As toddlers grow and explore their surroundings, they are exposed to an alarming number of chemicals that can have long-term effects on their health. A recent study published in Environmental Science & Technology has shed light on this critical issue, revealing that children aged 2 to 4 years in the United States are regularly exposed to a wide range of potentially hazardous substances.

Conducted by researchers from multiple institutions across the country, the study analyzed urine samples from 201 children and detected 96 chemicals in their bodies. The findings are alarming because early childhood is a critical period for brain and body development, and many of these chemicals can interfere with hormones, brain function, and immune response.

The research was part of the Environmental influences on Child Health Outcomes (ECHO) program, funded by the National Institutes of Health (NIH). The study looked at children from four states – California, Georgia, New York, and Washington – and found that they were exposed to chemicals through everyday activities such as eating, drinking, breathing indoor and outdoor air, and touching contaminated surfaces.

The researchers noted that children are particularly vulnerable due to frequent hand-to-mouth contact, playing close to the ground, and higher intake rates relative to their smaller body weight. In fact, many of the children had higher levels of certain chemicals in their bodies than their mothers did during pregnancy, including phthalates, bisphenol S, and pesticide biomarkers.

The study’s lead author, Deborah H. Bennett, emphasized that further research is needed to understand the long-term health implications of these chemical exposures. Jiwon Oh, first author of the study, added that exposure to certain chemicals in early childhood has been linked to developmental delays, hormone disruption, and other health issues.

While it may be impossible to eliminate all chemical exposures, parents can take simple steps to reduce their children’s contact with harmful substances. By being aware of these potential risks and taking precautions, we can help protect our toddlers’ health and well-being.

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.

The scientific community has made another groundbreaking discovery that reveals how our beloved morning coffee might be doing more than just waking us up. A recent study conducted by researchers at Queen Mary University of London’s Cenfre for Molecular Cell Biology sheds light on the potential anti-ageing properties of caffeine, the world’s most popular neuroactive compound.

The research, published in the journal Microbial Cell, delves into the intricate mechanisms within our cells and how they respond to stress and nutrient availability. The scientists used a single-celled organism called fission yeast as a model to understand how caffeine affects ageing at a cellular level.

One of the key findings was that caffeine doesn’t act directly on the growth regulator called TOR (Target of Rapamycin), which is responsible for controlling energy and stress responses in living things for over 500 million years. Instead, it works by activating another crucial system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.

“When your cells are low on energy, AMPK kicks in to help them cope,” explains Dr Charalampos (Babis) Rallis, Reader in Genetics, Genomics, and Fundamental Cell Biology at Queen Mary University of London, the study’s senior author. “And our results show that caffeine helps flip that switch.”

The implications of this discovery are significant, as AMPK is also the target of metformin, a common diabetes drug being studied for its potential to extend human lifespan together with rapamycin. The researchers demonstrated using their yeast model that caffeine’s effect on AMPK influences how cells grow, repair their DNA, and respond to stress – all of which are tied to ageing and disease.

These findings open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines. So, the next time you reach for your coffee, remember that it might be doing more than just boosting your focus – it could also be giving your cells a helping hand in slowing down your ageing process.