This "new generation" antidepressant, fluoxetine (Prozac®) could also restore youth to neurons that inhibit aging, reveal this work by the Picower Institute for Learning and Memory, MIT (Cambridge), conducted in mice and published in the Journal of Neuroscience.
Cognitive loss caused more by the loss of plasticity than the loss of cells:
the common belief would indeed be that the loss of neurons linked to cell death could explain functional and cognitive deficiencies related to age. However "this loss is very limited during normal aging and does not explain age-related cognitive decline", explains lead author Ronen Eavri and his colleague Elly Nedivi: "it seems rather that the structural alterations of neuronal morphology and synaptic connections are the factors most correlated with brain age and can therefore be considered the physical basis of age-related decline”.
Demonstration of the cause and its possible reversal:
this work provides new evidence that the decline in this ability of brain cells to evolve, called "plasticity", rather than a decrease in the total number of cells, may be the basis of sensory and cognitive declines associated with normal brain aging . In particular, the scientists show that the age-inhibiting interneurons in the visual cortex of mice remain just as abundant during aging, but that their "branches" become simpler and much less dynamic and structurally flexible. But they also provide proof of concept that it is possible to restore much of the lost plasticity in cells, by giving mice a commonly used antidepressant drug, fluoxetine (the active ingredient in Prozac).
The sudden drop in the “dynamism index”:
in the study, the researchers focused on the aging of inhibitory interneurons, which is less well understood than that of excitatory neurons, but which plays a key role in plasticity—essential for learning and memory and for sensory acuity. The researchers focused on the visual cortex. The team counted and chronically tracked the structure of inhibitory interneurons in dozens of mice aged 3, 6, 9, 12 and 18 months and showed that inhibitory interneurons retained the ability to dynamically remodel into adulthood. , but that on the other hand, the plasticity reaches a limit then decreases gradually from about 6 months. Thus, between 3 and 18 months, the dendrites gradually become simpler, presenting fewer branches and this,
Fluoxetine promotes the remodeling of the branches of the interneuron in mice:
with the addition of the drug in drinking water at the age of 3 months (in green on the lower visual) and for 6 months, 67% of the cells resume new growth at nine months of age, showing that early treatment can reverse the age-related decline in plasticity of neurons in the visual cortex.
This finding, in mice, that fluoxetine can attenuate age-related loss of plasticity suggests considerable hope for a therapeutic approach in reducing sensory and cognitive deficits associated with aging.