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Scientists have recorded the first-ever brain scan of a dying human.

A man suddenly died during a routine brain scan, revealing intriguing insights into what happens in our final moments.

An 87-year-old man undergoing a routine EEG for epilepsy suffered a fatal heart attack. Researchers found that in the 30 seconds before and after his heart stopped, his brain waves resembled those seen during dreaming, memory recall, and meditation.

This suggests that the commonly reported phenomenon of “life flashing before your eyes” may have a neurological basis. However, since this is a single case study, more research is needed to confirm how common this experience may be.

The findings, published by Dr. Ajmal Zemmar and his team, showed a surge in gamma waves — high-frequency neural oscillations linked to memory and consciousness — just before and after death.

These waves are typically observed when people recall memories, adding weight to the idea that the brain may replay key life events in its final moments. While this discovery cannot fully explain the mysteries of death, it offers a fascinating glimpse into the brain’s last activity and opens the door for further research on human consciousness at the end of life.


This innovation, called ALA-CART, helps the immune system better recognize and destroy resistant cancers. The new design not only improves treatment success but also promises fewer side effects.

A Powerful Upgrade to CAR-T Therapy

Researchers at the University of Colorado Anschutz Medical Campus have developed an enhanced version of CAR-T cell therapy designed to improve effectiveness and longevity, particularly against cancer cells that were previously difficult to detect and eliminate.

Sunburns and aging skin are obvious effects of exposure to harmful UV rays, tobacco smoke and other carcinogens. But the effects aren’t just skin deep. Inside the body, DNA is literally being torn apart.

Understanding how the body heals and protects itself from DNA damage is vital for treating genetic disorders and life-threatening diseases such as cancer. But despite numerous studies and medical advances, much about the molecular mechanisms of DNA repair remains a mystery.

For the past several years, researchers at Georgia State University have tapped into the Summit supercomputer at the Department of Energy’s Oak Ridge National Laboratory to study an elaborate molecular pathway called (NER). NER relies on an array of highly dynamic protein complexes to cut out (excise) damaged DNA with surgical precision.

Can Tesla REALLY Build Millions of Optimus Bots? ## Tesla is poised to revolutionize robotics and sustainable energy by leveraging its innovative manufacturing capabilities and vertical integration to produce millions of Optimus bots efficiently and cost-effectively ## Questions to inspire discussion ## Manufacturing and Production.

S low model count strategy benefit their production? A: Tesla s speed of innovation and ability to build millions of robots quickly gives them a key advantage in mass producing and scaling manufacturing for humanoid robots like Optimus. + s factory design strategies support rapid production scaling? A: Tesla## Cost and Efficiency.

S vertical integration impact their cost structure? A: Tesla s AI brain in-house, Tesla can avoid paying high margins to external suppliers like Nvidia for the training portion of the brain. +## Technology and Innovation.

S experience in other industries benefit Optimus development? A: Tesla s own supercomputer, Cortex, and AI training cluster are crucial for developing and training the Optimus bot## Quality and Reliability.

S manufacturing experience contribute to Optimus quality? A: Tesla## Market Strategy.

S focus on vehicle appeal relate to Optimus production? A: Tesla## Scaling and Demand.

For decades, scientists have focused on amyloid plaques—abnormal clumps of misfolded proteins that accumulate between neurons—as a therapeutic target for Alzheimer’s disease. But anti-amyloid therapies haven’t made strong headway in treating the devastating condition.

Now, researchers at Yale School of Medicine (YSM) are zeroing in on a byproduct of these plaques, called axonal spheroids, and exploring how to reverse their growth. They published their findings March 10 in Nature Aging.

Axonal spheroids are bubble-like structures on axons—the part of the neuron that sends messages through electrical impulses—that form due to swelling induced by amyloid plaques. Previous research at YSM has shown that as these spheroids grow, they block electricity conduction in the axons, which can hinder the ability to communicate with other neurons.

As Shakespeare put it, we all have our entrances and our exits on this grand stage we call life, and now researchers have identified the specific point in middle-age when our brain cells show the first signs of starting down a downward slope.

That age, based on brain scans and tests covering 19,300 individuals, is on average around 44 years. It’s here that degeneration starts to be noticeable, before hitting its most rapid rate at age 67. By the time we reach 90, the speed of brain aging levels off.

According to the team behind the new study, led by researchers from Stony Brook University in the US, the findings could be helpful in figuring out ways to promote better brain health during the later stages of life.

Dissecting the effects of hypothermic and hypometabolic states on aging processes, the authors show that activation of neurons in the preoptic area induces a torpor-like state in mice that slows epigenetic aging and improves healthspan. These pro-longevity effects are mediated by reduced Tb, reinforcing evidence that Tb is a key mediator of aging processes.

Regular use of math and reading skills could prevent cognitive decline with age, according to a new Science Advances study.


Cognitive skills of the population such as literacy and numeracy are important not only for individual incomes but also for the economic growth of nations (26). As a result, the aging of world populations presents an economic concern if the commonly assumed declines of these skills with age hold.

We use longitudinal variation in individual literacy and numeracy skills for a representative adult sample to create age-skill profiles that credibly separate age from cohort effects. The pure age component that we derive provides a different perspective on the impacts of aging populations. Overall, our results are not consistent with a view that a natural law dictates an inevitable decline in these skills with age. Potential cognitive declines only occur at later ages and are not inevitable with usage of skills.

This is consolation for countries with aging populations, but avoidance of skill losses is not automatic and appears related to stimulation from skill usage. These results thus suggest that age-skill relationships of adults deserve policy attention, consistent with concerns about the necessity of lifelong learning.