Skip to main content
News Icon

News categories: Publication

Alzheimer's Study published in Cell Reports

Alzheimer's disease: Inflammation triggers fatal cycle

University of Bonn study proves disastrous contribution of an ancient immune mechanism

An immune reaction in the brain seems to play a major role in the development of Alzheimer's disease. In a way, it "adds fuel to the fire" and apparently causes an inflammation that, in a sense, keeps kindling itself. The study has now been published in the journal Cell Reports. Alzheimer's disease is characterized by clumps of the protein Aß (amyloid beta), which form large plaques in the brain. Aß resembles molecules on the surface of some bacteria. Over many millions of years, organisms have therefore developed defense mechanisms against such structures. These mechanisms are genetically determined and therefore belong to the so-called innate immune system. They usually result in certain scavenger cells absorbing and digesting the molecule.

In the brain, the microglia cells take over this role. In doing so, however, they trigger a devastating process that appears to be largely responsible for the development of dementia. On contact with Aß, certain molecule complexes, the inflammasomes, become active in the microglia cells. They then resemble a wheel with enzymes on the outside. These can activate immune messengers and thereby trigger an inflammation by directing additional immune cells to the site of action.

"Sometimes the microglia cells perish during this process," explains Prof. Dr. Michael Heneka, head of a research group at the German Center for Neurodegenerative Diseases (DZNE) and director of the Department of Neurodegenerative Diseases and Gerontopsychiatry at the University Hospital Bonn. "Then they release activated inflammasomes into their environment, the ASC specks." Prof. Michael Heneka is a member of the Cluster of Excellence ImmunoSensation.


Publication

Lea L. Friker, Hannah Scheiblich, Inga V. Hochheiser, Rebecca Brinkschulte, Dietmar Riedel, Eicke Latz, Matthias Geyer and Michael T. Heneka: Amyloid Clustering around ASC Fibrils Boosts Its Toxicity in Microglia; Cell Reports; DOI: 10.1016/j.celrep.2020.02.025

Contact

Prof. Dr. Michael Heneka

Director of the Department of Neurodegenerative Diseases and Gerontopsychiatry

University Hospital Bonn

German Center for Neurodegenerative Diseases (DZNE)

Tel. +49-(0)228-28713091

E-mail: michael.heneka@dzne.de

Related news

Prof. Matthias Geyer, - together with Prof. Robert P. Fisher from New York, provides an overview of the current state of research on the transcriptional regulation of cyclin-dependent kinases (CDKs) and the prospects for cancer treatment.

News categories: Publication

A Ray of Hope in the Fight Against Cancer

Cancer is the second leading cause of death in Germany. In the search for new therapeutic approaches that target the uncontrolled growth of tumor cells, a class of enzymes known as cyclin-dependent kinases (CDKs) has come into focus. This is because this family of enzymes plays a fundamental role in gene expression and cell division. An overview of the current state of research on the transcriptional regulation of CDKs and the prospects for cancer treatment was compiled by Prof. Matthias Geyer of the UKB in collaboration with Prof. Robert P. Fisher and has now been published.
View entry
(from left) Julia Nicke and Dr. Mona Malek Mohammadi have identified a previously unknown signaling pathway in the immune system that helps newborn heart cells survive and regenerate after injury.

News categories: Publication

Central Hub for Heart Repair Discovered Bonn study: Heart muscle interaction enables cardiac regeneration in the neonatal heart

Researchers at the University Hospital of Bonn (UKB) and the University of Bonn have identified a previously unknown signaling pathway in the immune system that helps newborn heart cells survive and regenerate after injury. The findings could open new avenues for future therapies aimed at repairing damaged adult hearts after heart attacks or chronic cardiovascular disease. The study has now been published in the journal Cell Communication and Signaling (Springer Nature).
View entry
News Icon

News categories: Publication

Malaria Causes Permanent Damage to Phagocytes in the Spleen

Macrophages formed in the bone marrow can only assume the function of embryonal phagocytes, or “scavenger cells,” to a certain degree according to a study by the University of Bonn and the Peter Doherty Institute for Infection and Immunity at the University of Melbourne. The researchers have demonstrated that malaria infection causes permanent damage to resident CD163 macrophages in the spleen, which are responsible for cleaning the blood, recycling iron and communicating with other cells involved in the body’s immune response.
View entry

Back to the news overview