The Food and Drug Administration’s approval in 2023 of lecanemab—a novel Alzheimer’s therapy shown in clinical trials to modestly slow disease progression—was met with enthusiasm by many in the field as it represented the first medication of its kind able to influence the disease. But side effects—brain swelling and bleeding—emerged during clinical trials that have left some patients and physicians hesitant about the treatment.

Medications can have somewhat different effects once they are released into the real world with broader demographics. Researchers at Washington University School of Medicine in St. Louis set out to study the adverse events associated with lecanemab treatment in their clinic patients and found that significant adverse events were rare and manageable.

Consistent with the results from carefully controlled clinical trials, researchers found that only 1% of patients experienced severe side effects that required hospitalization.

Researchers in Australia have found evidence that bacteria that live in the nose can make their way into the brain through nasal cavity nerves, setting off a series of events that could lead to Alzheimer’s disease. The work adds to the growing body of evidence that Alzheimer’s may be initially triggered through viral or bacterial infections.

Chlamydia pneumoniae is a common bacterium that, as its name suggests, is a major cause of pneumonia, as well as a range of other respiratory diseases. But worryingly, it’s also been detected in the brain on occasion, indicating it could cause more insidious issues.

For the new study, researchers at Griffith University and the Queensland University of Technology set out to investigate how C. pneumoniae might get into the brain, and whether it could cause damage once there. The team already had an inkling about how this nose-dwelling bug might make the trek.

Researchers found the PHGDH gene directly causes Alzheimer’s and discovered a drug-like molecule, NCT-503, that may help treat the disease early by targeting the gene’s hidden function. A recent study has revealed that a gene previously identified as a biomarker for Alzheimer’s disease is not jus

“I think, therefore I am,” René Descartes, the 17th-century French philosopher and mathematician, famously wrote in 1637. His idea was straightforward: even if your senses, the world, or your body deceives you, the very act of thinking proves you exist because there’s a thinker doing the thinking. Cogito, ergo sum, as the phrase goes in Latin, cemented the way the Western world would continue to define the self for the next 400 years—as a thinking mind, first and foremost.

But a growing body of neuroscience studies suggest the father of modern thought got it backward: the true foundation of consciousness isn’t thought, some scientists say—it’s feeling. A massive international study published in Nature late last month is further driving the theory forward. That means “I feel, therefore I am” may be the new maxim of consciousness. We are not thinking machines that feel; we are feeling bodies that think. And it’s more than a philosophical debate, too. Determining where consciousness resides could reshape life-or-death decisions and force society to rethink who, or what, truly counts as being self-aware.

The experiment used a rare “adversarial collaboration” model, bringing together scientists with opposing views to test two major theories of consciousness: integrated information theory (IIT) and global neuronal workspace theory (GNWT). Put simply, IIT says consciousness arises when information in the brain is deeply connected, especially in the back of the brain. GNWT argues that consciousness arises when the front of the brain broadcasts important information across a wide network, like a brain-wide alert.