Washington : A study led by researchers at Bay Pines VA Healthcare System and the University of South Florida has found that Cotinine, a compound derived from tobacco, reduced plaques associated with dementia and prevented memory loss in a mouse model of Alzheimer''s disease.
"We found a compound that protects neurons, prevents the progression of Alzheimer''s disease pathology, enhances memory and has been shown to be safe," said Valentina Echeverria, a scientist at Bay Pines VA Healthcare System and an assistant professor of Molecular Medicine at USF Health.
"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,” she added.
The Bay Pines VA/USF team decided to look at the effects of cotinine, the major byproduct of nicotine metabolism, in Alzheimer''s disease mice. Cotinine is nontoxic and longer lasting than nicotine. Furthermore, its safety has already been demonstrated in human trials evaluating cotinine''s potential to relieve tobacco withdrawal symptoms.
The brains of Alzheimer''s mice treated with cotinine showed a 26-percent reduction in deposits of amyloid plaques, which are a hallmark of Alzheimer''s disease. Cotinine also inhibited the accumulation of the amyloid peptide oligomers – a predecessor of senile plaques – in the brains of these mice. Furthermore, the researchers discovered that cotinine stimulated the signaling factor Akt, which promotes the survival of neurons and enhances attention and memory.
Senile plaques likely had not yet formed or were just beginning to accumulate in the brains of the young adult mice when long-term cotinine treatment was started. The researchers suggested "cotinine may be useful in preventing cognitive deterioration when administered to individuals not yet exhibiting Alzheimer''s disease cognitive impairment or those with mild cognitive impairment at early stages of the disease."
The finding is detailed in the Journal of Alzheimer''s Disease. (ANI)