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Alzheimer’s is defined by the production of amyloid beta peptides that are prone to aggregation. However, clinical approaches that seek to directly intervene in amyloid production have been largely, but not completely, unsuccessful.
Some investigators now question whether amyloid is the primary toxin; perhaps, instead, it is the brain’s protective responses that result in neurodegeneration?
The innate immune system is one response that is both powerful, for good or evil, and has been implicated by the latest genetic evidence. I will review some of the basic biology and the therapeutic interventions that are shedding light on the role of amyloid and inflammation in Alzheimer’s disease.
Key Learning objectives:
Understand how amyloid plaques are generated and what the resulting therapeutic targets have been
Gain an overview of recent amyloid-based trials – for small and large molecules
Learn how genomics has implicated innate immunity in Alzheimer’s disease
Hear about the role of TREM2 in Alzheimer’s and other neurodegenerative disorders
Develop a view on whether blocking amyloid or inflammation is the better strategy
Damian Crowther Director
R&D, Neuroscience IMED Biotech Unit AstraZeneca
Technology Networks Limited
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