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Reversing Age-Related Cognitive Decline: A Possibility?

 New experiments conducted on mice have indicated that restoring brain plasticity might hold the key to reversing age-related cognitive decline.

The experiments focused on inhibitory interneurons in the visual cortex. These sensory neurons have rarely been studied to date, however, they’re believed to be crucial to brain plasticity.

The study’s researchers said: "Despite common belief, loss of neurons due to cell death is quite limited during normal aging and unlikely to account for age-related functional impairments. Rather, it seems that structural alterations in neuronal morphology and synaptic connections are features most consistently correlated with brain age, and may be considered as the potential physical basis for the age-related decline."

Mice at several key ages were used in the study, and this was important because the researchers wanted to track the decline in inhibitory brain cells as the mice aged. The research found that there was no significant age-related decline to speak of.

With that being said, the researchers did note a decline in several plasticity markers. The growth of dendrites, which are branches that connect neurons to each other, were observed to slow down progressively between the ages of three (when mice reach maturity) and 18 (when mice can be considered old) months. This is one of the key factors that prevents the brain from remodeling itself, thus reducing plasticity.

Another plasticity marker that was used for measurement is the stimulus-selective response potentiation. It essentially allowed the researchers to see how well the mice responded to visual stimuli, and they found that these responses declined with age. In fact, SRP measurements were solid for three months, but almost nonexistent by the time they reached nine months.

Last but not least, the researchers devoted the final part of the study to finding out whether plasticity reduction in the mice’s brains could be reversed. They used a drug called fluoxetine, which is more commonly known as Prozac, in three-month-old mice. They were treated with the drug for at least six months and displayed significant improvements in all plasticity markers.

"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," the researchers wrote.

Although the new hypothesis for normal age-related decline is compelling, using fluoxetine as a therapeutic agent isn’t especially practical. For instance, its side effects mean that it isn’t recommended for use by the elderly, and it would have to be administered at a young age, and for a very long time, for it to have any effect. The latter points are also based on the assumption that the drug’s effects on mice could be replicated in humans, which would take years of clinical trials to prove definitively.

Nevertheless, the study found that a decline in brain plasticity has the potential to be reversed, meaning that age-related cognitive decline we’ve come to accept as just part of getting older might actually be able to be managed in the future.


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