Author(s): Thomas G Ohm* and Volker Meske*
The by far most relevant genetic risk factor for Alzheimer’s disease is possession of the allelic epsilon 4 variant of the cholesterol transporter apolipoprotein E. The apolipoprotein E allelic polymorphism impacts on both histopathological hallmarks of Alzheimer’s disease, the intraneuronal tau-aggregates forming neuropil threads and neurofibrillary tangles and the extracellular plaques built-up by beta-amyloid. Autophagy is a crucial process in neurons and plays a central role in cellular degradation of protein aggregates including those composed of tau or beta-amyloid. We discuss available evidence for a role of the apolipoprotein E polymorphism in autophagy.
