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Category: neuroscience

Genetic risk for Alzheimer’s disease could depend on how well you sleep

A compelling longitudinal study of over 350 older adults with early beta-amyloid accumulation reveals that the genetic risk for Alzheimer’s disease is not strictly deterministic, but is profoundly modulated by sleep quality through the AQP4 gene—a critical regulator of the brain’s glymphatic waste-clearance system. By cross-referencing specific AQP4 variants with multi-year MRI and PET imaging alongside cognitive assessments, researchers demonstrated that poor sleep parameters, such as shorter duration and delayed onset, significantly accelerate neurodegenerative markers like gray matter loss and ventricle expansion in carriers of specific risk alleles. Paradoxically, however, carriers of certain rare variants exhibited slower cognitive decline even in the presence of sleep disturbances. Ultimately, these findings illuminate a complex gene-environment interplay, proving that identical genetic predispositions can either expedite or buffer against brain atrophy depending on sleep architecture, thereby highlighting the critical necessity of personalized, sleep-targeted lifestyle interventions as a highly actionable strategy for Alzheimer’s prevention.

Scientists have discovered an important link between sleep, genetics, and Alzheimer’s disease. New findings suggest that getting poor sleep can accelerate brain shrinkage and memory loss in older adults carrying specific genetic variants.

Intelligence Without Brains: A Radical New Idea

What if intelligence doesn’t require a brain? Biologist Michael Levin argues that intelligence is not confined to neurons, but exists on a continuum of goal-directed behavior and problem-solving across a wide range of species and systems. Using a framework he calls the “cognitive light cone,” Levin explores diverse forms of intelligence extending all the way down to the cellular level. His research suggests that cells communicate through electrical networks, enabling them to make collective decisions and adapt to unexpected challenges, evidenced by engineered tadpoles capable of seeing through eyes located on their tails. Levin radically challenges the conventional wisdom even further, proposing that forms of intelligence may extend beyond biology to molecular systems and maybe even the weather.

00:00 What is intelligence?
01:03 The field of diverse intelligence.
01:33 Intelligence at the cellular level.
02:08 The cognitive light cone.
03:01 The intelligence of groups of cells.
03:52 The bioelectric language of cells.
04:20 The mind of the body.
04:23 Cells that solve problems.
05:17 The tadpole experiment.
06:25 The cognitive spectrum.
06:48 Can you train a hurricane?
07:03 A new science of intelligence.
07:28 Beyond human biases.

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What one sleepless night does to brain connections and why sleep may reset them

A night without sleep produced increased markers of connections between brain cells, showing that sleep in humans may be important for restoring cellular balance in the brain, according to a study published in PLOS Biology by David Elmenhorst from the Forschungszentrum Jülich Institute of Neuroscience and Medicine in North Rhine-Westphalia, Germany, and colleagues.

Scientists have long wondered why humans and other animals need to sleep. One potential mechanism is that sleep is required to restore synaptic connections and homeostasis in the brain. Synapses—the connections between brain cells—become stronger during wakefulness.

This increases the amount of energy the brain needs and leads to a buildup of proteins in the brain. Sleep is thought to reset these levels, reducing synaptic connections and restoring homeostasis, but evidence has thus far been limited to animal models.

Functionalism (Stanford Encyclopedia of Philosophy/Winter 2016 Edition)

Functionalism in the philosophy of mind is the doctrine that what makes something a mental state of a particular type does not depend on its internal constitution, but rather on the way it functions, or the role it plays, in the system of which it is a part. This doctrine is rooted in Aristotle’s conception of the soul, and has antecedents in Hobbes’s conception of the mind as a “calculating machine”, but it has become fully articulated (and popularly endorsed) only in the last third of the 20th century. Though the term ‘functionalism’ is used to designate a variety of positions in a variety of other disciplines, including psychology, sociology, economics, and architecture, this entry focuses exclusively on functionalism as a philosophical thesis about the nature of mental states.

The following sections will trace the intellectual antecedents of contemporary functionalism, sketch the different types of functionalist theories, and discuss the most serious objections to them.

Vagus nerve stimulation may quiet pain through newly mapped brainstem pathway

Physical pain is essential for survival, as it allows animals to detect when they are injured or unwell, seek shelter and address their ailments. Yet when it becomes chronic, pain can also become highly distressing and debilitating.

While there are now several therapeutic strategies for managing chronic pain, an emerging one that has been found to be particularly promising is vagus nerve stimulation (VNS). VNS entails the delivery of mild electrical pulses to the nerve that connects the brain to organs throughout the body.

Past studies suggest that VNS-based therapy can reduce the pain associated with various medical conditions, including chronic headaches, fibromyalgia and joint inflammation. The neural processes by which it can ease pain, however, are still poorly understood.

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.

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