Future “you” could be quietly shaping your reality.
Category: neuroscience
Explore consciousness theories and implications
It is because the phantom primal eye is centrally evoked by the cellular as generic APS identically with all the contents of special sense information that Leibniz’s “like can only interact with like” condition is satisfied by the non-physical primal eye “monad”—as opposed to Descartes’s cellular pineal gland.
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The circuit that lets your brain think and see
Nuttida Rungratsameetaweemana is challenging a story neuroscience has told for decades. According to the conventional account, our eyes collect raw information and relay it through a series of nerves and waystations that lead deep into the brain, eventually reaching the cortex. There, the thinking begins as information is processed and put to use for higher tasks such as reasoning, judgment and decision-making.
Her group’s work is complicating that account. Last year, the team published fMRI scans showing unexpected levels of activity in the earliest visual areas of the cortex, the regions that first receive visual signals. Rather than passively relaying what the eyes take in, those early areas seemed to process the same information differently depending on what the research participant was doing. When asked to sort shapes by one set of rules, a participant’s early visual system behaved one way. When asked to apply a different set of rules to the same shape, it behaved differently.
In a new paper published today in PLOS Biology, Rungratsameetaweemana and her team at Columbia Engineering show how the brain might pull this off. They built a simple neural network that follows many of the rules that govern real brains. Like the brain, their model contained one class of neurons that drive other neurons to fire and another class that suppress firing.
Cognitive flexibility problems may arise months before memory impairment in Alzheimer’s
When most people think about Alzheimer’s disease, memory loss is usually the first thing that comes to mind. Forgetting a loved one’s name, missing appointments or repeatedly misplacing everyday items are often considered early warning signs. But what if the disease begins affecting the brain long before memory problems become noticeable? New research from scientists at Texas A&M Health suggests that another change in brain function may appear even earlier: difficulty adapting when circumstances change.
In a recent study published in Nature Communications, researchers found that animal models with Alzheimer’s-related brain changes developed problems with cognitive flexibility months before they showed signs of memory impairment. Cognitive flexibility refers to the brain’s ability to adjust behavior, learn new rules and adapt when situations change.
“We found that this function was impaired before we could detect deficits in spatial memory,” said neuroscientist Jun Wang, Ph.D., professor in the Texas A&M University Naresh K. Vashisht College of Medicine at Texas A&M Health.
Fear-learning circuit shows how stress disrupts brain’s ability to suppress trauma
Fear is often thought of as a negative emotion but is actually a natural protective response to perceived threats or danger. It helps us survive. When we experience a situation that causes fear, it becomes stored in our brain as a fear memory. These fear memories prevent us from touching a hot stove after being burned or from stepping onto a busy street.
What about fear memories that take over? Post-traumatic stress disorder, or PTSD, is caused by severe acute or chronic stress that disrupts the learning process designed to suppress fear memories. These memories then begin to negatively affect a person’s quality of life.
Typically, our fear memories can be suppressed through extinction learning. The original memory or fear isn’t forgotten, but a new memory is formed and suppresses the original fear memory. However, extinction learning can become tricky in situations that involve traumatic memories.
Trisomic rescue via allele-specific multiple chromosome cleavage using CRISPR-Cas9 in trisomy 21 cells
Human trisomy 21, responsible for Down syndrome, is the most prevalent genetic cause of cognitive impairment and remains a key focus for prenatal and preimplantation diagnosis. However, research directed toward eliminating supernumerary chromosomes from trisomic cells is limited. The present study demonstrates that allele-specific multiple chromosome cleavage by clustered regularly interspaced palindromic repeats Cas9 can achieve trisomy rescue by eliminating the target chromosome from human trisomy 21 induced pluripotent stem cells and fibroblasts. Unlike previously reported allele-nonspecific strategies, we have developed a comprehensive allele-specific (AS) Cas9 target sequence extraction method that efficiently removes the target chromosome. The temporary knockdown of DNA damage response genes increases the chromosome loss rate, while chromosomal rescue reversibly restores gene signatures and ameliorates cellular phenotypes. Additionally, this strategy proves effective in differentiated, nondividing cells. We anticipate that an AS approach will lay the groundwork for more sophisticated medical interventions targeting trisomy 21.
Keywords: CRISPR/Cas; Down syndrome; allele specificity; chromosome cut; chromosome loss; human trisomy 21.
© The Author(s) 2025. Published by Oxford University Press on behalf of National Academy of Sciences.
Consciousness likely not unique to earthlings, paper says
Does consciousness depend on flesh and blood?
The answer is almost certainly no, according to Eric Schwitzgebel, a distinguished professor of philosophy at the University of California, Riverside.
In a new working paper, Schwitzgebel and Jeremy Pober, a former UCR graduate student who is now a postdoctoral researcher at the University of Lisbon, assert that consciousness is likely possible in life forms made of much different stuff. Think of the five-limbed alien with a rock-like exterior in the recent blockbuster movie “Project Hail Mary.”
Research progress on 40 Hz sensory stimulation for the treatment of Alzheimer’s disease
Abstract:
Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder characterized by β-amyloid (Aβ) deposition, tau protein hyperphosphorylation, and synaptic dysfunction. In recent years, 40 Hz sensory stimulation—including visual, auditory, and multimodal modalities—has emerged as a novel, non-invasive intervention demonstrating potential efficacy in both animal models and preliminary clinical studies. Preclinical evidence indicates that such stimulation can markedly reduce cerebral Aβ burden (by approximately 37%–53%), inhibit tau protein phosphorylation, enhance neuronal network synchrony and synaptic plasticity, and improve learning and memory performance. Limited human trials suggest that 40 Hz sensory stimulation is safe and well tolerated in patients with mild cognitive impairment (MCI) and early-stage AD, with a slowing trend in cognitive scale score decline following intervention. This review summarizes the mechanisms of action, experimental evidence from animal models, and advances in clinical application of 40 Hz sensory stimulation in AD prevention and treatment. It further explores the potential for multimodal combination therapies integrating sensory stimulation with cognitive training, pharmacological interventions, and lifestyle modifications, and addresses challenges such as optimal timing of intervention and the influence of ambient electromagnetic fields in real-world settings. Current evidence supports 40 Hz sensory stimulation as a feasible, multi-target, and safe adjunctive intervention; however, its efficacy and applicability must be verified through multicenter, randomized controlled trials with long-term follow-up.