Toggle light / dark theme

More than 25 years ago, biologists in Arkansas began to report dozens of bald eagles paralyzed, convulsing, or dead. Their brains were pocked with lesions never seen before in eagles. The disease was soon found in other birds across the southeastern United States. Eventually, researchers linked the deaths to a new species of cyanobacteria growing on an invasive aquatic weed that is spreading across the country. The problem persists, with the disease detected regularly in a few birds, yet the culprit’s chemical weapon has remained unknown.

Today in Science, a team identifies a novel neurotoxin produced by the cyanobacteria and shows that it harms not just birds, but fish and invertebrates, too. “This research is a very, very impressive piece of scientific detective work,” says microbiologist Susanna Wood of the Cawthron Institute. An unusual feature of the toxic molecule is the presence of bromine, which is scarce in lakes and rarely found in cyanobacteria. One possible explanation: the cyanobacteria produce the toxin from a bromide-containing herbicide that lake managers use to control the weed.

The discovery highlights the threat of toxic cyanobacteria that grow in sediment and on plants, Wood says, where routine water quality monitoring might miss them. The finding also equips researchers to survey lakes, wildlife, and other cyanobacteria for the new toxin. “It will be very useful,” says Judy Westrick, a chemist who studies cyanobacterial toxins at Wayne State University and was not involved in the new research. “I started jumping because I got so excited.”

Summary: People with cerebral small vessel damage who also had a leaky blood-brain barrier had more tissue damage after two years than those whose blood-brain barrier was intact.

Source: AAN

As people age, changes in the tiniest blood vessels in the brain, a condition called cerebral small vessel disease, can lead to thinking and memory problems and stroke. These changes can also affect the blood-brain barrier, a layer of cells that protect the brain from toxins circulating in the blood.

Using an ordinary light microscope, MIT engineers have devised a technique for imaging biological samples with accuracy at the scale of 10 nanometers — which should enable them to image viruses and potentially even single biomolecules, the researchers say.

The new technique builds on expansion microscopy, an approach that involves embedding biological samples in a hydrogel and then expanding them before imaging them with a microscope. For the latest version of the technique, the researchers developed a new type of hydrogel that maintains a more uniform configuration, allowing for greater accuracy in imaging tiny structures.

This degree of accuracy could open the door to studying the basic molecular interactions that make life possible, says Edward Boyden, the Y. Eva Tan Professor in Neurotechnology, a professor of biological engineering and brain and cognitive sciences at MIT, and a member of MIT’s McGovern Institute for Brain Research and Koch Institute for Integrative Cancer Research.

Summary: Mimicking a muscular stress system can provide neuroprotection against aging in both the brain and retina. The signal helps prevent the buildup of misfolded protein aggregates.

Source: St. Jude Children’s Research Hospital.

How do different parts of the body communicate? Scientists at St. Jude are studying how signals sent from skeletal muscle affect the brain.

Stanford University neurobiologist Sergiu Pașca has been making brain organoids for about 10 years, and his team has learned that some of these tissue blobs can thrive in a dish for years. In the new study, they teamed up with neurogeneticist Daniel Geschwind and colleagues at the University of California, Los Angeles (UCLA), to analyze how the blobs changed over their life spans…

…They noticed that when an organoid reached 250 to 300 days old—roughly 9 months—its gene expression shifted to more closely resemble that of cells from human brains soon after birth. The cells’ patterns of methylation—chemical tags that can affix to DNA and influence gene activity—also corresponded to increasingly mature human brain cells as the organoids aged, the team reports today in Nature Neuroscience.


Organoids develop genetic signatures of postnatal brains, possibly broadening their use as disease models.

Sleep deprivation causes an inflammatory response that results in negative health outcomes.


Summary: Study sheds light on DNA methylation related to sleep deprivation in those with shift-work disorder.

Source: University of Helsinki

Long-term sleep deprivation is detrimental to health, increasing the risk of psychiatric and somatic disorders, such as depression and cardiovascular diseases. And yet, little is known about the molecular biological mechanisms set in motion by sleep deprivation which underlie related adverse health effects.

In a recently published study, the University of Helsinki, the Finnish Institute for Health and Welfare, the Finnish Institute of Occupational Health and the Finnair airline investigated dynamic changes to DNA methylation in shift workers. DNA methylation denotes epigenetic regulation that modifies gene function and regulates gene activity without changing the sequence of bases in the DNA.

In autism, male-female imbalance is especially pronounced. Boys are as much as four times more likely to have some form of autism and are also more likely to have severe symptoms.


HAMILTON, ON, March 3, 2021 — Evolutionary forces drive a glaring gender imbalance in the occurrence of many health conditions, including autism, a team of genetics researchers has concluded.

The human genome has evolved to favour the inheritance of very different characteristics in males and females, which in turn makes men more vulnerable to a host of physical and mental health conditions, say the researchers responsible for a new paper published in the Journal of Molecular Evolution.

Their analysis shows that while there are certain conditions that occur only in women (cervical cancer and ovarian cancer, for example), or much more frequently in women (such as multiple sclerosis), men are more prone to medical conditions overall and, as a result, on average die sooner than women.

Stress may improve intelligence. That does not mean you should desire problems.


Summary: People who experience fewer stressors in daily life report better emotional stability, moods, and overall health. However, those who are less stressed score lower on cognitive tests than those who experience daily stressors. Those who are stress-free are also less likely to give emotional support or experience positive things happening throughout the day.

Source: Penn State

Stress is a universal human experience that almost everyone deals with from time to time. But a new study found that not only do some people report feeling no stress at all, but that there may be downsides to not experiencing stress.

The researchers found that people who reported experiencing no stressors were more likely to experience better daily well-being and fewer chronic health conditions. However, they were also more likely to have lower cognitive function, as well.

Studies on postmortem tissue may need to adjust for postmortem cell activity.


In the hours after we die, certain cells in the human brain are still active. Some cells even increase their activity and grow to gargantuan proportions, according to new research from the University of Illinois Chicago.

In a newly published study in the journal Scientific Reports, the UIC researchers analyzed gene expression in fresh brain tissue — which was collected during routine brain surgery — at multiple times after removal to simulate the post-mortem interval and death. They found that gene expression in some cells actually increased after death.

These ‘zombie genes’ — those that increased expression after the post-mortem interval — were specific to one type of cell: inflammatory cells called glial cells. The researchers observed that glial cells grow and sprout long arm-like appendages for many hours after death.

Furthermore, it implies that defects in the repair process, not the DNA damage itself, can potentially lead to developmental or neurodegenerative diseases.


Researchers at the National Institutes of Health (NIH) have discovered specific regions within the DNA of neurons that accumulate a certain type of damage (called single-strand breaks or SSBs). This accumulation of SSBs appears to be unique to neurons, and it challenges what is generally understood about the cause of DNA damage and its potential implications in neurodegenerative diseases.

Because neurons require considerable amounts of oxygen to function properly, they are exposed to high levels of free radicals—toxic compounds that can damage DNA within cells. Normally, this damage occurs randomly. However, in this study, damage within neurons was often found within specific regions of DNA called “enhancers” that control the activity of nearby genes.

Fully mature cells like neurons do not need all of their genes to be active at any one time. One way that cells can control gene activity involves the presence or absence of a chemical tag called a methyl group on a specific building block of DNA. Closer inspection of the neurons revealed that a significant number of SSBs occurred when methyl groups were removed, which typically makes that gene available to be activated.