Scientists may have finally found how Alzheimer's kills brain cells

Scientists have identified evidence of a previously unknown process that may explain how brain cells die in Alzheimer's disease and frontotemporal dementia (FTD). The discovery, centered on a mechanism known as karyoptosis, could point researchers toward new ways to slow the progression of these devastating conditions.

Many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and FTD, are marked by the buildup of harmful proteins inside neurons. Over time, these nerve cells die, contributing to memory loss and other symptoms. Although scientists have long known about several forms of cell death, including apoptosis, those mechanisms have never fully explained the extensive neuron loss seen in these disorders.

Now, researchers from King's College London, working with the UK Dementia Research Institute and supported in part by Alzheimer's Research UK, have identified karyoptosis as a potential missing link connecting toxic protein accumulation to the death of brain cells.

Karyoptosis refers to a series of chemical reactions set in motion when toxic proteins accumulate inside a cell. As the process unfolds, the cell's nucleus, which contains its genetic material, gradually shrivels before ultimately breaking apart.

Evidence Found in Alzheimer's and FTD Brains

The findings, published in Nature Communications, are based on an analysis of 3,000 brain cells collected from 28 people with either FTD or end stage Alzheimer's disease. Using computational algorithms, the researchers identified different forms of cell death occurring within the tissue.

They found signs of karyoptosis in 35 percent of cells from the frontal cortex of people with Alzheimer's disease, compared with just 15 percent of cells from healthy older adults.

"This study is the culmination of a 10-year journey at King's, from when we first identified karyoptosis in a relatively rare disease to discovering that it is a common feature of dementias which affect millions of people."

A Possible New Target for Dementia Treatments

The researchers also uncovered a key molecular pathway that appears to control karyoptosis. They found that forcing proteins inside neurons to clump together, a hallmark of many neurodegenerative diseases, can trigger this destructive process.

According to the study, the buildup of toxic proteins destabilizes the outer membrane of the nucleus, causing it to shrink and eventually disintegrate.

The team then investigated proteins known as kinases, which act as molecular switches in this pathway. In laboratory experiments using rat neurons, blocking these switches reduced markers associated with karyoptosis. In particular, the interaction between the kinase p38 MAP kinase and the protein LaminB1 emerged as a promising target for slowing or preventing the breakdown of the nucleus.

The researchers believe this pathway could eventually lead to therapies that reduce brain cell loss in dementia. Their next goal is to develop ways to selectively target the interaction between p38 MAP kinase and LaminB1 in humans.

"By specifically targeting the interaction between p38 MAP kinase and LaminB1 we may slow down the process of cell death, buying time for more pinpointed therapies against specific neurodegenerative diseases," said Dr. Manolis Fanto, Reader in Functional Genomics, Institute of Psychiatry, Psychology and Neuroscience, King's College London.

Building a Road Map for Future Therapies

"The death and loss of cells in the brain drives many symptoms experienced by people living with dementia. Our study uncovers a new series of chemical events which can coordinate cell death in brain cells. We have started to lay out the road map of how karyoptosis works, and I'm excited to see future breakthroughs this may drive in the dementia research community and beyond," said Dr. Rebecca Casterton, Senior Researcher at the UK Dementia Research Institute at King's and first author on the paper.

"For decades, we've known that toxic proteins build up in Alzheimer's disease and frontotemporal dementia, but exactly how they lead to the loss of brain cells has remained unclear.

"The identification of karyoptosis is a crucial step towards finding targets for treatments that could stop or slow cell loss. It could help widen the window for therapies that tackle the underlying causes of disease, bringing us closer to a cure for dementia. This is why Alzheimer's Research UK funds and supports research," said Dr. Sara Rodrigues, Senior Research Manager at Alzheimer's Research UK.

The study, "Karyoptosis mediates cell death and neurodegeneration upon proteotoxic stress," was published in Nature Communications.

The research was primarily funded by Alzheimer's Research UK and the Biotechnology and Biological Sciences Research Council International Partnership. Additional support came from a studentship provided by the UK Medical Research Council and the UK Dementia Research Institute.

Journal Reference:

1. Rebecca Casterton, Aitana Martinez-Cotrina, Jodi Barnard, Eleanor Wycherley, Yanling Hu, Rhys Anderson, Sebastien Janel, Jiin Byun, Olivia Houghton, Daniel A. Solomon, Juan Alcalde, Frank Lafont, Marc-David Ruepp, Frank Hirth, Bart Tummers, Yong-Yeon Cho, Gian De Nicola, Sarah Mizielinska, Manolis Fanto. Karyoptosis mediates cell death and neurodegeneration upon proteotoxic stress. Nature Communications, 2026; 17 (1) DOI: 10.1038/s41467-026-73802-w

Courtesy:

King's College London. "Scientists may have finally found how Alzheimer's kills brain cells." ScienceDaily. ScienceDaily, 5 July 2026. <www.sciencedaily.com/releases/2026/06/260626124701.htm>.

 

 

Streetlights are trapping thousands of pill bugs in giant “death spirals”

 

Researchers have uncovered a surprising side effect of artificial lighting: ordinary streetlights can lure thousands of tiny land dwelling isopods into giant synchronized "death spirals." The newly documented behavior, observed in Israel, is the first of its kind and suggests that human made lighting can dramatically disrupt the instincts of small ground dwelling animals.

The study was led by PhD student Idan Sheizaf under the supervision of Prof. Ariel Chipman at The Hebrew University of Jerusalem. Published in Ecology and Evolution, the research describes how land dwelling isopods, relatives of crabs and shrimp that are better known as woodlice or pill bugs, abandon their normally solitary habits to join enormous circular formations containing more than 5,000 individuals.

A surprising discovery in northern Israel

The unusual behavior first came to light after amateur naturalist Eviatar Itzkovich noticed huge swirling groups of isopods during summer nights in the Golan Heights.

The researchers focused on the species Armadillo sordidus, a little studied isopod that typically spends its time hidden beneath rocks and damp leaf litter, where moisture helps prevent it from drying out.

Although woodlice commonly cluster together to conserve moisture, scientists had never documented coordinated movement on this scale. Before this work, very little was known about A. sordidus. The study also expanded the species' known range. Previously, it had only been recorded in southern Syria and the Golan Heights. Researchers have now documented it in the Jezreel Valley for the first time.

Experiments reveal the role of artificial light

To determine what was causing the strange circular marches, the team tested several possible explanations, including magnetic fields and different types of lighting.

Strong magnets placed near the moving isopods had no effect, even though the Golan Heights is known for unusual magnetic properties. The animals continued circling uninterrupted.

Ultraviolet flashlights attracted only a small number of isopods and never triggered the swirling formations.

White light, however, consistently produced the dramatic behavior. When researchers positioned a white lamp so that its beam shone straight down, the isopods repeatedly gathered into large rotating circles.

The experiments showed that the shape of the illuminated area is what matters most. A vertical beam creates a circular boundary of light on the ground. Drawn toward that edge, the isopods begin walking along its perimeter. As more individuals join, the movement reaches a tipping point and develops into a large, self sustaining circular procession.

Reflecting on the findings, Idan Sheizaf said: "While collective movement is common in the animal kingdom, seeing it in this form in isopods was entirely unexpected. It appears that the geometry of our modern world -- specifically the circular pools of light created by streetlights, is interacting with the natural instincts of these creatures to create a mesmerizing, yet potentially harmful, emergent phenomenon."

Why the "death spirals" may be dangerous

Although the swirling formations are visually striking, researchers believe they represent an unintended trap created by artificial light at night (ALAN), not a natural social behavior.

Most of the participants were female, and many were carrying eggs, making it unlikely that the gatherings were related to mating. Instead, the evidence suggests that artificial lighting is disrupting the animals' normal instincts.

The consequences could be severe. During one observation, a centipede preyed on the distracted isopods while they remained caught in the swirling formation. By pulling these animals out of their sheltered habitats and keeping them moving in circles, streetlights may leave them vulnerable to predators while also wasting energy needed for survival.

The findings highlight how even a simple change to the environment, such as installing a streetlight, can reshape ancient behaviors in small animals that often go unnoticed.

Journal Reference:

1. Idan Sheizaf, Eviatar Itzkovich, Ariel D. Chipman. A Novel Light‐Induced Collective Circular Movement in Armadillo sordidus Isopods. Ecology and Evolution, 2026; 16 (4) DOI: 10.1002/ece3.73487

Courtesy:

 The Hebrew University of Jerusalem. "Streetlights are trapping thousands of pill bugs in giant “death spirals”." ScienceDaily. ScienceDaily, 6 July 2026. <www.sciencedaily.com/releases/2026/06/260626125707.htm>.