Alzheimer's disease (AD) is the most common cause of dementia in the elderly population, with a projected cost of over $100 billion annually in the US alone (www.alzdiscovery.org). Late-onset AD (LOAD), the most common form of the disease, develops after age 60. The e4 allele of the apolipoprotein E (apoE) gene is the most widely reproduced susceptibility allele for LOAD with e4 carriers having an earlier age of disease onset as well as a greater probability of LOAD. Despite the strong genetic association of e4 with LOAD, there are significant gaps in our understanding of how apoE participates in disease pathogenesis, and why this role is differentiated by the various apoE isoforms. Known beneficial roles for apoE in brain include cholesterol transport from astrocytes to neurons for maintenance of neuronal function and synapse generation. ApoE also mediates the uptake and clearance of the Aß peptides by neurons and astrocytes, and possibly across the BBB. However, apoE has also been reported to correlate with increase Aß production and aggregation, and is co-deposited in neuritic plaques, a neuropathological hallmark of LOAD. This symposium brings together experts in the field of Aß and ApoE biology as well as brain lipid metabolism to address whether apoE is friEnd or foE in the pathogenesis of LOAD, and to discuss potential therapeutic strategies based on the apoE pathway that may be amenable for the prevention and treatment of LOAD.
Networking reception to follow.