We tend to assume that emotionally charged words are more likely to grab our attention. An insult shouted across a crowded room or a disturbing phrase overheard on television can seem impossible to ignore. But a new study published in Psychological Science suggests the opposite may happen before words reach conscious awareness.
Researchers at the Hebrew University of Jerusalem found that when people were focused on a visual task, they were less likely to consciously notice negative spoken words than neutral ones. The findings offer new insight into how the brain determines which information enters conscious awareness and which remains outside it.
“This study is a nice example of how our conscious intuitions regarding what we notice are not always what our unconscious is doing,” said lead author Gal R. Chen, a doctoral candidate in psychology at the Hebrew University of Jerusalem.
Mutations in human LIS1 cause lissencephaly, a severe developmental brain malformation. Although most studies focus on development, LIS1 is also expressed in adult mouse tissues. We previously induced LIS1 knock-out (iKO) in adult mice using a Cre-Lox approach with an actin promoter driving CreERT2 expression. This proved to be rapidly lethal, with evidence pointing toward nervous system dysfunction. CreERT2 activity was observed in astrocytes, brainstem and spinal motor neurons, and axons and Schwann cells in the sciatic and phrenic nerves, suggesting dysfunctional cardiorespiratory and motor circuits. However, it is unclear how LIS1 knock-out in these different cell types contributes to the lethal phenotype.
One of the most detailed maps to date of meningioma—the most common brain tumor in adults—reveals how the tumor’s surrounding environment helps drive disease behavior and patient outcomes, according to new research from Mayo Clinic.
The study, published in Nature Genetics and conducted in collaboration with scientists at Princess Margaret Cancer Center in Toronto, combines several advanced laboratory techniques to examine tumors at an unprecedented level of detail, offering clues to why some meningiomas grow slowly while others recur or become more aggressive. The findings could lead to more precise ways to predict risk and guide treatment decisions.
Growing evidence suggests that traditional grading systems for meningioma do not fully capture the behavior of these complex tumors, prompting the development of molecular classification tools that more accurately predict which tumors are more likely to recur after surgery.
For many people who suffer from depression, the condition is not just about feeling down but also about a loss of motivation and difficulty finding pleasure in activities they used to enjoy. A new study conducted in Sweden shows that a medicine used to treat Parkinson’s disease can be used as an add-on therapy to alleviate these symptoms in some patients with treatment-resistant depression. The study has been published in Nature Medicine.
The researchers at Lund University and the psychiatric services in Region Skåne have identified the potential new therapy for the condition associated with depression that involves a reduced ability to feel joy, pleasure or motivation—known as anhedonia. Those affected may lose interest in things that they previously found meaningful or rewarding.
The study is an example of what is known as drug repurposing, whereby an already approved medicine is used to treat a different condition. In this study, the researchers investigated pramipexole, which has long been used to treat Parkinson’s disease, as an add-on therapy for depression with marked anhedonia.
A popular over-the-counter supplement taken for joint pain might increase people’s risk for Alzheimer’s disease, a new study says.
Glucosamine use is associated with a 25% higher odds that a person will progress from mild cognitive impairment to dementia and Alzheimer’s disease, researchers report in the journal Nature Metabolism.
“While it’s an association and not proof of causality, it does raise an important clinical question that now deserves much more attention,” researcher Matt Gentry said in a news release. He’s chair of biochemistry and molecular biology at the University of Florida.
Though protein clumps associated with Alzheimer’s and Parkinson’s were discovered more than a century ago, researchers remain largely unable to prevent them from forming or eliminate them from the brain. And though a variety of therapies have taken aim at tau tangles, beta-amyloid plaques and Lewy bodies, among other notorious aggregates, none have been very effective at stopping disease progression.
Rockefeller’s Hermann Steller and his team in the Strang Laboratory of Apoptosis and Cancer Biology have long been focused on understanding how the cell’s protein-degrading machines, called proteasomes, are regulated. His lab discovered that a transporter protein termed PI31 shuttles proteasomes over long distances from the nerve cell body to synapses. When this system fails, synapses become depleted of degradative capacity, and proteins that should have been eliminated accumulate. As a result, synaptic communication breaks down, protein clumps form and neuronal health deteriorates.
Now a new study in Nature Communications, led by researchers from University College London and contributed to by Steller’s lab, has identified mutations in PSMF1, the gene that produces PI31, that cause the protein to malfunction. Moreover, the scientists demonstrated that these mutations cause a spectrum of severe, very early-onset neurological disorders.
People with Alzheimer’s disease who took the common supplement glucosamine were 25% more likely to die within five years than those who didn’t.
That’s the key finding of a new study that my colleagues and I published in the journal Nature Metabolism.
Glucosamine is a sugar molecule that’s sold over the counter as a remedy for joint pain and arthritis. More than 40 million Americans take it each year.