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Category: neuroscience – Page 2

Mitochondrial Ca2+ efflux controls neuronal metabolism and long-term memory across species

Mitochondrial calcium regulates neuronal metabolism and memory.

Brain metabolism is important for long-term memories (LTMs) and various brain functions, Although it is well known that impairing neuronal metabolism limits brain performance, it is not clear if expanding the metabolic capacity of neurons boosts brain function.

In this study, the authors demonstrate that increasing mitochondrial metabolism can enhance LTM formation in flies and mice.

The authors increase mitochondrial Ca2+ by knocking down the mitochondrial Ca2+ exporter Letm1 and demonstrate over-activation of mitochondrial metabolism in neurons of central memory circuits, leading to improved LTM storage. sciencenewshighlights Science Mission https://sciencemission.com/Mitochondrial-Ca2-efflux

Boosting mitochondrial metabolism in neurons in central memory circuits by enhancing Ca2+ retention in the mitochondrial matrix is shown to improve long-term memory formation in flies and mice.

Degenerating Tanycytes Disrupt Tau Removal, Shaping Alzheimer’s Progression

“Tanycytes, whose cell bodies line the walls and floor of the third ventricle and extend long, slim processes that terminate in ‘endfeet’ that contact these fenestrated capillaries,” act as a shuttle between the CSF and the blood, the authors wrote. The new study suggests they also act as a kind of molecular “exit ramp,” moving tau out of the CSF and into the bloodstream for disposal. When these cells become fragmented, that clearance system falters. Tau, which should be ferried away, instead lingers—much like traffic backing up when a major off‑ramp closes—allowing toxic protein species to accumulate.

“Our findings reveal a previously underappreciated, disease‑relevant role for tanycytes in neurodegeneration,” said corresponding author Vincent Prévot, PhD, of INSERM. “Focusing on tanycyte health could be a way to improve tau clearance and limit disease progression.”

Using rodent and cellular models, the researchers showed that tanycytes take up tau from the CSF and release it into pituitary portal capillaries, enabling its entry into the systemic circulation, according to the authors. When the team blocked vesicular transport in tanycytes, tau clearance from CSF to blood slowed dramatically, and tau pathology intensified. As the authors wrote, “Blocking tanycytic vesicular transport blunts CSF‑to‑blood tau efflux and potentiates tau pathology.”

Can a wealthy family change the course of a deadly brain disease?

A wealthy family fighting its own disease boosted research on a little-studied brain protein, progranulin. Can it spur new dementia treatments?

Bluefield investigators, and eventually drug companies, saw something compelling about FTD-GRN, the form of the condition Alice had. In other genetic neurodegenerative disorders, such as familial Alzheimer’s and Huntington disease, mutations spark the production of toxic proteins, generating complex cascades of pathology. But the culprit mutations driving FTD-GRN block progranulin production, leaving carriers with less than half as much of the protein as noncarriers. Many dementia researchers came to describe FTD-GRN as a “low-hanging fruit” among neurodegenerative diseases, using words such as “intuitive” and “tractable” to characterize its biology. The solution seemed obvious: A treatment just needed to raise progranulin levels in the brain.

Fueled in part by that confidence, six clinical trials have been launched to test progranulin-boosting therapies in FTD-GRN. Companies also hope the anti-inflammatory properties of a progranulin-boosting agent could help in Parkinson’s disease, Alzheimer’s, amyotrophic lateral sclerosis (ALS), and FTD caused by other mutations or without a known genetic cause.

All has not gone according to plan, however. In October 2025, a landmark phase 3 clinical trial of a progranulin-boosting drug in people with FTD-GRN did not keep their disease from progressing. In February, a small trial of a gene therapy delivering a healthy copy of GRN to the brain was halted, also for lack of effect.

Researchers detect complex emotions by combining multiple optical signals

Researchers have developed a new way to recognize human emotions by combining fiber-based physiological signals with thermal images of the face. The portable emotional recognition system could eventually be used to support at-home mental health monitoring, improve driver safety and make technology more responsive to human emotions.

“Unlike many existing approaches, our method does not rely on facial expressions, which can be consciously controlled or exaggerated,” said research team leader Rui Min from Beijing Normal University at Zhuhai (BNU Zhuhai) in China.

“Instead, it focuses on natural bodily responses that occur automatically. By combining multiple types of optical sensing and higher-level physiological interpretation, our system can more accurately capture emotion than those using a single type of input.”

New study shows how sickle cell affects brain function

Sickle cell disease is often thought of solely as a blood disorder, but new research from the Wood Neuro Research Group provides measurable evidence that it can reshape how brain networks function. Previous neuroimaging studies have relied on functional connectivity to show that adults with sickle cell disease may experience changes in how brain networks communicate among one another, potentially compensating for reduced oxygen delivery. However, this method is limited in determining the directionality or influence between networks.

“Red blood cells that carry oxygen to the brain are altered by the disease, resulting in reduced oxygen delivery to all regions of the brain and long-term changes in how it functions,” outlined Nahom Mossazghi, biomedical engineering Ph.D. student and the study’s first author. “The brain actively recruits other regions to help process information, which we do not see in people without the disease.”

The study, published in Human Brain Mapping, used MRI and advanced analytical tools originally developed in economics to examine how different brain networks influence one another. Instead of functional connectivity, effective connectivity was used to address a gap in the field and interpret how specific networks support one another in response to the disease-related changes.

Temporal lobe epilepsy: A new strategy to correct abnormal electrical activity

Many patients suffer from epilepsy that cannot be controlled by current medications. Surgical removal of epileptogenic brain regions is effective in only about half of cases, and not all patients are eligible for the procedure. For these individuals, therapeutic options remain severely limited. Researchers from the Paris Brain Institute and the Institut du Fer à Moulin in Paris have now taken an important step forward: they have identified two molecules capable of reducing seizure frequency by targeting a mechanism that has so far received little attention. Their findings are published in Proceedings of the National Academy of Sciences.

For the brain to function normally, it must continuously regulate its electrical activity. One of the key mechanisms involved is GABAergic signaling, a natural inhibitory system that controls neuronal activity and prevents the electrical bursts that characterize epileptic seizures. This braking system depends on a delicate balance: the concentration of chloride inside neurons.

An ion transporter known as KCC2 is responsible for removing excess chloride from nerve cells. When it functions poorly—as observed in many neurological disorders, including mesial temporal lobe epilepsy, the most common form of focal epilepsy in adults—chloride accumulates inside neurons. As a result, GABAergic signals, instead of inhibiting neuronal activity, can paradoxically excite it.

Targeting amyloid-β pathology by chimeric antigen receptor astrocyte (CAR-A) therapy

Researchers at Washington University in St. Louis have developed a novel cell therapy for Alzheimer’s disease using genetically modified astrocytes — the brain’s most abundant cells. By equipping these cells with a chimeric antigen receptor (CAR), scientists enabled them to specifically target and clear beta-amyloid plaques, the toxic protein deposits that accumulate in brain tissue and drive neurodegeneration. In mouse trials, a single injection prevented plaque formation in young healthy rodents and reduced existing plaque levels by half in older mice. While the approach is still being refined to minimize side effects and must be evaluated for human safety, it holds promise both as a preventive measure and as a treatment at various stages of Alzheimer’s. The same technology may eventually be adapted for cancer therapy by reprogramming the cells to target tumor markers.

Alzheimer’s disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration. Despite advances in anti-amyloid immunotherapies, important limitations remain, highlighting the need for new therapeutic strategies. Here, we introduce anti-amyloid chimeric antigen receptors expressed in astrocytes (CAR-A) and validate their function in vitro. We show that two CAR-A designs reduce amyloid and associated pathology after plaque formation and prevent early plaque deposition in vivo. Single-nucleus RNA sequencing shows that CAR-A treatment induces a distinct glial response to amyloid pathology involving coordinated activity of astrocytes and microglia. Each construct additionally elicits distinctive, receptor-specific effects in astrocytes or microglia.

Why organisms are more than machines

We are living in the age of maximum AI hype: A superintelligence that surpasses humanity is going to emerge at any moment, according to the most breathless corners of the tech world.

There are basic technical grounds to be skeptical of that claim, but beyond that, a much deeper issue lies at the boundary between science and philosophy: What makes life different from non-life? Why is a rock inert and insensate, while even the simplest cell manifests open-ended activity in the relentless pursuit of staying alive? Since the only systems that indisputably display intelligence are alive, if we can’t understand life, we’re probably missing something essential about intelligence.

Sixty years ago, an influential but little-known philosopher named Hans Jonas gave a potent, creative, and radical answer to this question of what makes life different from non-life. In the decades since, the power and reach of his perspective have gained traction. Today, for a growing group of researchers — in fields ranging from neuroscience to the physics of complex systems — Jonas has become an incisive voice arguing forcefully that organisms are more than just machines, and minds are more than just computers.

Creating less trippy, more therapeutic ‘magic mushrooms’

Psilocybin—the psychoactive compound in “magic mushrooms”—is gaining scientific attention for its potential in treating neuropsychiatric conditions including depression, anxiety, substance use disorders and certain neurodegenerative diseases. However, its hallucinogenic effects may limit broader therapeutic applications. Researchers publishing in the Journal of Medicinal Chemistry synthesized modified versions of psilocin, the active form of psilocybin, that retained its activity while producing fewer hallucinogenic-like effects than pharmaceutical-grade psilocybin in a preliminary study in mice.

“Our findings are consistent with a growing scientific perspective suggesting that psychedelic effects and serotonergic activity may be dissociated,” says Andrea Mattarei, a corresponding author of the study. “This opens the possibility of designing new therapeutics that retain beneficial biological activity while reducing hallucinogenic responses, potentially enabling safer and more practical treatment strategies.”

Mood disorders and some neurodegenerative diseases, such as Alzheimer’s disease, involve imbalances of the neurotransmitter molecule serotonin, which helps regulate mood and other brain functions. For decades, scientists have been investigating the therapeutic use of psychedelics such as psilocybin on serotonin-signaling pathways. However, the hallucinations that can accompany these drugs may make people wary of taking them, even if there is a medical benefit.

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