Little was then known about the origin of neural plaques, and the necessary technologies were still lacking. That Haass did not follow up his early work on inflammation processes should not be held against him. “In the initial phase, the microglia help to restrict the size of the plaques, thus preventing nerve-cell death,” says Haass, who holds a Chair in Metabolic Chemistry at LMU and is Coordinator of the Munich Site of the German Center for Neurodegenerative Diseases (DZNE). They promote progression of the disease, but in its early stages their activation has a protective effect. To complicate things further, the phagocytes in the central nervous system play a dual role in this context. Researchers now know that inflammation reactions trigger the activation of the microglia. Over a period of several decades, a cascade of physiological and pathological processes leads to the accumulation of characteristic protein aggregates called plaques, and to the progressive loss of nerve cells, in the brain. Indeed, much of the work done by the Cluster of Excellence SyNergy – funding for which has now been extended – has underlined their importance. Nowadays, Haass and his Munich colleagues are no longer unaware of the crucial contribution of immunological mechanisms to the progression of dementia.

All of us in the Alzheimer field ignored it for far too long.” But I didn’t pursue the topic further for over 20 years. Even then, he was interested in the part played by the brain’s phagocytes (the ‘microglia’) in the pathogenesis of Alzheimer’s disease and, more generally, in the role of the immune system in dementias – and he had published work on these issues. Professor Christian Haass, Speaker of the SyNergy Cluster of Excellence | © Jan Greune / LMUĬhristian Haass is an old hand in the business, but this story takes him back to the very beginnings of his scientific career.

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