Poly-N-methylated Aβ-Peptide C-Terminal fragments (MEPTIDES) reverse the deleterious effects of amyloid-β in rats.

Alzheimer's disease (AD) is characterized by extracellular deposition of amyloid-β (Aβ) plaques. These protein deposits impair synaptic plasticity thereby producing a progressive decline in cognitive function. Current therapies are merely palliative and only slow cognitive decline.