Donations Granted

EarlyAD project takes a groundbreaking approach for the research of Alzheimer’s disease (AD) by using idiopathic normal pressure hydrocephalus (iNPH) as a model for early stages of AD providing a rare chance to study AD before symptoms appear. The project utilizes brain biopsies, cerebrospinal fluid, blood and imaging data from iNPH and AD patients for the discovery of disease mechanisms and discovery of novel biomarkers related to immunometabolic alterations. Strong collaboration between the university and hospitals, expertise in advanced tissue function measurement techniques, genetics, and imaging technologies and integration of multi-level data with clinical information offer a unique opportunity to study disease mechanisms and identification of new biomarkers.

High entropy alloys (HEAs) are materials that contain more than four constituent elements at nearly equal concentrations; a feature that yields enhanced structural stability and performance superior to that of contemporary engineering alloys. Yet, the unique features of HEAs can only be harnessed to their full extent if the positions of constituent atoms are tuned with atomic to nanoscale precision. This is currently not possible, and our project seeks to address this challenge by combining cutting edge experiments with advanced computer simulations.  The knowledge generated from the project will provide the scientific foundation for unlocking the full potential of HEAs for use in extreme conditions, including high mechanical and thermal loads, corrosive environments, and high radiation.

The vascular homing peptide CAR reaches the healing tissue via the bloodstream. It not only acts as a transport vehicle for drugs, but also binds to the syndecan-4 in the healing tissue and activates the syndecan-4-mediated signaling pathway critical for wound healing. CAR induces the skin wounds to heal, i.e. close rapidly (Nat Comms 2023). Now our aim is to build two different drug molecules, so-called recombinant fusion proteins. One of the recombinant proteins to be built contains multiple copies of the CAR peptide, and the other protein is a fusion of the CAR peptide and a therapeutic protein to yield a fusion protein that contains two parts that accelerate tissue regeneration independently in the same molecule.

In osteoporosis, bone loss results in fractures. Muscle loss, sarcopenia, often coexists and contributes to skeletal fragility. We study patients with monogenic osteoporosis to understand contribution of various signaling pathways for musculoskeletal health. Our translational study applies clinical and imaging tools, bone and muscle biopsies, and biomarkers to provide in-depth clinical, tissue-level, cellular and molecular data on skeletal and muscular characteristics in affected patients. We use various cell-based strategies and animal models for detailed musculoskeletal analyses, drug discovery and pre-clinical treatment trials. Our goal is to elucidate disease mechanisms in osteoporosis and interconnections between osteoporosis and sarcopenia.

Syövät lisääntyvät, ja keuhkosyöpä on yleisin syöpään liittyvä kuolinsyy. Useimmat potilaat diagnosoidaan myöhäisessä vaiheessa, jolloin hoidot ovat rajallisia. Kohdennetut lääkkeet ja immuunihoidot ovat parantaneet ennusteita, mutta valtaosalle kehittyy nopeasti lääkeresistenssi, ja syöpä uusiutuu. Tämä johtuu kasvainten monimuotoisuudesta ja aggressiivisesta mikroympäristöstä, jotka rajoittavat hoitojen tehoa. Nykyiset mallit, kuten 2D-soluviljelmät ja hiiret, eivät ennusta ihmisen syöpien monimutkaisuutta, mikä vaikeuttaa uusien hoitojen kehitystä. Kehitämme uudenlaisen lääkekehitysalustan hyödyntäen yksisolu-multiomiikkaa, koneoppimista ja ihmislähtöisiä syöpäsiruja. Tavoitteena on tunnistaa lääkeresistenssin ja immuunivasteen mekanismeja sekä kehittää tehokkaampia hoitoja, jotka nopeuttavat lääkekehitystä, vähentävät kustannuksia ja parantavat potilaiden ennustetta.

A child’s early motor development is important for all subsequent development, but the lack of objective assessment methods has formed a global bottleneck for improving the well-being of young children. The MOPO project uses a new Finnish innovation, the MAIJU smart jumpsuit, to measure a child’s motor development during natural play in home conditions. The project investigates factors affecting a child’s motor development and how motor development affects a child’s sleep or later cognitive development. The MOPO project also explores the potential of smart clothing in healthcare, increasing regional and cultural equality, and supporting clinical research. If successful, the MOPO project could change practices in healthcare and other child-related activities, both in Finland and internationally.

This project aims to generate new, unique information on the effectiveness of treatment for difficult-to-treat mental disorders and the comparative effectiveness of treatments based on work capacity, mortality, and the need for hospitalization. The project will investigate the effectiveness of pharmacotherapies and psychotherapy in severe depression and borderline personality disorder, by using Finnish and Swedish registry data. The project also aims to identify retargetable drugs for the treatment of mental disorders, such as GLP-1 receptor agonists. In addition, machine learning models to assess individual prognosis and treatment response in clinical decision-making will be developed.

The aim of the study is to develop a drug therapy to halt the degeneration process in retinal dystrophies. Specifically, we aim to prove our hypothesis on the cause-and-effect relationships of the mechanisms of action of our drug treatment candidate and to obtain more information on the efficacy of the treatment, especially in retinal diseases related to the Finnish disease heritage. Although the first clinical trial should be carried out with oral drugs to speed up the process, the project is also working on innovative eye delivery techniques so that in the future, drugs to retinal diseases can be administered directly into the eye. The treatment based on drug repurposing can lead to clinical applications on an accelerated schedule compared to the traditional drug development pipeline.

The project aims to develop new applications and targets for antibody-based drugs. With current administration methods, these drugs typically affect all organs and tissues in the entire body. The goal of the project  is to locally direct therapeutic antibodies that regulate the immune response to only those lymph nodes that are actively involved in initiating the immune reaction. By targeting treatment in this way, the project aims to enhance, for example, vaccine responses and the ability of the body’s own immune system to recognize and destroy cancer cells in a cost-effective and safe manner.

Tuberculosis is an infection caused by the bacterium Mycobacterium tuberculosis, which leads to more than 1.5 million deaths annually. The use of the current vaccine, Bacillus Calmette-Guérin (BCG), is limited by its side effects and limited efficacy. The aim of the research project is to develop a new mRNA vaccine against tuberculosis. The project is based on our own research, which has led to the identification of several protective vaccine antigens in a zebrafish model of tuberculosis. On this basis, we have developed an mRNA vaccine, the efficacy, safety and the resulting immune response of which we are studying in mammalian models of tuberculosis. The aim of the project is to enable clinical trials of the vaccine in humans. 

Cancer remains one of the most complex diseases to treat, especially when tumors become aggressive or therapy-resistant. This project develops deep learning and network science methods to map gene regulatory networks in cancer at unprecedented resolution. By integrating multiple types of molecular data, we aim to reveal how regulatory programs rewire across patients, tumor types, and tumor subpopulations. Applied to large public datasets and the Finnish iCAN cohort, our models are expected to uncover hidden cancer subtypes and drivers of aggressiveness and therapy resistance, linking molecular mechanisms to clinical outcomes and laying the foundation for network-based precision oncology.

Multiple sclerosis (MS) is the most common cause of non-traumatic neurological disability affecting young adults. Epstein-Barr virus (EBV) infection is the outstanding risk factor of MS. We will analyze, whether particular variants of this common virus underly the development of MS. A part of the patients and controls will be collected from Kyrönmaa, which is a high-risk geographic focus of MS. In collaboration with Finnish biobanks we will also perform a state-of-the-art analysis of EBV antibodies in MS patients and controls. We will use a more precise antibody detection methodology than in previous studies and control for confounders such as genetic factors and other viral infections, which may affect EBV antibody levels.

Regulatory RNA genes are genes that regulate the expression of other genes. Often, such regulatory RNA genes mutate rapidly, with no homologs found in close relatives. In this research, we will screen recent and ancient mutation clusters in the human genome and identify their impact on the origin of regulatory RNA genes using comparative genomic methods. This research will provide information on how new genetic information is generated and how gene regulation can change rapidly. In a broader context, this research will provide insights into diseases associated with dysfunctional gene regulation and how species receive genetic material to adapt to changing environments.

Acute myeloid leukemia is the most common acute leukemia. The prognosis remains poor, especially in relapsed disease and in patients ineligible for intensive chemotherapy. Venetoclax has improved treatment outcomes by sensitizing cancer cells to programmed cell death (apoptosis), but one third of patients do not benefit from the therapy and most eventually develop resistance. Our preliminary analyses (VenEx study, 104 patients) suggest that apoptosis regulation is altered in leukemia cells of resistant patients and that the PRAME gene is strongly overexpressed. We are investigating the combination of PRAME-targeted immunotherapies with new agents that modulate apoptosis. These findings may open new opportunities for the development of combination therapies and for improving prognosis.

The research focuses on uterine leiomyomas and endometrial polyps. These common tumors cause significant morbidity for women and major economic burden on societies. Occasionally, they may also transform into malignancy, leiomyomas to leiomyosarcomas and polyps to endometrial cancer. The aim of this project is to continue our long-term efforts to reveal the molecular background of uterine tumors. We aim to identify the genetic changes that lead to tumor development, to understand the tumorigenic mechanisms of the identified alterations, and to develop new clinically translatable tools that benefit diagnostics and improve patient management.

We investigate mitochondrial dysfunction as a central disease mechansim of Parkinson’s disease specifically focusing on muscle tissue and myogenic cells. We aim to detect mitochondrial dysfunction-related clinical features and characterize mitochondrial subtypes in Parkinson’s disease to improve diagnostics and predictability of the disease progression. Our aim is to provide essential basis for disease-modifying therapies. Furthermore, as much as one-fifth of the Finnish patients with Parkinson’s disease have familial disease, but currently known hereditary forms explain only rare cases in Finland. Our aim is to investigate novel population-specific forms of PD, which, in part, direct the research of disease mechanisms.

Mitochondria are cell organelles that provide energy for cellular processes via oxidative phosphorylation (OXPHOS) that also produces heat, making the mitochondria 15°C warmer than the surrounding cell. We will develop new tools to measure mitochondrial heat production in homeotherm and poikilotherm in vitro and in vivo models. Our aim is to reveal the role of mitochondrial heat generation in three important phenomena: mitochondrial diseases, immune response and adaptation to different temperature regimes. 

Many brain disorders involve disturbances in synaptic connections between neurons, regulated in part by cell signaling mediated through the neurotrophin receptor TrkB. Our preliminary results suggest that a drop in brain temperature during sleep regulates neurotrophic signaling mechanisms, which may be disrupted in pathological conditions. This project aims to map these temperature-dependent mechanisms that influence neural plasticity and to investigate their significance for brain function using state-of-the-art research methods. The study will enhance our understanding of fundamental principles of brain function and may enable significant breakthroughs in the study of disease processes and the development of therapeutic interventions.ä.