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Here’s what you’ll learn when you read this story:
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For decades, scientists have looked at various mechanisms responsible for the decline of our mental faculties as we age.
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A new discovery shows that the accumulation of a certain protein called the ferritin light chain 1, or FTL1, plays a big role.
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In experiments with mice, scientists found that less FTL1 present in neural cells promoted healthier, younger brains.
The brain may lie at the biological center of our lived experience, but the scientific underpinnings of the brain—specifically, how it forms subjective consciousness—remain mysterious. Sadly, one truth is well-known: As we age, so does our brain. Because this all-important organ filled with 86 billion neurons forms our experience, dysregulation within the brain has outsized impacts on someone’s quality of life.
For years, scientists have tried to find ways to stave off these negative effects and make a person’s healthspan largely match their ever-increasing lifespan. In 2021, Stanford University investigated the debris-cleaning role of the myeloid cells within the brain, and three years later, a study from the University of Rochester on the broader glymphatic system (which interacts with myeloid cells) found ways to restart the flow of brain-cleaning fluids.
In another installment of this ongoing research to improve the aging brain, scientists from the University of California San Francisco (UCSF) identified a protein that’s central to aging the brain in humans. By analyzing how genes and proteins changed over time in mice, the team identified a troublesome protein named ferritin light chain 1, or FTL1. When scientists reduced the presence of this protein in the hippocampus, the mice regained some of their youthful characteristics, including improved nerve connections and better permorfance on memory tests. The results of the study were published in the journal Nature Aging.
“It is truly a reversal of impairments […]. It’s much more than merely delaying or preventing symptoms,” Saul Villeda, a co-author of the study from UCSF, said in a press statement. “We’re seeing more opportunities to alleviate the worst consequences of old age. It’s a hopeful time to be working on the biology of aging.”
To test this idea even further, the team artificially stimulated the production of FTL1 in young mice, and soon, their mental abilities began to match those of older rodents. When analyzing the effects of FTL1 protein in a petri dish, Villeda and his team discerned that nerve cells engineered simple, one armed neural wires—known as “neurites”—rather than the branching neurites typical of normal neural cells.
“To identify potential therapeutic targets to restore cognitive function in older people, we first need to gain mechanistic insight into the molecular drivers of cognitive decline in the aging brain,” the authors wrote. “It has become clear that cognitive dysfunction in the aged brain in the absence of neurodegenerative disease is not paralleled by cell death but, instead, by a decline in neuronal function at the synaptic level.”
The authors also note that a 2015 study found that increased ferritin levels in cerebrospinal fluid negatively impacted cognitive performance and accurately predicted conversion from mild cognitive impairment to Alzheimer’s disease. The researchers hope that by targeting FTL1, future therapies may not only improve natural cognitive decline, but will also benefit people with neurodegenerative diseases.
As this study—and many studies before it—have clearly demonstrated, there is no singular cause of mental decline. But with each new study, scientists work toward a holistic picture of neurodegenerative decline as we age, and with that new perspective comes the hope of new therapies that could make cognitive decline a thing of the past.
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