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Dementia

Decoding Cell Development: Unveiling the Formation of the Brain and Inner Ear

Researchers have developed a method that shows how the nervous system and sensory organs are formed in an embryo. By labeling stem cells with a genetic ‘barcode’, they have been able to follow the cells’ developmental journey and discover how the inner ear is formed in mice. The discovery could provide important insights for future treatment of hearing loss.

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The groundbreaking research at Karolinska Institutet has shed new light on how the nervous system and sensory organs are formed in an embryo. By employing a revolutionary method that labels stem cells with a unique genetic ‘barcode’, scientists have been able to track the developmental journey of these cells, ultimately revealing the intricate processes behind the formation of the inner ear in mice.

“Our study provides a comprehensive family tree for the cells of the nervous system and the inner ear,” explains Emma Andersson, docent at the Department of Cell and Molecular Biology. “This breakthrough could lead to significant insights into treating hearing loss and potentially shed light on the mechanisms driving other genetic and developmental diseases.”
Andersson’s team used a cutting-edge technique where they injected a virus containing a genetic ‘barcode’ into mouse stem cells during an early stage of development. As these cells divided, they inherited this unique code, allowing researchers to follow their progression into distinct types of neurons and cells within the inner ear.
The results demonstrated that crucial cells in the inner ear, responsible for hearing, arise from two primary types of stem cells. This knowledge could pave the way for novel treatments targeting damaged cells in the inner ear.

“The ability to track cell origin and development offers a unique window into understanding the fundamental mechanisms behind hearing loss,” says Andersson. “This discovery may enable us to find innovative ways to repair or replace these cells, ultimately improving treatment outcomes.”
The team now intends to leverage this method to study other aspects of the nervous system’s development, as well as the broader processes governing embryonic growth. Their ultimate goal is to unlock new insights and treatments for various developmental diseases.
“We are just beginning to grasp the intricate processes driving nervous system development,” says Andersson. “Our technique opens up numerous opportunities to explore how the brain, inner ear, and other parts of the body form during embryonic development.”
Andersson led this research alongside Jingyan He, a postdoctoral fellow, and Sandra de Haan, a former PhD student within her research group. The study was funded by Karolinska Institutet, the European Union, and several prominent foundations, including the Erling-Persson Foundation and the Swedish Research Council.

No conflicts of interest are declared, except for co-author Jonas Frisén’s consulting role with 10x Genomics.

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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Alzheimer's

The Common Blood Test That Could Predict Alzheimer’s Progression

A simple blood test could reveal which early Alzheimer’s patients are most at risk for rapid decline. Researchers found that people with high insulin resistance—measured by the TyG index—were four times more likely to experience faster cognitive deterioration. The study highlights a major opportunity: a common lab value already available in hospitals could help guide personalized treatment strategies. This discovery also uncovers a unique vulnerability in Alzheimer’s disease to metabolic stress, offering new possibilities for intervention while the disease is still in its early stages.

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The common blood test known as the triglyceride-glucose (TyG) index has long been used to detect insulin resistance. New research presented at the European Academy of Neurology Congress 2025 suggests that this simple test could also be used to predict how fast Alzheimer’s disease progresses in individuals with mild cognitive impairment.

A team of neurologists from the University of Brescia reviewed records for 315 non-diabetic patients with cognitive deficits, including 200 with biologically confirmed Alzheimer’s disease. All subjects underwent an assessment of insulin resistance using the TyG index and a clinical follow-up of 3 years. The results showed that when patients were divided according to their TyG index levels, those in the highest third of the Mild Cognitive Impairment subgroup deteriorated far more quickly than their lower-TyG peers.

The researchers found that high TyG was associated with blood-brain barrier disruption and cardiovascular risk factors, yet it showed no interaction with the APOE ε4 genotype. This suggests that metabolic and genetic risks may act through distinct pathways.

Identifying high-TyG patients could refine enrolment for anti-amyloid or anti-tau trials and prompt earlier lifestyle or pharmacological measures to improve insulin sensitivity.

“If targeting metabolism can delay progression, we will have a readily modifiable target that works alongside emerging disease-modifying drugs,” concluded Dr. Bianca Gumina.

The study aimed to fill the gap in understanding how quickly Alzheimer’s progresses by focusing on its impact during the prodromal mild cognitive impairment (MCI) stage.

This research has significant implications for individuals with mild cognitive impairment and their families, as it could provide a simple and cost-effective way to predict the pace of cognitive decline.

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Alternative Medicine

Iron Overload: The Hidden Culprit Behind Early Alzheimer’s in Down Syndrome

USC researchers have uncovered a hidden driver behind the early and severe onset of Alzheimer’s in people with Down syndrome: iron overload in the brain. Their study revealed that individuals with both conditions had twice the iron levels and far more oxidative damage than others. The culprit appears to be ferroptosis, an iron-triggered cell death mechanism, which is especially damaging in sensitive brain regions.

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Scientists at the USC Leonard Davis School of Gerontology have made a groundbreaking discovery that sheds light on the unique challenges faced by people with Down syndrome who develop Alzheimer’s disease. Their research reveals a crucial link between high levels of iron in the brain and increased cell damage, providing a potential explanation for why Alzheimer’s symptoms often appear earlier and more severely in individuals with Down syndrome.

Down syndrome is caused by having an extra third copy (trisomy) of chromosome 21, which includes the gene for amyloid precursor protein (APP). People with Down syndrome tend to produce more APP, leading to an increased risk of developing Alzheimer’s disease. In fact, about half of all people with Down syndrome show signs of Alzheimer’s by the age of 60, which is approximately 20 years earlier than in the general population.

The researchers studied donated brain tissue from individuals with Alzheimer’s, those with both Down syndrome and Alzheimer’s (DSAD), and those without either diagnosis. They found that the brains of people with DSAD had twice as much iron and more signs of oxidative damage in cell membranes compared to the brains of individuals with Alzheimer’s alone or those with neither diagnosis.

This excess iron leads to ferroptosis, a type of cell death characterized by iron-dependent lipid peroxidation. In other words, iron builds up, drives the oxidation that damages cell membranes, and overwhelms the cell’s ability to protect itself.

The researchers also discovered that lipid rafts, tiny parts of the brain cell membrane crucial for cell signaling and protein processing, had more oxidative damage and fewer protective enzymes in DSAD brains compared to Alzheimer’s or healthy brains. These lipid rafts showed increased activity of the enzyme β-secretase, which interacts with APP to produce Aβ proteins, potentially promoting the growth of amyloid plaques.

The findings have significant implications for future treatments, especially for people with Down syndrome who are at high risk of Alzheimer’s. Early research in mice suggests that iron-chelating treatments may reduce indicators of Alzheimer’s pathology. Medications that remove iron from the brain or help strengthen antioxidant systems might offer new hope.

The study was supported by various organizations, including the National Institute on Aging and Cure Alzheimer’s Fund. These findings highlight the importance of understanding the biology of Down syndrome for Alzheimer’s research and could lead to new therapeutic approaches for this vulnerable population.

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