A groundbreaking new study has shed light on the surprising link between hearing loss, loneliness, and lifespan. Researchers from the USC Caruso Department of Otolaryngology – Head and Neck Surgery found that adults with hearing loss who used hearing aids or cochlear implants were more socially engaged and felt less isolated compared to those who didn’t use them.

The study, published in JAMA Otolaryngology – Head & Neck Surgery, is the first to link hearing aids and cochlear implants to improved social lives among adults with hearing loss. The researchers conducted a comprehensive review of 65 previously published studies, encompassing over five thousand participants, on how hearing aids and cochlear implants affect three key measures: social quality of life, perceived social handicap, and loneliness.

The findings suggest that hearing devices can help prevent the social disconnection and broader health consequences that can follow untreated hearing loss. When left unaddressed, hearing loss can make communication difficult, leading people to withdraw from conversations and social activities. This can lead to mental stimulation reduction, increased risk of loneliness, anxiety, depression, cognitive decline, and dementia.

The researchers found that adults using hearing devices feel more socially connected and less limited in social situations. They are better able to engage in group conversations and feel more at ease in noisy or challenging listening environments. Participants also reported feeling less socially handicapped by their hearing loss, with fewer barriers and frustrations during interactions and an improved ability to stay engaged without feeling excluded.

Those with cochlear implants reported the most improvement in their social quality of life, likely because cochlear implants offer greater hearing restoration than hearing aids, especially for individuals with more severe hearing loss. As a result, they may experience more noticeable improvements in social engagement once their hearing is restored.

While it was outside the scope of the study to measure how better social lives relate to improved cognitive outcomes, the researchers believe there may be a connection. Previous research has found managing hearing loss may be key to reducing the risk of cognitive decline and dementia. The study’s lead researcher, Janet Choi, MD, MPH, an otolaryngologist with Keck Medicine, believes that by restoring clearer communication, hearing devices may help preserve cognitive health by keeping the brain more actively involved and people more connected.

This research follows a January 2024 study by Choi showing that adults with hearing loss who use hearing aids have an almost 25% lower risk of mortality, suggesting that treating hearing loss can improve lifespan as well as social quality of life. These findings add to a growing body of research showing that hearing health is deeply connected to overall well-being.

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Scientists have taken a groundbreaking step towards reversing Parkinson’s symptoms in mice, paving the way for potential treatments for humans. A team of researchers at the University of Sydney has identified a new brain protein involved in the development of Parkinson’s disease and found a way to modify it.

Parkinson’s disease is a degenerative neurological disorder that affects over 150,000 people in Australia alone, making it the second most common condition after dementia. The research team, led by Professor Kay Double from the Brain and Mind Centre, has spent more than a decade studying the biological mechanisms behind the condition.

In their latest study, published in Acta Neuropathologica Communications, the researchers found that targeting the faulty SOD1 protein with a drug treatment improved motor function in mice bred to have Parkinson-like symptoms. The mice treated with the special copper supplement showed significant improvements in their motor skills, which is a promising sign for potential human treatments.

Professor Double said: “We were astonished by the success of the intervention. We had hoped that treating this malfunctioning protein might improve the Parkinson-like symptoms in the mice, but even we were surprised by the dramatic improvement.”

The study involved two groups of mice: one group received the special copper supplement, while the other received a placebo. The results showed that the mice receiving the placebo experienced a decline in their motor symptoms, whereas those receiving the copper supplement did not develop movement problems.

Professor Double said: “The results were beyond our expectations and suggest that this treatment approach could slow the progression of Parkinson’s disease in humans.”

Parkinson’s disease is caused by the death of dopamine-producing cells in the brain, leading to a range of symptoms including tremors, muscle stiffness, slow movement, and impaired balance. Currently, there is no known cure, and only limited treatments are available.

The researchers hope that their discovery will lead to improved treatments for Parkinson’s disease. Professor Double said: “As our understanding of Parkinson’s disease grows, we are finding that there are many factors contributing to its development and progression in humans – and faulty forms of the SOD1 protein is likely one of them.”

Their next step is to identify the best approach to targeting the faulty SOD1 protein in a clinical trial, which could be the start of a new therapy to slow the development of Parkinson’s disease.

The battle against Alzheimer’s disease and other forms of dementia has just received a surprise player: brain sugar metabolism. A new study from scientists at the Buck Institute for Research on Aging has revealed that breaking down glycogen – a stored form of glucose – in neurons may protect the brain from toxic protein buildup and degeneration.

Glycogen is typically thought of as a reserve energy source stored in the liver and muscles, but small amounts also exist in the brain. The research team, led by postdoc Sudipta Bar, PhD, discovered that in both fly and human models of tauopathy (a group of neurodegenerative diseases including Alzheimer’s), neurons accumulate excessive glycogen. This buildup appears to contribute to disease progression.

Tau, the infamous protein that clumps into tangles in Alzheimer’s patients, physically binds to glycogen, trapping it and preventing its breakdown. When glycogen can’t be broken down, the neurons lose an essential mechanism for managing oxidative stress, a key feature in aging and neurodegeneration.

By restoring the activity of an enzyme called glycogen phosphorylase (GlyP), which kicks off the process of glycogen breakdown, the researchers found they could reduce tau-related damage in fruit flies and human stem cell-derived neurons. Rather than using glycogen as a fuel for energy production, these enzyme-supported neurons rerouted the sugar molecules into the pentose phosphate pathway (PPP) – a critical route for generating NADPH (nicotinamide adenine dinucleotide phosphate) and Glutathione, molecules that protect against oxidative stress.

The team demonstrated that dietary restriction (DR) naturally enhanced GlyP activity and improved tau-related outcomes in flies. They further mimicked these effects pharmacologically using a molecule called 8-Br-cAMP, showing that the benefits of DR might be reproduced through drug-based activation of this sugar-clearing system.

Researchers also confirmed similar glycogen accumulation and protective effects of GlyP in human neurons derived from patients with frontotemporal dementia (FTD), strengthening the potential for translational therapies. The study emphasizes the power of the fly as a model system in uncovering how metabolic dysregulation impacts neurodegeneration.

The researchers acknowledge the Buck’s highly collaborative atmosphere as a major factor in the work, highlighting the expertise in fly aging and neurodegeneration, proteomics, human iPSCs, and neurodegeneration. The study not only highlights glycogen metabolism as an unexpected hero in the brain but also opens up a new direction in the search for treatments against Alzheimer’s and related diseases.

By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell’s inner chemistry to fight age-related decline. As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain’s hidden sugar code could unlock powerful tools for combating dementia.