Lifeboat Foundation

Scientists in Denmark believe the psychedelic substance psilocybin might produce rapid and lasting antidepressant effects in part because it enhances neuroplasticity in the brain. Their new research, published in the International Journal of Molecular Sciences, has found evidence that psilocybin increases the number of neuronal connections in the prefrontal cortex and hippocampus of pig brains.

Psilocybin — the active component in so-called “magic” mushrooms — has been shown to have profound and long-lasting effects on personality and mood. But the mechanisms behind these effects remain unclear. Researchers at Copenhagen University were interested in whether changes in neuroplasticity in brain regions associated with emotional processing could help explain psilocybin’s antidepressant effects.

“Both post-mortem human brain and in vivo studies in depressed individuals have shown a loss of synapses through the down-regulation of synaptic proteins and genes,” the authors of the study wrote. “Hence, upregulation of presynaptic proteins and an increase in synaptic density may be associated with the potential antidepressive effects of psychedelics.”

A study of Japanese university students and recent graduates has revealed that writing on physical paper can lead to more brain activity when remembering the information an hour later. Researchers say that the complex, spatial and tactile information associated with writing by hand on physical paper is likely what leads to improved memory.

“Actually, paper is more advanced and useful compared to electronic documents because paper contains more one-of-a-kind information for stronger memory recall,” said Professor Kuniyoshi L. Sakai, a neuroscientist at the University of Tokyo and corresponding author of the research recently published in Frontiers in Behavioral Neuroscience. The research was completed with collaborators from the NTT Data Institute of Management Consulting.

Typically, pyramidal cells and GABAergic interneurons in the brain are activated simultaneously. A team of neuroscientists at New York University, however, recently identified a unique class of neurons that do not fire at the same time as all principal neurons, cells and interneurons. Interestingly, the team found that these specific neurons are most active during the DOWN state of non-REM (NREM) sleep, when all other neuron types are silent.

“As is often the case in science, our discovery was a true serendipity,” György Buzsáki, one of the researchers who carried out the study, told MedicalXpress. “By collecting sleep recordings in deep layers of the cortex, we observed that spikes of some rare neurons occasionally occurred during the so-called ‘DOWN state’ epochs of sleep. No neuron was supposed to do such thing, as DOWN state is known (and identified by) by its complete neuronal silence (lack of spikes).”

The neocortex, a set of layers in a region of the brain called cerebral cortex, is rebooted thousands of times every night from the transient (50−300 ms long) DOWN state. In their study, Buzsáki and his colleagues identified a class of neurons that appear to be most active when all other neurons (i.e., excitatory pyramidal and inhibitory neurons) are silent, in the DOWN state, during NREM stages of sleep. In their follow up experiments, they showed that these neurons are neuroglia-form cells found in the deeper layers of the neocortex, which specifically express genes known as ID2 and Nkx2.1.

Summary: Study sheds light on what causes normal proteins to convert to a diseased form associated with CJD and Kuru.

Source: Imperial College London.

For the first time, researchers have pinpointed what causes normal proteins to convert to a diseased form, causing conditions like CJD and Kuru.

In this episode of Lifespan News:

Binary Clock Predicts Biological Age Longevity company funding roundup Lifespan.io just turned 7 CAR T-cell therapy generates lasting remissions in patients with multiple myeloma CBD Reduces Plaque and Improves Cognition in Model of Familial Alzheimer’s.

Summary: When the ventral tegmental area was stimulated, monkeys were better able to identify details associated with subconscious visual stimuli they were exposed to.

Source: KU Leuven.

Researchers uncovered for the first time what happens in animals’ brains when they learn from subconscious, visual stimuli. In time, this knowledge can lead to new treatments for a number of conditions.

The debate holds a special interest for neuroscientists; since computer programming has only been around for a few decades, the brain has not evolved any special region to handle it. It must be repurposing a region of the brain normally used for something else.

So late last year, neuroscientists in MIT tried to see what parts of the brain people use when dealing with computer programming. “The ability to interpret computer code is a remarkable cognitive skill that bears parallels to diverse cognitive domains, including general executive functions, math, logic, and language,” they wrote.

Since coding can be learned as an adult, they figured it must rely on some pre-existing cognitive system in our brains. Two brain systems seemed like likely candidates: either the brain’s language system, or the system that tackles complex cognitive tasks such as solving math problems or a crossword. The latter is known as the “multiple demand network.”

With powerful engines, near-photorealistic graphics, and the ability to build incredible, immersive worlds, it’s hard to imagine what the next big technological advance in gaming might be.

Based on a recent tweet by Neuralink co-founder and President Max Hodak, the word might not even apply. In it, he hinted — vaguely, to be fair — that whatever forms of entertainment get programmed into neural implants and brain-computer interfaces will represent a paradigm shift that moves beyond the current terminology.

“We’re gonna need a better term than ‘video game’ once we start programming for more of the sensorium,” Hodak tweeted.

While topline results from TRAILBLAZER-ALZ showed a 32% slowing of cognitive decline with the anti-amyloid drug donanemab, highly anticipated phase 2 findings provide a more detailed analysis.