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Category: neuroscience – Page 15

A team of researchers at UCL and UCLH have identified the key brain regions that are essential for logical thinking and problem solving.

The findings, published in Brain, help to increase our understanding of how the human brain supports our ability to comprehend, draw conclusions, and deal with new and novel problems—otherwise known as reasoning skills.

To determine which are necessary for a certain ability, researchers study patients with brain lesions (an area of damage in the brain) caused by stroke or . This approach, known as “lesion-deficit mapping,” is the most powerful method for localizing function in the human brain.

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We’re closer than ever to being able to upload our minds and become “digitally immortal.” But should we?

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What if our minds could live after our bodies have died? What if mortality became obsolete? Steven Kotler, award-winning journalist and executive director of the Flow Research Collective, has studied these seemingly sci-fi ideas, and it turns out that they’re not so fictional, after all. In fact, mind-uploading technology is expected to be available as early as 2045.

“Digital immortality” would have its upsides; we could preserve the minds of modern geniuses and have their guidance through future conflicts. Or, alternatively, things could get dark, as we have never before interfered with such complex evolutionary processes. Kotler explains that the ability to store human personalities and consciousness on computers poses profound ethical and societal questions.

By developing and using this mind-uploading technology, we are simultaneously redefining what it means to be a human being, pushing the boundary between life, death, and whatever is in between. It seems, whether we’re ready or not, that it is going to happen soon.

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🧠💥 Quantum Particle Zeta‑9 Just Broke the Human Thought Barrier.
A newly discovered particle is doing something no subatomic entity should be capable of — reacting to human thought before it happens. Welcome to the edge of physics, where consciousness and quantum mechanics collide.

In this video, we unpack the stunning results from recent Fermilab experiments involving Zeta‑9, a particle that appears to anticipate human intention. Is it just quantum weirdness—or evidence that the human mind is more than biology?

You’ll discover:

What Zeta‑9 is and how it was discovered.

Why its behavior defies causality and classical physics.

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Driven by genetic and environmental factors, aging is a physiological process responsible for age-related degenerative changes in the body, cognitive decline, and impaired overall wellbeing. Notably, premature aging as well as the emergence of progeroid syndromes have posed concerns regarding chronic health conditions and comorbidities in the aging population. Accelerated telomere attrition is also implicated in metabolic dysfunction and the development of metabolic disorders. Impaired metabolic homeostasis arises secondary to age-related increases in the synthesis of free radicals, decreased oxidative capacity, impaired antioxidant defense, and disrupted energy metabolism. In particular, several cellular and molecular mechanisms of aging have been identified to decipher the influence of premature aging on metabolic diseases. These include defective DNA repair, telomere attrition, epigenetic alterations, and dysregulation of nutrient-sensing pathways. The role of telomere attrition premature aging in the pathogenesis of metabolic diseases has been largely attributed to pro-inflammatory states that promote telomere shortening, genetic mutations in the telomerase reverse transcriptase, epigenetic alteration, oxidative stress, and mitochondrial dysfunctions. Nonetheless, the therapeutic interventions focus on restoring the length of telomeres and may include treatment approaches to restore telomerase enzyme activity, promote alternative lengthening of telomeres, counter oxidative stress, and decrease the concentration of pro-inflammatory cytokines. Given the significance and robust potential of delaying telomere attrition in age-related metabolic diseases, this review aimed to explore the molecular and cellular mechanisms of aging underlying premature telomere attrition and metabolic diseases, assimilating evidence from both human and animal studies.

Aging is defined as a physiological phenomenon driven by genetic and biological processes, which are related to the lifespan of an individual and are associated with all age-related pathologies (Li et al., 2021). The aging process increases the susceptibility of individuals to factors leading to death as they grow older. Aging is a complex multifactorial phenomenon that involves the simultaneous interaction between various factors at different levels of functional organization. The role of genetic and environmental factors is represented by the heterogenous aging phenotype across different individuals, hence, these factors influence the lifespan of an individual via the process of aging (Jayanthi et al., 2010). With the deterioration of physiological functions critical to the survival and fertility of humans, the process of aging is known to relate to the notion of natural selection (Gilbert, 2000).

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Chronic pain—or pain that lasts at least three months—is closely intertwined with depression. Individuals living with pain’s persistent symptoms may be up to four times more likely to experience depression, research shows.

Almost 30% of people worldwide suffer from a chronic pain condition such as and migraines, and one in three of these patients also report co-existing pain conditions.

Now, a new study published in Science Advances shows that a person’s risk of depression increases alongside the number of places in the body in which they experience pain. Furthermore, inflammatory markers such as C-reactive protein (a protein produced by the liver in response to inflammation) help explain the association between pain and depression.

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A research team at the Institute for Basic Science (IBS) has identified a previously unknown enzyme, SIRT2, that plays a key role in memory loss associated with Alzheimer’s disease (AD). The study, led by Director C Justin LEE, of the IBS Center for Cognition and Sociality, provides critical insights into how astrocytes contribute to cognitive decline by producing excessive amounts of the inhibitory neurotransmitter GABA.

Astrocytes, once thought to only support neurons, are now known to actively influence brain function. In Alzheimer’s disease, astrocytes become reactive, meaning they change their behavior in response to the presence of amyloid-beta (Aβ) plaques, a hallmark of the disease. While astrocytes attempt to clear these plaques, this process triggers a harmful chain reaction. First, they uptake them via autophagy (Kim and Chun, 2024) and degrade them by the urea cycle (Ju et al, 2022), as discovered in previous research. However, this breakdown results in the overproduction of GABA, which dampens brain activity and leads to memory impairment. Additionally, this pathway generates hydrogen peroxide (H2O2), a toxic byproduct that causes further neuronal death and neurodegeneration.

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Immune molecules called cytokines play important roles in the body’s defense against infection, helping to control inflammation and coordinating the responses of other immune cells. A growing body of evidence suggests that some of these molecules also influence the brain, leading to behavioral changes during illness.

Two new studies from MIT and Harvard Medical School, focusing on a cytokine called IL-17, now add to that evidence. The researchers found that IL-17 acts on two distinct brain regions—the amygdala and the somatosensory cortex—to exert two divergent effects. In the amygdala, IL-17 can elicit feelings of anxiety, while in the cortex it promotes sociable behavior.

These findings suggest that the immune and nervous systems are tightly interconnected, says Gloria Choi, an associate professor of brain and cognitive sciences, a member of MIT’s Picower Institute for Learning and Memory, and one of the senior authors of the studies.

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For many years, some parents have noticed that their autistic children’s behavioral symptoms diminished when they had a fever. This phenomenon has been documented in at least two large-scale studies over the past 15 years, but it was unclear why fever would have such an effect.

A new study from MIT and Harvard Medical School sheds light on the cellular mechanisms that may underlie this phenomenon. In a study of , the researchers found that in some cases of infection, an immune molecule called IL-17a is released and suppresses a small region of the brain’s cortex that has previously been linked to social behavioral deficits in mice.

“People have seen this phenomenon before [in people with autism], but it’s the kind of story that is hard to believe, which I think stems from the fact that we did not know the mechanism,” says Gloria Choi, the Samuel A. Goldblith Career Development Assistant Professor of Applied Biology and an assistant professor of brain and cognitive sciences at MIT. “Now the field, including my lab, is trying hard to show how this works, all the way from the and molecules to receptors in the brain, and how those interactions lead to behavioral changes.”

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