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Scientists Finally Figured Out Why 90% of Humans Are Right-Handed

Not to toot my own horn or anything, but I can extend my empathy beyond myself just enough to imagine someone else’s perspective, fully knowing I’ll never completely understand the texture of their experience. But as a right-handed person, I will never, ever be able to do that for left-handed people. There’s just something in my brain preventing me from understanding how someone can navigate the world primarily using the hand I mostly rely on to accidentally test the sharpness of kitchen knives.

So naturally, it always made sense to me that around 90 percent of humans are right-handed. What never made sense was why. According to new research published in PLOS Biology, we may have finally figured it out: humans became overwhelmingly right-handed because we started walking upright and developed massive brains.

Researchers from the University of Oxford analyzed more than 2,000 primates across 41 species, comparing handedness with factors like social behavior, diet, body size, and movement. Nothing fully explained humanity’s innate steadfast dedication to right-handedness until researchers started factoring in brain size and the ratio between leg and arm length.

Light-triggered arrhythmia reveals rapid brain oxygen shifts in mice

An irregular heartbeat, or arrhythmia, leads to inefficient pumping of blood by the heart, which then prevents blood and oxygen from getting to the body’s other organs. When blood and oxygen flow poorly to the brain, the risk of stroke and cognitive decline increases.

A team of researchers based at Washington University in St. Louis used cardiac optogenetics to noninvasively study arrhythmia and its impact on the brain. Using highly sensitive imaging in a mouse model, they found that arrhythmia in a mouse heart alters oxygen concentration in the brain during and after arrhythmia.

Results of the research are published in Science Advances.

Fragile X deficits in mice respond to gene therapy

A gene therapy designed to replace a missing brain protein restored normal brain activity and improved behavior in a mouse model of fragile X syndrome (FXS), according to a study led by researchers at the University of California, Riverside. The findings, published in Molecular Therapy Nucleic Acids, suggest that gene therapy may one day address the underlying cause of FXS rather than simply treating its symptoms.

FXS affects approximately 2–3% of individuals diagnosed with autism and is one of the best-defined genetic causes of neurodevelopmental disability. The condition occurs when a mutation in the FMR1 gene prevents the production of fragile X messenger ribonucleoprotein (FMRP), a protein that regulates communication between brain cells.

“In a typical brain, FMRP acts like a brake or a volume control,” said Iryna Ethell, the paper’s senior author and a professor of biomedical sciences in the UCR School of Medicine. “Without it, neural circuits become overactive and less efficient, which contributes to many of the developmental and behavioral challenges associated with FXS.”

Faster aging, chronic disease linked to WTC responders with PTSD

Post-traumatic stress disorder (PTSD) remains a common condition affecting World Trade Center (WTC) responders 25 years after the attack on the Twin Towers. While the condition is considered mainly psychological, a new study sheds light on changes in the biological processes of WTC patients with PTSD that may explain why PTSD is associated with a variety of chronic diseases that ultimately contribute to aging.

Completed by a team of researchers affiliated with the Stony Brook World Trade Center Health and Wellness Program, which monitors the health of and provides patient care to some 10,000 WTC responders, and scientists at Duke University, the study is published in Nature Communications.

The work represents more than a decade of research led by Benjamin J. Luft, MD, senior author, the Edmund D. Pellegrino Professor of Medicine in the Renaissance School of Medicine (RSOM) at Stony Brook University and director of the WTC Health and Wellness Program; and Pei-Fen Kuan, Ph.D., first author and professor in the Department of Applied Mathematics and Statistics in the College of Engineering and Applied Sciences at Stony Brook University.

A selective, brain-penetrant GalR1 antagonist restores cholinergic signaling in vitro and rescues cholinergic cognitive deficits in mice

In this study, we characterized PAC-832, a small-molecule GalR1 antagonist with sub-micromolar potency (IC50 = 0.28 μM), 30-fold selectivity over GalR2 and GalR3, and excellent brain penetration and drug-like properties. In functional cell-based assays, PAC-832 reversed galanin-mediated suppression of acetylcholine release. In a scopolamine challenge model, PAC-832 attenuated cognitive deficits in the Y-maze and NOR tasks, with effect sizes comparable to donepezil.

The scopolamine model is widely used in behavioral mouse research to evaluate compounds for procognitive activity. However, because scopolamine impairs cognition by blocking muscarinic receptors rather than by reducing acetylcholine release, our behavioral results do not directly assess whether PAC-832 acts by restoring cholinergic signaling in vivo, or whether it acts through an alternative downstream mechanism. Establishing the former will require direct measurement of acetylcholine release in the CNS (e.g. using microdialysis or biosensor-based approaches) and/or GalR1-dependent in vivo validation (e.g. using transgenic GalR1-knockout mice).

Nonetheless, our work addresses a longstanding pharmacological gap in the galanin field. Despite decades of work implicating galanin signaling in CNS function and disease, translational progress has been limited by a lack of subtype-selective, brain-penetrant small molecule galanin modulators. Recent therapeutic development within the galanin field has largely focused on GalR2 agonism, while GalR1-targeting approaches have remained dependent on peptide tools unable to pass the blood-brain barrier. PAC-832 is, to our knowledge, the first GalR1-selective small molecule antagonist with sufficient brain exposure to test the effects of GalR1 antagonism following peripheral administration.

A 13-second eye test may help predict recovery of consciousness after severe brain injury

A simple bedside eye test may help predict recovery of consciousness in patients with severe brain injuries, according to new research presented at the European Academy of Neurology (EAN) Congress 2026.

The study found that a previously overlooked phase of the pupil response to light, known as the late light-off response (LOR), predicted improvements in consciousness seven days later in patients with acute brain injury. In contrast, standard pupil measurements already widely used in intensive care units (ICUs), including the Neurological Pupil Index (NPi) and pupillary light reflex (PLR) latency, did not predict later gains in consciousness.

Breastfeeding may protect against ADHD symptoms

A new study from the University of Bergen shows an association between breastfeeding up to 6 months of age and a reduced risk of ADHD symptoms from ages 3 to 8.

Breast milk is the primary source of nutrition for infants. It is uniquely tailored for the child and contains numerous components beneficial for growth and brain development, including long-chain fatty acids, amino acids, antibodies and beneficial bacteria.

“It is well established that psychiatric symptoms and disorders can be influenced by both genetic and environmental factors,” says Berit Skretting Solberg, psychiatrist and researcher at the Department of Biomedicine, University of Bergen, and senior consultant at Betanien Hospital.

Humans Were Injected: BREAKTHROUGH Age Reversal For Every Tissue

Life Biosciences just dosed the first human patient with ER-100 — an OSK gene therapy built from three Yamanaka factors, designed to reprogram old cells back toward a younger state. The first target is the eye. But the real implication is much bigger: this method appears to work on every tissue type it has been tried on.

If this first eye trial comes back safe, it could be the first domino in a much larger age-reversal wave: eye, liver, brain, skin, muscle, heart, kidney, blood vessels — potentially every tissue in the body.

This episode reveals the tidal wave of companies racing toward human trials using the same basic strategy: epigenetically reprogramming old cells so they behave young again. Billions of dollars are pouring into this from Jeff Bezos, Sam Altman, Brian Armstrong, Peter Thiel, and the biggest names in longevity biotech.

We walk through who they are, what they are trying to cure, why the eye came first, what worked in mice and monkeys, why NewLimit is going after liver rejuvenation, and whether the cheap pill version could be right behind the expensive gene therapy.

Bottom line: real age reversal is now in a human trial.

LONGEVITY LATTE PRE-ORDER:

The Neuroscience of Happiness and Pleasure

The evolutionary imperatives of survival and procreation, and their associated rewards, are driving life as most animals know it. Perhaps uniquely, humans are able to consciously experience these pleasures and even contemplate the elusive prospect of happiness. The advanced human ability to consciously predict and anticipate the outcome of choices and actions confers on our species an evolutionary advantage, but this is a double-edged sword, as John Steinbeck pointed out as he wrote of “the tragic miracle of consciousness” and how our “species is not set, has not jelled, but is still in a state of becoming” (). While consciousness allows us to experience pleasures, desires, and perhaps even happiness, this is always accompanied by the certainty of the end.

Nevertheless, while life may ultimately meet a tragic end, one could argue that if this is as good as it gets, we might as well enjoy the ride and in particular to maximize happiness. Yet, it is also true that for many happiness is a rare companion due to the competing influences of anxiety and depression.

In order to help understand happiness and alleviate the suffering, neuroscientists and psychologists have started to investigate the brain states associated with happiness components and to consider the relation to well-being. While happiness is in principle difficult to define and study, psychologists have made substantial progress in mapping its empirical features, and neuroscientists have made comparable progress in investigating the functional neuroanatomy of pleasure, which contributes importantly to happiness and is central to our sense of well-being.

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