Turku University Hospital

Researchers have found a new function for an existing protein. They discovered that TIMP-1, a protein traditionally known to prevent damage to the body's cells and tissues, plays a critical role in the immune system's defense against cancer. The findings of the study could improve the effectiveness of current cancer immunotherapies. Researchers at the University of Turku in Finland have found a new function for an existing protein. They discovered that TIMP-1, a protein traditionally known to prevent damage to the body's cells and tissues, plays a critical role in the immune system's defence against cancer. The findings of the study could improve the effectiveness of current cancer immunotherapies. TIMP-1 protein is produced by dendritic cells, which are responsible for initiating immune responses and boosting the immune system's ability to recognise and destroy cancer cells. The protein enhances antitumor immunity through self-stimulation and by activating surrounding immune cells. As a result, increasing TIMP-1 expression or targeting its negative regulators in tumours with deficient immune responses could potentially improve the effectiveness of current cancer immunotherapies. "For patients deficient in TIMP-1 expression, our discovery helps create rational therapeutic innovations," says Carlos Rogerio Figueiredo, Docent and InFLAMES researcher at the University of Turku. According to Figueiredo, the new findings are also relevant for fighting infections by viruses and bacteria, as the process is part of a universal mechanism that fights microorganisms and cancer in a similar fashion. The study used samples from the Finnish Auria Biobank for clinical-oriented discoveries, which were further validated with the latest biochemical and immunological tools to propose a new molecular view of how the body fights cancer. Figueiredo thanks the patients as well as Oncologist Maria Sundvall and Pathologist Eva-Maria Birkman from Turku University Hospital for their significant contributions to this project. "The published research shows how the reverse translational method works in practice. Traditional translational research typically starts with basic laboratory discoveries, which are later tested on patients in clinical trials. The reverse translational approach, on the other hand, starts with real-world data from patient samples to guide focused laboratory studies, thereby enhancing the likelihood of success when applied to patients," explains Figueiredo. Figueiredo heads the Medical Immuno-Oncology Research Group (MIORG) at the Faculty of Medicine at the University of Turku, which is affiliated with the Turku Bioscience Centre and supported by the Research Council of Finland, InFLAMES Flagship, the Sigrid Juselius Foundation, and the Jane and Aatos Erkko Foundation. The findings of the study were published in the journal Genes & Immunity, which is part of the Nature Portfolio series. InFLAMES Flagship is a joint initiative of University of Turku and Åbo Akademi University, Finland. The goal of the Flagship is to integrate the immunological and immunology-related research activities to develop and exploit new diagnostic and therapeutic tools for personalised medicine. InFLAMES is part of Research Council of Finland's Flagship Programme.

An international research group succeeded in identifying the probable origin of stuttering in the brain. An international research group led by researchers from the University of Turku and Turku University Hospital in Finland has succeeded in identifying the probable origin of stuttering in the brain. Stuttering is a speech rhythm disorder characterised by involuntary repetitions, prolongations or pauses in speech that prevent typical speech production. Approximately 5-10% of young children stutter, and an estimated 1% continue to stutter into adulthood. A severe stutter can have a profound negative impact on the life of the individual affected. "Stuttering was once considered a psychological disorder. However, with further research, it is now understood to be a brain disorder related to the regulation of speech production," says Professor of Neurology Juho Joutsa from the University of Turku. Stuttering may also be acquired as a result of certain neurological diseases, such as Parkinson's disease or a stroke. However, the neurobiological mechanisms of stuttering are not yet fully understood, and where it originates in the brain remains uncertain. The findings from brain imaging studies are partly contradictory, and it is challenging to determine which changes are the root cause of stuttering and which are merely associated phenomena. Stuttering localised in the same brain network regardless of its cause Researchers from Finland, New Zealand, the United States and Canada developed a new research design that could provide a solution to this problem. The study included individuals who had suffered a stroke, some of whom developed a stutter immediately after it. The researchers discovered that although the strokes were located in different parts of the brain, they all localised to the same brain network, unlike the strokes that did not cause stuttering. In addition to people who had suffered a stroke, the researchers used magnetic resonance imaging (MRI) to scan the brains of 20 individuals with developmental stuttering. In these individuals, the stuttering was associated with structural changes in the nodes of the brain network originally identified in relation to causal stroke lesions -- the greater the changes, the more severe the stuttering. This finding suggests that stuttering is caused by a common brain network, regardless of the aetiology (developmental or neurological). The key nodes of the network identified by the researchers were putamen, amygdala and claustrum located deep within the brain, and the connections between them. "These findings explain well-known features of stuttering, such as the motor difficulties in speech production and the significant variability in stuttering severity across emotional states. As major nuclei in the brain, the putamen regulates motor function and the amygdala regulates emotions. The claustrum, in turn, acts as a node for several brain networks and relays information between them," explains Joutsa. The results of the study provide a unique insight into the neurobiological basis of stuttering. Locating stuttering in the brain opens up new possibilities for medical treatment. Researchers hope that in the future, stuttering could be effectively treated, for example, with brain stimulation that can be targeted specifically to the now identified brain network.

Regular high caffeine consumption affects dopamine function in patients with Parkinson's disease, shows a new international study. Caffeine consumption before undergoing diagnostic brain dopamine imaging may also affect the imaging results. Regular high caffeine consumption affects dopamine function in patients with Parkinson's disease, shows a new international study led by the University of Turku and Turku University Hospital in Finland. Caffeine consumption before undergoing diagnostic brain dopamine imaging may also affect the imaging results. Previous research has shown that regular caffeine intake is associated with a reduced risk of developing Parkinson's disease. However, there is limited research on the effects of caffeine on disease progression in patients who have already been diagnosed. A follow-up study led by the University of Turku and Turku University Hospital (Tyks) in Finland examined how caffeine consumption affects brain dopamine function over an extended period in patients diagnosed with Parkinson's disease. The dopamine function of the brain was assessed with single photon emission computed tomography (SPECT) to measure dopamine transporter (DAT) binding. "The association between high caffeine consumption and a reduced risk for Parkinson's disease has been observed in epidemiological studies. However, our study is the first to focus on the effects of caffeine on disease progression and symptoms in relation to dopamine function in Parkinson's disease," says Valtteri Kaasinen, Professor of Neurology at the University of Turku and principal investigator of the study. Caffeine consumption had no effect on Parkinson's symptoms A clinical study compared 163 patients with early-stage Parkinson's disease to 40 healthy controls. The examinations and imaging were conducted on two occasions for a subsample, with an average interval of six years between the first and second imaging session. Changes in brain dopamine transporter binding were compared with patients' caffeine consumption, which was assessed both by a validated questionnaire and by determining concentrations of caffeine and its metabolites in blood samples. The findings revealed that patients with a high caffeine consumption exhibited a 8.3-15.4% greater decrease in dopamine transporter binding compared to those with a low caffeine consumption. However, the observed decline in dopamine function is unlikely to be due to a greater reduction in dopamine neurons following caffeine consumption. Rather, it is more likely to be a downregulatory compensatory mechanism in the brain that has also been observed in healthy individuals following caffeine and other stimulant use. "While caffeine may offer certain benefits in reducing risk of Parkinson's disease, our study suggests that high caffeine intake has no benefit on the dopamine systems in already diagnosed patients. A high caffeine intake did not result in reduced symptoms of the disease, such as improved motor function," says Kaasinen. Another significant finding of the study was the observation that a recent dose of caffeine, for example in the morning of the imaging session, temporarily increases the person's DAT binding values. This could potentially complicate the interpretation of clinically commonly used brain DAT imaging results. The research results suggest that patients should refrain from consuming coffee and caffeine for 24 hours before undergoing diagnostic DAT imaging.