagnosis (biomarkers) and/or effective disease therapies. Our research mainly involves studies of intracellular transport and proteome and lipidome cell-type specific changes.

Within the proposed research we will test the hypothesis that changes in non-neuronal cells, glia cells, precede neurodegeneration and are triggers of neurodegenerative diseases. We are conducting the aforementioned research using a model of the juvenile neurodegenerative disorder Niemann-Pick type C (NPC)—a rare lipid-storage and lysosomal-dysfunction disease—which shares several similarities with the more common Alzheimer’s disease (AD).

The research is primarily carried out using a mouse model of NPC (BALB/cNctr-Npc1m1N/J (003092), The Jackson Laboratory, Bar Harbor, Maine, USA), which is maintained at the Animal Facility at the Ruđer Bošković Institute (RBI). In collaboration with partners from the German Center for Neurodegenerative Diseases in Munich, the ACCESS center at the University of Geneva, and the University Hospital Centre in Zagreb, our goal is to validate our findings and translate them into human models.

Research by Silva Katušić’s group is currently funded by the following projects:

1. Ruđer Bošković Institute (IRB), internal program funding (KP2-25): “Investigating the role of NPC1 protein in myelination,” March 20, 2025 – December 31, 2026, 15,000 EUR, Role: Principal Investigator.
2. Croatian Science Foundation – “Career Development Project for Young Researchers – Training of New PhDs,” DOK-NPOO-2023-10-6286 (2024–2029), Role: Principal Investigator/Mentor.
3. Croatian Science Foundation (HRZZ), research project IP-2022-10-7325, “Endosome biogenesis in Niemann-Pick disease type C” (ENDOGENESIS), December 31, 2023 – December 30, 2027, 197,611.12 EUR, Role: Principal Investigator.