Incontro programmato fra le iniziative promosse dall’Università di Catania nell’ambito del Festival dello Sviluppo Sostenibile 2025
Mercoledì 3 settembre 2025 | Ore 11:30
Ex Cappella – Villa San Saverio, Via Valdisavoia 9 (CT)
MICHAEL HENEKA – Director Luxembourg Centre for Systems Biomedicine, University of Luxembourg
Michael Heneka is a board-certified neurologist and clinician-scientist with a 25 years of track record in studying neurodegenerative disease at the experimental, preclinical and clinical level.
He has a long-standing interest in immunology and neuroscience.
While the main focus of his work is related to dementia and Alzheimer’s disease, he has also been working on Amyotrophic Lateral Sclerosis and Parkinson’s disease. To date he has published about 260 peer-reviewed manuscripts.
At the clinical level he has established a neurodegenerative outpatient unit at both the University of Münster and of Bonn.
From 2016 to 2021, he led the department of Neurodegenerative Disease and Geriatric Psychiatry in Bonn.
He is from January 2022 onwards the Director of the Luxembourg Centre of Systems Biomedicine at the University of Luxembourg.
ABSTRACT
The accumulation of neurotoxic amyloid beta peptides along with neurofibrillary tangle formation are key pathological hallmarks of Alzheimer’s disease. The brain has been considered as an immune-privileged organ, however, increasing evidence from translational, genetic, and pathological studies suggests that activation of distinct innate immune pathways are a third important disease hallmark which actively contributes to disease progression and chronicity.
Microglia play a pivotal role in this immune response and are activated by binding of aggregated proteins or aberrant nucleic acids to pattern recognition receptors. This immune activation initially aims to resolve the pathological challenge through TAM receptor ligation- Over time however, it results in the chronic release of inflammatory mediators and diverts microglia cells from their physiological functions and tasks. Sustained NLRP3 inflammasome activation in causes a hyperinflammatory microglial cell death called pyroptosis which is the release of ASC specks. The latter contributes to seeding of pathology by enhancing the propensity of beta-amyloid peptides to aggregate. This mechanism may account for the spread of pathology within a brain region, but also from one brain area to another. Increased cell death in turn will cause proliferation of microglial cells generating a subpopulations. Interestingly these subpopulations show changes in the transcriptome when compared to non-proliferating cells and also restricted Ab clearance capacity.
