{"id":37240,"date":"2026-04-01T12:03:36","date_gmt":"2026-04-01T10:03:36","guid":{"rendered":"https:\/\/uni-freiburg.de\/en\/?p=37240"},"modified":"2026-04-01T12:03:37","modified_gmt":"2026-04-01T10:03:37","slug":"first-steps-towards-cell-therapy-for-brain-disorders","status":"publish","type":"post","link":"https:\/\/uni-freiburg.de\/en\/first-steps-towards-cell-therapy-for-brain-disorders\/","title":{"rendered":"First steps towards cell therapy for brain disorders"},"content":{"rendered":"\n
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Freiburg, 31\/03\/2026<\/em><\/p>\n\n\n\n

Researchers in Freiburg have found a way to selectively replace defective immune cells in the blood vessels of the brain using an animal model. This is an important first step towards cell therapies for Alzheimer\u2019s disease and other brain disorders. The findings were recently published in the journal Nature Immunology<\/em>.<\/strong><\/strong><\/p>\n<\/div>\n\n\n\n

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\"Artistic<\/figure>\n\n\n\n

Artistic illustration showing the peripheral regions of the brain, from the dura mater to the parenchyma, with clusters of resident macrophages (blue) and infiltrating macrophages derived from monocytes (yellow). Image: Medical Center \u2013 University of Freiburg \/ Maximilian Fliegauf<\/em><\/p>\n<\/div>\n\n\n\n

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The brain and its interfaces are monitored by specialised immune cells. Researchers at the University of Freiburg\u2019s Faculty of Medicine have now investigated macrophages in the meninges and in the brain\u2019s blood vessels, which regulate the removal of waste products from the brain and control inflammatory processes. As scientists from the Institute of Neuropathology at the Medical Center \u2013 University of Freiburg, in collaboration with an international research team, have demonstrated the brief administration of a drug triggers controlled cell death in these cells. This results in them being specifically replaced by newly arriving cells, thereby influencing their function. This method could form the basis of a new therapy in the future to combat harmful vascular deposits in Alzheimer\u2019s disease. Their research, published in the journal Nature Immunology<\/em>, was conducted on genetically modified mouse strains. The data obtained are an essential building block for enabling the future use of cell-based therapeutic approaches in brain diseases.<\/p>\n<\/div>\n<\/div>\n\n\n\n

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\u201cUsing our method, we can selectively replace phagocytes \u2013 also known as macrophages \u2013 in the blood vessels of the brain. The macrophages within the brain, which are located directly adjacent to the sensitive nerve cells, remain unaffected, however,\u201d says study leader Prof. Dr Marco Prinz<\/strong>, Medical Director of the Institute of Neuropathology at the Medical Center \u2013 University of Freiburg and a member of the CIBSS \u2013 Centre for Integrative Biological Signalling Studies at the University of Freiburg. \u201cThe cells we investigated are all part of the blood-brain barrier, which makes access for therapeutic agents extremely difficult. The fact that we can now, for the first time, specifically replace these macrophages represents a significant step forward,\u201d adds Dr Lukas Amann<\/strong>, group leader at the Institute of Neuropathology at the Medical Center \u2013 University of Freiburg and co-last author of the study.<\/p>\n\n\n\n

The brain can be divided into two regions: the border zones and the functional tissue. In both, macrophages are the predominant type of immune cell. The macrophages at the brain\u2019s borders are located directly at the blood-brain barrier, which is formed at the brain\u2019s blood vessels. There, they control which substances enter the brain, thereby protecting it from harmful substances, deposits and pathogens. At the same time, waste products are also removed from the brain via the blood vessels, with the macrophages playing an important regulatory role in this process.<\/p>\n<\/div>\n\n\n\n

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Prof. Dr Marco Prinz, Medical Director of the Institute of Neuropathology at the University Medical Centre Freiburg. Photo: CIBSS University of Freiburg<\/em><\/p>\n<\/div>\n<\/div>\n\n\n\n

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The implications for Alzheimer\u2019s and other conditions<\/strong><\/h2>\n\n\n\n

\u201cRemoving waste products from the brain is very important, as these are highly damaging to the brain\u2019s nerve cells. If macrophages are not fully functional, this plays a decisive role in the development of brain diseases. For example, in Alzheimer\u2019s patients, the inadequate removal of harmful proteins from the brain\u2019s blood vessels causes what is known as cerebral amyloid angiopathy. The protein deposits impair the brain\u2019s oxygen supply, which can lead to memory loss and even haemorrhages. We intend to use our findings in future to restore or even improve the function of brain macrophages in such diseases,\u201d Prinz continued.<\/p>\n\n\n\n

Glowing immune cells in a stroke model<\/strong><\/h2>\n\n\n\n

The research team led by lead author Maximilian Fliegauf<\/strong>, a pharmacist and PhD student at the Institute of Neuropathology at the Medical Center \u2013 University of Freiburg, tracked the immune cells in an animal model as they travelled from the bone marrow to the brain and demonstrated that these cells settle long-term specifically in the interfaces of the brain. This was achieved using genetically modified mice in which immune cells were made to glow, allowing them to be observed using high-resolution microscopy. Studies in a stroke model demonstrated that diseases can be influenced by this replacement. \u201cWe are demonstrating here for the first time that the immune cells in the brain\u2019s blood vessels can be replaced in a highly targeted manner \u2013 and immune cells that can be replaced can also be positively influenced. In the next step, we want to use this knowledge to develop new therapeutic approaches for various vascular diseases of the brain.\u201d<\/p>\n\n\n\n

Researchers from Freiburg and Caen (France), as well as from Bonn and Munich, were involved in the study.<\/p>\n<\/div>\n\n\n\n

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Further information<\/strong><\/strong><\/h3>\n\n\n\n
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