Multi-scale modeling of altered synaptic plasticity related to Amyloid β effects.

As suggested by Palop and Mucke (2010) pathologically elevated β-amyloid (Aβ) impairs long term potentiation (LTP) and enhances long term depression (LTD) possible underlying mechanisms in Alzheimer's Disease (AD). In the present paper we adopt and further elaborate a phenomenological computational model of bidirectional plasticity based on the calcium control hypothesis of Shouval et al. (2002).