Rather technical piece about a natural variant of amyloid-beta that combines with wild-type amyloid-beta to hinder conformational changes in the molecule thought to be toxic to neutrons. It is interesting if only to point up what a really complicated problem amyloid-beta is: is it toxic to neurons, in what form is it toxic, and does it progress to larger fibrils of polymer that may be present in the brain in large quantities but are no longer toxic? See this quote:
"As prototypic compound we designed a six-mer mutated peptide (Aβ1-6A2V), linked to the HIV-related TAT protein, which is widely used for brain delivery and cell membrane penetration of drugs. The resulting molecule [Aβ1-6A2VTAT(D)] revealed strong anti-amyloidogenic effects in vitro and protected human neuroblastoma cells from Aβ toxicity. Preclinical studies in AD mouse models showed that short-term treatment with Aβ1-6A2VTAT(D) inhibits Aβ aggregation and cerebral amyloid deposition, but a long treatment schedule unexpectedly increases amyloid burden, although preventing cognitive deterioration."