Scientists used diverse genomes to complete a fuller human DNA map. This unlocks hidden risks and improves diagnoses.
The Argentine microbiologist Federico Rey and Indian pathologist Vaibhav Vemuganti applaud the “exciting opportunities” that the new study opens for the prevention and treatment of cardiovascular disease. In a commentary also published Wednesday in Nature, the two experts emphasize that exposure to imidazole propionate worsens plaque formation in the arteries of mice. “This effect occurs independently of changes in cholesterol levels, a surprising result given the central role of cholesterol in the development of atherosclerosis,” note the two specialists, from the University of Wisconsin-Madison. “This discovery offers an interesting clue about a possible new factor involved in the origin of atherosclerosis. This is very relevant because, although lowering cholesterol — through drugs called statins, for example — can effectively reduce the risk of cardiovascular disease, a considerable proportion of people still experience adverse cardiovascular events, such as myocardial infarctions or strokes,” they warn. The CNIC itself said in a statement that the new study “could revolutionize” the diagnosis and treatment of atherosclerosis.
Sancho stresses that the work has been made possible thanks to the collaboration of thousands of volunteer employees of Banco Santander in Madrid, but also thanks to grants of €1 million from the “la Caixa” Foundation, €150,000 from the European Research Council and €100,000 from the State Research Agency.
The discovery of the decisive effect of imidazole propionate on atherosclerosis takes place against a backdrop in which the scientific community is revealing the unknown role of intestinal microbes in some human diseases. The biotechnologist Cayetano Pleguezuelos and his colleagues at the Hubrecht Institute (The Netherlands) demonstrated in February 2020 that a strain of the bacterium Escherichia coli produces a toxic molecule, called colibactin, which damages the DNA of human cells and causes malignant tumors.
0,
In a study published last week in the journal L’Anthropologie, researchers re-analyzed fragments of Skhūl I, the name for remains belonging to a likely female child between the ages of 3 and 5. While the individual is currently recognized as an anatomically modern human, Homo sapiens, its classification remains contentious, given that it has some Neanderthal-like features. Now, the new study suggests the child might have been a hybrid—and potentially had one Homo sapiens parent and one Neanderthal parent.
To reach this conclusion, the team conducted CT scans of the child’s neurocranium—the part of the skull that protects the brain—and jaw. They compared the resulting 3D models to remains of other Homo sapiens and Neanderthal children. In short, they found the neurocranium to be more similar to that of a modern human, while the jaw was more akin to a Neanderthal’s.
“The combination of features seen in Skhūl I may suggest that the child is a hybrid,” the researchers write in the study. “In the Middle Pleistocene, the Levant was the crossroad of gene flows between Indigenous lineages and other taxa from Africa and Eurasia, which is likely the explanation for Skhūl I anthropological.”
Their results align with genetic evidence indicating that modern humans and Neanderthals didn’t just cross paths—they interbred for thousands of years. In fact, some research has suggested Homo sapiens drove Neanderthals to extinction not with violence, but by absorbing them into their population through interbreeding. Regardless of the reason for Neanderthals’ demise, many humans have Neanderthal DNA today.
nouvelle analyse du neurocr ne et de la mandibule de l’enfant Skhūl I : conclusions taxonomiques et implications culturelles.
Scientists at UCSF have uncovered how certain immune cells in the brain, called microglia, can effectively digest toxic amyloid beta plaques that cause Alzheimer’s. They identified a key receptor, ADGRG1, that enables this protective action. When microglia lack this receptor, plaque builds up quickly, causing memory loss and brain damage. But when the receptor is present, it seems to help keep Alzheimer's symptoms mild. Since ADGRG1 belongs to a drug-friendly family of receptors, this opens the door to future therapies that could enhance brain immunity and protect against Alzheimer’s in more people.