A study conducted by researchers at Bay Pines VA Healthcare System and the University of South Florida found that Cotinine, a compound derived from tobacco, helped reduce plaques associated with dementia in genetically altered mice with Alzheimer's disease.
Valentina Echeverria, a scientist at Bay Pines VA Healthcare System, said, "We found a compound that protects neurons, prevents the progression of Alzheimer's disease pathology, enhances memory and has been shown to be safe. It looks like cotinine acts on several aspects of Alzheimer's pathology in the mouse model. That, combined with the drug's good safety profile in humans, makes it a very attractive potential therapy for Alzheimer's disease."
As part of the study, young mice were genetically altered to suffer memory problems akin to Alzheimer's disease. Cotinine was administered regularly for five months.
During the end of the study period, findings revealed that mice which received cotinine performed better at tasks involving their working memory and thinking skills as compared to mice which did not receive cotinine.
Long-term cotinine treatment caused a 26% reduction in deposits of amyloid plaques, which is an indicator of Alzheimer's disease. Cotinine also activated the signaling factor Akt, which helps neurons survive, thus improving memory.