Christian Haass is a German biochemist and neuroscientist specializing in Alzheimer's disease research. His work has focused on understanding the molecular mechanisms of amyloid-beta metabolism and the role of microglia in neurodegeneration. He has made significant contributions to our understanding of how genetic risk factors influence Alzheimer's disease pathogenesis and has pioneered research into immune-based therapeutic approaches. He is a leading authority on amyloid-beta metabolism and the role of microglia in neurodegeneration.
Christian Haass received his PhD from the University of Munich (Ludwig Maximilian University of Munich). He completed his postdoctoral training at the Massachusetts General Hospital and Harvard Medical School. He currently holds the chair of Metabolic Biochemistry at the Ludwig Maximilian University of Munich and is a senior scientist at the German Center for Neurodegenerative Diseases (DZNE). His research career has spanned over three decades, with major contributions to understanding the amyloid hypothesis and microglial biology in Alzheimer's disease.
Haass's research has revolutionized our understanding of Alzheimer's disease pathogenesis:
- Pioneered research on the proteolytic processing of APP by secretases
- Characterized the amyloidogenic pathway that generates amyloid-beta peptides
- Demonstrated how mutations in APP and presenilins cause familial Alzheimer's disease
- Identified the role of alpha- and beta-secretases in amyloid processing
- Investigated the molecular mechanisms of amyloid-beta aggregation
- Studied the role of metal ions in amyloid fibril formation
- Explored therapeutic strategies targeting amyloid-beta oligomerization
- Researched the toxic species of amyloid-beta (oligomers vs. fibrils)
¶ Microglia and Neuroinflammation
- Discovered that microglia undergo transformation in Alzheimer's disease
- Identified the role of TREM2 in microglial function
- Investigated how genetic variants in immune genes modify AD risk
- Pioneered research on the neurodegenerative microglia phenotype (DAM)
- Haass C, et al. (1992). Amyloid beta-peptide is produced by cultured cells during normal metabolism
- De Strooper B, et al. (1998). A presenilin-1 mutation at codon 385
- Haass C, Selkoe DJ. (2007). Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide
- Ulrich JD, et al. (2017). Elucidating the Role of TREM2 in Alzheimer's Disease
- Condello C, et al. (2018). Microglia constitute a barrier to neurofibrillary pathology
- Haass C, et al. (2022). TREM2 in Alzheimer's disease: from genetics to therapy
¶ Awards and Honors
- Ernst Jung Prize for Science and Medicine (2000)
- Metlife Foundation Award (2002)
- Brain Prize (2018)
- Gairdner International Award (2022)
- Member of the German National Academy of Sciences Leopoldina
- European Academy of Sciences member
- Haass C, et al. (1992). Nature.
- Selkoe DJ, Hardy J. (2016). The amyloid hypothesis of Alzheimer's disease at 25 years. EMBO Molecular Medicine.
- Sims MR, et al. (2017). TREM2, microglia and Alzheimer's disease. Nature Reviews Neurology.