doctor holding brain scan results

ANK6 dipeptide improves cognition in Alzheimer’s disease transgenic mouse model

Alzheimer’s disease is a neurodegenerative disease whose contributing factors are not well understood. It is thought that overproduction, the decreased clearance, and the increased deposition of amyloid beta leads to the cognitive decline associated with Alzheimer’s disease. Our lab previously found that treatment with monomeric D3 peptide (an amyloid beta oligomer directed D-enantiomeric peptide) improves cognition and decreases levels of amyloid-beta deposition and inflammation in a double transgenic mouse model.1 This study tests the hypothesis that the ANK6 dipeptide (a D3 dimer) causes a similar decrease in amyloid-beta oligomer deposits in the brains of transgenic mice (Mus musculus) with the Swedish-Dutch-Iowa amyloid precursor protein mutation (APPSwDI), and improves cognition. APPSwDI mice were treated with ANK6 peptide or a saline control, delivered via Alzet minipumps surgically inserted beneath the peritoneal layers, for four weeks.

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