neurons from fetal donors only to develop Lewy bodies within those neurons a few years after transplantation.130 Other models emphasize the role of network-based dysregulation of excitation-inhibition balance (especially at the local microcircuit level),131 disruption of activity- or connectivity-based inter-neuronal trophic factor support,132 and the long-term metabolic demands of high synaptic plasticity and turnover.133,134 These accounts need not be considered mutually exclusive and each presents a potential therapeutic target for exploration.
