Endogenous Aβ₄₂ is a critical player in synaptic plasticity and memory within the normal central nervous system. This needs to be taken into consideration when designing therapies aiming at reducing Aβ levels to treat Alzheimer disease.
No takes yet. Share an insight, caveat, or question.
Puzzo et al. (2010) studied this question.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: