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Category: biotech/medical

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.

Accelerating and Streamlining Microbial Process Development

CDMO Fujifilm Biotechnologies unveiled its ShunzymeX precision purification technology, which is aimed at simplifying downstream processing for complex biologics. The technology will be presented this week at the Festival of Biologics conference in San Diego.

Fujifilm Biotechnologies, in collaboration with the University of Edinburgh, developed ShunzymeX, a proprietary technology that leverages a novel protease to enable purification of complex biologics with a simplified process, according to the company. This technology enables the addition of an affinity tag to the protein, allowing the biologic protein to be purified with an off-the-shelf affinity resin. After purification, the novel protease cleaves off the tag without leaving a scar on the native protein.

ShunzymeX addresses some of the inherent challenges in traditional microbial downstream purification due to the diversity of microbial-expressed proteins, including variability in size and sequence, leading to a lack of suitable affinity resins, says John Stewart, senior vice president of global process development, Fujifilm Biotechnologies.

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.

RAB3GAP2 is a regulator of skeletal muscle endothelial cell proliferation and associated with capillary-to-fiber ratio

Ström et al. identify the rs115660502 variant in RAB3GAP2 associated with increased skeletal muscle capillary-to-fiber ratio and enriched in endurance athletes. This variant reduces RAB3GAP2 expression, enhancing endothelial proliferation, tube formation, and TNC secretion, thereby promoting exercise-like angiogenesis and microvascular remodeling in skeletal muscle.

Prognostic and Therapeutic Implications of Alamandine Receptor MrgD Expression in Clear Cell Renal Cell Carcinoma with Development of Metastatic Disease

Despite advances in the management of advanced clear cell renal cell carcinoma (ccRCC), robust biomarkers for prognosis and therapeutic response prediction remain elusive.

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.

Light-guided ‘optovolution’ evolves proteins that switch states on schedule

EPFL researchers have developed a light-based method that can produce proteins that switch states, respond to signals, and even compute, using light and the cell cycle.

Evolution is biology’s powerful method of engineering. It works by generating many variants of DNA, RNA, and proteins inside cells and letting nature “select” the organism that performs best. Early farmers started taking advantage of evolution by interfering with natural selection and letting only the most productive livestock and crops mate.

In laboratories, researchers have developed methods for directed evolution of proteins, especially enzymes and antibodies, that are used in household detergents, medicine, and industry.

A bicistronic viral genome uses a compact type IV IRES near its 3′ end to express a transmembrane protein

Sherlock et al. examine an IRES RNA that initiates translation of a small downstream coding region within a viral genome. The structure, function, and mechanism of this IRES are interrogated experimentally. Differential translation efficiencies between two IRESs within one viral genome exemplify RNA-structure-based tuning of gene expression.

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