Sara J. Fernandez

TL;DR: The hypothesis that targeting and functional disruption of particular synapses by Aβ oligomers may provide a molecular basis for the specific loss of memory function in early Alzheimer's disease is suggested.

TL;DR: This response provides a pathologically specific mechanism for the therapeutic action of memantine, indicates a role for ROS dysregulation in ADDL-induced cognitive impairment, and supports the unifying hypothesis that ADDLs play a central role in AD pathogenesis.

TL;DR: It is suggested that insulin resistance in AD brain is a response to ADDLs, which disrupt insulin signaling and may cause a brain‐specific form of diabetes as part of an overall pathogenic impact on CNS synapses.

TL;DR: Aβ 1−42 (Aβ1-42) is a self-associating peptide that becomes neurotoxic upon aggregation as discussed by the authors, and its toxicity originally was attributed to the presence of large, readily formed Aβ fibrils.

TL;DR: It is shown that, independent of the presence of fibrils, ADDLs stimulate tau phosphorylation in mature cultures of hippocampal neurons and in neuroblastoma cells at epitopes characteristically hyperphosphorylated in AD.