Antidepressant can delay aging of brain cells

The study provides evidence that the decline in the capacity of brain cells to change, called "plasticity," rather than a decline in total cell numbers may underlie some of the sensory, cognitive declines associated with normal brain aging.

Representational Image:Pixabay

New York: Administering commonly used antidepressant fluoxetine to mice helped restore youthful flexibility to their aging brain cells, showed a study.

The study provides fresh evidence that the decline in the capacity of brain cells to change, called "plasticity," rather than a decline in total cell numbers may underlie some of the sensory and cognitive declines associated with normal brain aging. 

Scientists at the MIT revealed that in mice treated with fluoxetine, also known as Prozac, the inhibitory interneurons in the visual cortex remained just as abundant during aging, but their arbors become simplified and they become much less structurally dynamic and flexible. They could also restore a significant degree of lost plasticity to the cells.

"Here we show that fluoxetine can also ameliorate the age-related decline in the structural and functional plasticity of visual cortex neurons," said the scientists including lead author Ronen Eavri from MIT. 

"Our finding that fluoxetine treatment in aging mice can attenuate the concurrent age-related declines in interneuron structural and visual cortex functional plasticity suggests it could provide an important therapeutic approach towards mitigation of sensory and cognitive deficits associated with aging provided it is initiated before severe network deterioration," they added.

A previous study had shown that fluoxetine promotes interneuron branch remodeling in young mice, so the team decided to see whether it could do so for older mice and restore plasticity as well.

In the new study, appearing in the Journal of Neuroscience, they put the drug in the drinking water of mice at various ages for various amounts of time. 

Three-month-old mice treated for three months showed little change in dendrite growth compared to untreated controls, but 25 percent of the cells in six-month-old mice treated for three months showed significant new growth (at the age of 9 months). 

But among 3-month-old mice treated for six months, 67 percent of cells showed new growth by the age of 9 months, showing that treatment starting early and lasting for six months had the strongest effect.