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Learning makes brain cells work together, not apart

When you get better at a skill—recognizing a familiar face in a crowd, spotting a typo at a glance, or anticipating the next move in a game—sensory neurons in your brain become more coordinated, sharing information rather than acting more independently. That’s the conclusion of a new study by researchers at the University of Rochester and its Del Monte Institute for Neuroscience, published in Science, which challenges a long-held assumption in neuroscience that learning improves efficiency by minimizing repetition across neural signals.

Led by Shizhao Liu, a graduate student in the labs of Ralf Haefner and Adam Snyder, both faculty members in the Department of Brain and Cognitive Sciences, the study shows that learning instead increases shared activity among neurons. The findings could provide insights into learning disorders and inspire more flexible, human-like artificial intelligence tools.

“The dominant view in neuroscience has been that learning makes the brain more efficient by pushing neurons to act more independently, so information can be read out more cleanly,” Liu says. “Our results support a different idea, that sensory areas of the brain aren’t just passively encoding the world. They’re actively performing inference by combining what’s coming in with what the brain has learned to expect.”


A new University of Rochester study could reshape how scientists think about perception, learning disorders, and artificial intelligence.

Pharmacologic reversal of advanced Alzheimer’s disease in mice and identification of potential therapeutic nodes in human brain

Here, we show that pharmacologic restoration of NAD+ homeostasis via P7C3-A20, a neuroprotective compound that restores NAD+ homeostasis without producing supraphysiologic NAD+ levels,51,52,53,54,55,56 reverses cognitive deficits and neuropathology in advanced Aβ- and tau-driven AD models. We identify conserved molecular signatures between human and mouse AD and show that the magnitude of NAD+ homeostasis disruption correlates with pathology and symptom severity in mouse and human AD. We also demonstrate that NDAN brains display transcriptional profiles compatible with preserved NAD+ homeostasis and that P7C3-A230 restores NAD+ homeostasis and prevents oxidative damage and mitochondrial dysfunction in oxidatively stressed human brain microvascular endothelial cells (HBMVECs), a key component of the BBB. We additionally identify 46 conserved protein alterations in human and mouse AD brain that are corrected by AD reversal, together with overlapping transcriptomic changes in human AD. This highlights potential mechanisms and therapeutic targets for preserving and restoring brain resilience to AD.

These findings of cognitive recovery and pathological reversal in diverse models of advanced AD support disease progression as modifiable and driven by diminished brain resilience, with early cognitive impairment resulting from processes that promote neurodegeneration rather than solely from fixed neuronal loss. We propose that therapies to restore brain resilience, such as normalization of NAD+ homeostasis, merit clinical evaluation for prevention and reversal of AD and related dementias.

Weaponising the Mind: Rethinking Trust in Times of Cognitive Warfare

🧠 Cognitive warfare is real and it’s here already.

That is why the Konrad Adenauer Foundation is putting the topic on the agenda at the Munich Security Conference.

From now on, the focus will be on the following key issues: • Cognitive warfare as a security policy reality • Resilience instead of alarmism • Strategic advantage through the ability to act • Protection of democratic decision-making processes.

Cognitive warfare is changing the logic of modern conflicts. It does not target infrastructure or territory, but rather perception, trust and decision-making ability, thereby blurring the line between war and peace.

More about #MSC2026: https://www.kas.de/de/veranstaltungsberichte/detail/-/conten…t-begonnen.

#munichsecurityconference

Within-Person Association Between Daily Screen Use and Sleep in Youth: A Systematic Review and Meta-Analysis

A meta-analysis found that on days with more screen use, youths went to bed slightly later but had no significant changes in total sleep time, sleep quality, or efficiency.


Question What is the within-person association between daily screen use and sleep in children and youth?

Findings In this systematic review and meta-analysis, daily screen use was significantly related to later sleep onset but was not significantly related to total sleep time, sleep onset latency, sleep efficiency, wake after sleep onset, or subjective sleep quality.

Meaning When young people use screens, they may displace sleep when doing so; however, using screens more than usual is not necessarily detrimental to sleep.

Targeting mitochondrial metabolism with combined metabolic activators

Combined metabolic activators to treat mitochondrial dysfunction.

Mitochondrial dysfunction is a common feature of many human diseases and is emerging as a therapeutic target.

Systems biology and multiomics approaches have revealed that deficits in glutathione and NAD+ metabolism, impaired fatty acid oxidation, and disrupted redox balance are key drivers of disease pathogenesis.

Combined metabolic activators (CMA) were developed to address these metabolic deficits through the complementary actions of serine, Nacetylcysteine, L-carnitine, and NAD+ precursors.

CMA have been shown to lower hepatic fat, reduce systemic inflammation, accelerate recovery from infection, and improve cognitive performance in clinical studies. sciencenewshighlights ScienceMission https://sciencemission.com/Targeting-mitochondrial-metabolism


Mitochondria play a central role in energy metabolism, redox balance, and cellular homeostasis, and their dysfunction has been implicated in the pathogenesis of complex human diseases. Advances in systems biology and omics technologies have elucidated the mechanisms underlying these conditions, including metabolic dysfunction, mitochondrial impairment, inflammation, and redox imbalance. Preclinical and early clinical studies of combined metabolic activators (CMA), a formulation of bioactive metabolites, have demonstrated improvements in mitochondrial function and systemic metabolic profiles across multiple diseases.

Cheek cells may provide clues to schizophrenia risk

A simple cheek swab could one day provide a quick and noninvasive diagnostic test for schizophrenia. A new study published in Science Advances has identified higher levels of two biological markers in the cheek swabs of patients with schizophrenia compared with people who don’t have this mental health disorder. Schizophrenia is a long-term condition with a range of symptoms including hallucinations, delusions, muddled thoughts and loss of interest in everyday activities.

There is no single test for the illness, and diagnosis can be challenging because symptoms vary widely between people and typically relies on observing a patient’s behavior. It can, therefore, sometimes take months for a professional to make a diagnosis with any degree of certainty, as they have to rule out other possible causes. That is a lot of time for someone to wait without the right treatment if it is needed.

So researchers led by a team at Rutgers University in New Jersey decided to investigate whether molecular signatures in easy-to-collect buccal (cheek) cells could serve as reliable biomarkers.

The Observer Effect in Everyday Life

Daily reflection is a way to apply this principle in our everyday lives. It shines a spotlight on the behavior itself. And when behavior is observed consistently, it solidifies into neural pathways in the brain. We start behaving differently, not because someone else is judging us, but because we are measuring ourselves. The simple act of asking ourselves reflective questions each day shapes the behaviors in our lives, which, in turn, make us the people who exhibit those behaviors.

Another principle from quantum theory, entanglement, might also be at play when we do daily reflection. Quantum entanglement describes how particles can become linked to one another so that a change in one results in a change in the other. In the same way, the effort we make to change in one part of our lives is rarely confined to that part. Instead, our behaviors extend outward and affect those in relationship to us and around us. For example, your attempt to speak in positive terms, rather than negative ones, can influence your colleagues at work. Your intention to control your emotional outbursts can affect your family. Your efforts to build positive relationships at work or in your community can change the dynamics of those relationships. And when you combine these intentions with daily reflection, you’re not only strengthening a positive personal trait within yourself, but also influencing the bigger, interpersonal systems around you.

Philosophers, physicians, and physicists are forever debating what consciousness is. Is who we are just a byproduct of biology and the brain’s physiology, or is who we are more fundamental and exists irrespective of the brain’s neural firing? We may never know. That said, one thing is true: Conscious awareness shapes who we are. Without reflection, behavior defaults to habit. With reflection, possibility re-enters the system. The practice of asking yourself daily reflective questions puts you in the role of an observer rather than an actor. And from there, you can be intentional about who you choose to be tomorrow.

A new mechanism for motor-learning circuit rewiring

To address this question, the researchers used mouse models undergoing repeated motor training tasks, including the rotarod test, which measures motor coordination and learning. Using advanced imaging tools that can track individual synaptic components, the team observed a marked increase in astrocyte-mediated synapse elimination as motor learning progressed. In contrast, other glial cell types, such as microglia and oligodendrocyte precursor cells, showed no significant changes under the same experimental conditions, indicating a specific role for astrocytes in this process.

The researchers identified MEGF10, a phagocytic receptor expressed in astrocytes, as a key molecular mediator of this remodeling. When MEGF10 was selectively deleted in astrocytes, mice exhibited impaired motor learning and significant disruptions in communication between the motor cortex and the striatum. In addition, both long-term potentiation (LTP) and long-term depression (LTD)—two fundamental mechanisms of synaptic plasticity—were compromised. These results demonstrate that astrocyte-mediated synapse elimination is not merely a housekeeping function, but a necessary component of functional circuit refinement during learning.

The team further investigated how astrocytes determine which synapses to remove and identified two major regulatory signals. First, increasing neuronal activity between the motor cortex and the striatum significantly enhanced astrocyte-mediated synaptic elimination (a process in which astrocytes engulf and remove synapses), indicating that circuit engagement promotes remodeling. Second, manipulating dopamine levels, a key neuromodulator for movement and reward, also strongly influenced astrocytic synapse elimination. ScienceMission sciencenewshighlights.


When we learn a new motor skill—whether mastering a piano passage or refining balance while walking—the brain must reorganize the circuits that control movement. For decades, this process of synaptic remodeling has been attributed primarily to neurons strengthening or weakening their connections. However, the new study reveals that another cell type in the brain called astrocytes actively participates in this rewiring process.

A research team has demonstrated that astrocytes actively eliminate synapses in the striatum, a brain region that plays a central role in controlling voluntary movement and learning. This process is regulated by dopamine signaling and neural activity and is critical for proper motor skill acquisition.

Although synapse formation and elimination have long been studied in the context of neuronal plasticity, increasing evidence suggests that glial cells—particularly astrocytes and microglia—also contribute to synapse turnover. Until now, however, the precise role of astrocytes in motor learning and the mechanisms underlying their synaptic remodeling remained unclear.

Decoding alzheimer’s: The role of EEG rhythms and aperiodic components in cognitive decline

[Alzheimer’s disease: AD] Zhang et al.: “Increased theta band power was statistically significant in AD patients, highlighting its critical role in AD pathology.”


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