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Diet and Weight Loss

“Parkinson’s Reversal? One Drug Brings Dying Brain Cells Back to Life”

Stanford researchers discovered that dialing down an overactive enzyme, LRRK2, can regrow lost cellular “antennae” in key brain cells, restoring vital dopamine communication and neuroprotective signals in a mouse model of genetic Parkinson’s. After three months on the LRRK2-blocking drug MLi-2, damaged circuits revived and early signs of neuronal recovery emerged, hinting that timely treatment could not only halt but reverse disease progression—and perhaps benefit other Parkinson’s forms.

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In a groundbreaking study led by Stanford Medicine, researchers have discovered that inhibiting an overactive enzyme called LRRK2 can reverse the effects of Parkinson’s disease in mice with a specific genetic mutation. The study found that when mice consumed a molecule called MLi-2 LRRK2 kinase inhibitor for three months, their brain cells regained primary cilia, restored communication between dopamine neurons and the striatum, and began producing neuroprotective factors again.

The research team was initially unsure whether cilia could regrow in fully mature neurons that were no longer reproducing through cell division. However, recent findings on neurons involved in regulating circadian rhythms inspired them to try again. After three months of treatment, the percentage of striatal neurons and glia affected by overactive LRRK2 enzyme with primary cilia was indistinguishable from those without the genetic mutation.

This breakthrough has significant implications for patients with Parkinson’s disease. The earliest symptoms begin about 15 years before someone notices a tremor, typically manifesting as a loss of smell, constipation, and sleep disorders. Researchers hope that people with the LRRK2 genetic mutation can start treatment early enough to prevent or delay the onset of symptoms.

The next step for the research team is to test whether other forms of Parkinson’s disease not associated with the LRRK2 genetic mutation could benefit from this type of treatment. If successful, this approach has great promise in restoring neuronal activity and improving quality of life for patients. The study was funded by The Michael J. Fox Foundation for Parkinson’s Research, the Aligning Science Across Parkinson’s initiative, and the United Kingdom Medical Research Council.

Diet and Weight Loss

Tiny Gut “Sponge” Bacteria Found to Flush Out Toxic PFAS “Forever Chemicals”

Cambridge scientists have spotted gut bacteria that greedily soak up PFAS “forever chemicals,” then ferry them safely out of the body in animal tests, removing up to three-quarters of the toxins within minutes. Their findings hint at probiotic pills that could shield people from PFAS-linked cancers, fertility issues, and heart disease while lawmakers scramble to rein in 4,700 widespread compounds.

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The discovery of certain microbe species in the human gut that can absorb toxic PFAS chemicals has brought hope for a potential solution to mitigate their harmful effects. Scientists at the University of Cambridge have found that these bacterial species can soak up various PFAS molecules from their surroundings, including those ingested through food and water.

Researchers introduced nine bacterial species into the guts of mice to “humanize” the mouse microbiome and observed that they rapidly accumulated PFAS eaten by the mice, which were then excreted in feces. The study found that as the mice were exposed to increasing levels of PFAS, the microbes worked harder, consistently removing the same percentage of the toxic chemicals.

Within minutes of exposure, the bacterial species tested absorbed between 25% and 74% of the PFAS molecules. This is the first evidence that the gut microbiome could play a helpful role in removing toxic PFAS chemicals from our bodies.

The researchers plan to use their discovery to create probiotic dietary supplements that boost the levels of these helpful microbes in our gut, protecting against the toxic effects of PFAS. However, this has not yet been directly tested in humans.

PFAS, or Perfluoroalkyl and Polyfluoroalkyl Substances, are man-made chemicals used for their resistance to heat, water, oil, and grease. They are found in many everyday items, including waterproof clothing, non-stick pans, lipsticks, and food packaging. Due to their persistence in the environment, PFAS have accumulated in large quantities, affecting human health.

The study’s findings open up possibilities for developing ways to get PFAS out of our bodies where they do the most harm. Researchers are exploring various ways to turbocharge the microbes’ performance and create probiotics that remove PFAS from the body.

In addition to using probiotics, experts recommend avoiding PFAS-coated cooking pans and using a good water filter to help protect ourselves against PFAS.

The UK has launched a parliamentary inquiry into the risks and regulation of PFAS, highlighting the growing concern about their environmental and health impacts. The discovery of gut bacteria that can absorb PFAS molecules brings hope for a potential solution to mitigate these effects.

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Children's Health

“Chemical Exposure: A Growing Concern for Toddlers’ Health”

Researchers testing urine from 2- to 4-year-olds in four U.S. states uncovered 96 different chemicals, many of them unmonitored and linked to hormone and brain disruption. Legacy toxins like triclosan are slowly declining, yet replacements such as DINCH plasticizer and modern pesticides are rising. Toddlers—especially the youngest, later-born, and those from minority groups—often carried higher levels than their own mothers. Scientists urge expanded biomonitoring and stricter regulations before these invisible pollutants derail early development.

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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.

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Alzheimer's

Unlocking the Brain’s Sugar Code: Scientists Discover a New Player in the Battle Against Alzheimer’s

Scientists have uncovered a surprising sugar-related mechanism inside brain cells that could transform how we fight Alzheimer’s and other dementias. It turns out neurons don’t just store sugar for fuel—they reroute it to power antioxidant defenses, but only if an enzyme called GlyP is active. When this sugar-clearing system is blocked, toxic tau protein builds up and accelerates brain degeneration.

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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.

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