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Category: neuroscience – Page 76

The brain on books: How reading reshapes language processing

Learning to read reshapes how the brain processes language. New research from Baycrest and the University of São Paulo shows that learning to read fundamentally changes how the brain responds to spoken language, even when no written words are present. While previous brain imaging studies have demonstrated that literacy strongly affects how the brain responds to written words, this study is among the first to show differences in brain activity during listening alone.

The findings confirm that as people learn to read, they develop a skill known as phonemic awareness, the ability to hear and manipulate the individual sounds that make up spoken words, a core foundation of reading. The study shows that learning to read improves how the brain processes spoken language by increasing sensitivity to these component sounds. This, in turn, strengthens short-term verbal memory, supporting the ability to learn complex skills and manage the cognitive demands of daily life.

The work is published in the journal Cortex.

The role of the Cer1 transposon in horizontal transfer of transgenerational memory

Could a hybrid biohardware using neural orgamoids and silicon make minduploading easier.

Animals face both external and internal dangers: pathogens threaten from the environment, and unstable genomic elements threaten from within. C. elegans protects itself from pathogens by “reading” bacterial small RNAs, using this information to both induce avoidance and transmit memories for four generations. Here, we found that memories can be transferred from either lysed animals or from conditioned media to naive animals via Cer1 retrotransposon-encoded virus-like particles. Moreover, Cer1 functions internally at the step of transmission of information from the germline to neurons and is required for learned avoidance. The presence of the Cer1 retrotransposon in wild C. elegans strains correlates with the ability to learn and inherit small-RNA-induced pathogen avoidance. Together, these results suggest that C.

Scientists identify key brain mechanism behind ayahuasca’s ability to reduce PTSD symptoms

A study in European Neuropsychopharmacology finds that ayahuasca helps rats learn that a previously dangerous environment is safe. This effect appears to rely on BDNF signaling within the infralimbic cortex, suggesting a potential biological pathway for treating trauma.

Multi-omic analysis of guided and unguided forebrain organoids reveals differences in cellular composition and metabolic profiles

The differences in guided and unguided forebrain organoids.

The differences arising from guided or unguided differentiation of human forebrain organoids is not well understood.

The researchers perform a multiomic analysis of forebrain organoids generated by these two key methods.

The researchers demonstrate that guided forebrain organoids contained a larger proportion of neurons, including GABAergic interneurons, whereas the unguided organoids contained significantly more choroid plexus, radial glia, and astrocytes at later stages.

They also show increased levels of oxidative phosphorylation and fatty acid β-oxidation in the unguided forebrain organoids and a higher reliance on glycolysis in the guided forebrain organoids. sciencenewshighlights ScienceMission https://sciencemission.com/guided-and-unguided-forebrain-organoids

Øhlenschlæger et al. perform a multi-omic analysis of forebrain organoids generated by two key methods, guided and unguided differentiation. They document significant differences in the cell type composition and metabolic profiles of the two forebrain organoid types, providing a resource and methodological guide for the neural organoid field.

Continue reading “Multi-omic analysis of guided and unguided forebrain organoids reveals differences in cellular composition and metabolic profiles” | >

Tumor-derived aminopeptidase N promotes early stages of brain metastatic colonization

In this study, we identified the aminopeptidase CD13 as a key mediator in a subset of human BrMs originating from breast and lung cancers, with approximately 30% of samples exhibiting cancer cell-specific CD13 expression. Notably, this prevalence aligns with previous reports in breast and lung primary tumors. In BC, CD13 cancer cell expression was documented in 36% of patient samples analyzed, with higher rates in invasive ductal carcinoma,31 while in lung cancer, 35% of patients analyzed were positive for cancer cell CD13 expression.32 These observations suggest that CD13 expression is maintained during metastatic progression to the brain, underscoring its potential as a therapeutic target. Importantly, CD13 expression in primary lung cancer is associated with significantly reduced survival, with a similar trend in BC.31,32 Consistent with these data, we show here that patients with HER2+ BC with CD13high tumors have significantly poorer clinical outcomes. These findings emphasize the importance of stratifying patients by CD13 status to better assess both its prognostic significance and therapeutic potential.

To gain mechanistic insight into CD13 function, we employed murine BrM models from three primary origins (breast, lung, and melanoma) that recapitulate distinct stages of the metastatic cascade. Notably, only the breast-BrM model exhibited robust CD13 expression, suggesting that lung cancer and melanoma may rely on alternative, CD13-independent mechanisms to colonize the brain. CD13 knockdown in breast-BrM cells significantly prolonged survival and reduced metastatic seeding following intracardiac injection. This effect was less pronounced when cancer cells were introduced directly into the brain parenchyma (intracranial injection) or implanted at the primary site (MFP), underscoring CD13’s predominant role during the initial colonization phase of metastasis.

Both gain-and loss-of-function experiments confirmed CD13’s functional importance in metastatic seeding. CD13 has been described as a moonlighting enzyme with diverse cellular functions relevant to regulating metastasis,16,17 including β1 integrin recycling,21 cell migration,21 and activation of the MAPK and PI3K pathways.33 Based on our RNA-seq analysis, CD13 overexpression may further enhance metastatic efficiency through activation of Rho family GTPases and effectors that orchestrate cytoskeletal remodeling, endothelial cell adhesion, and transendothelial migration.34 These features position CD13 as a compelling anti-cancer target; indeed, CD13 inhibition has been explored in several therapeutic development efforts. However, no brain-permeable CD13 inhibitor has yet been approved worldwide for clinical use,16 representing a critical gap in the translational landscape.

A New Alzheimer’s Target Emerges: Blocking One Protein Restores Memory in Mice

Researchers have identified a protein that links brain immune activity, metabolism, and amyloid clearance, suggesting a new way to enhance current Alzheimer’s treatments. Alzheimer’s disease can look like a set of grim headlines: soaring case counts, ballooning health care costs, and an aging pop

Mitochondrial specialization and signaling shape neuronal function

How neuronal function is shaped by mitochondria.

Despite the established links between mitochondrial dysfunction and neuronal disorders, the specialization of mitochondria to support the specific demands of neurons has been less extensively explored.

Proper mitochondrial positioning influences an array of neuronal functions and processes, from neurodevelopment through synaptic transmission, due to the participation of mitochondria as local ATP suppliers, Ca2+ sinks, and sites of neurotransmitter synthesis.

In neurons, mitochondria are also crucial for local translation in axons and dendrites, to which they provide both local ATP and mRNA transport. In this way, mitochondria emerge as centers for neuronal plasticity sciencenewshighlights ScienceMission https://sciencemission.com/Mitochondrial-specialization

Neurons are specialized cells designed to process information and transmit it, often across long distances. In many neurons, the axonal volume far exceeds the somato-dendritic volume, creating a need for long-range transport and local polarization mechanisms. In addition, action potential firing and restoration of ionic gradients, as well as dynamic changes in synaptic plasticity, further increase the energetic demands of neurons. In this review, we highlight the roles mitochondria play in vertebrate neuronal biology and how mitochondrial functionality is tuned to support the unique demands of neurons. We cover the influence of mitochondrial positioning, ATP generation and Ca2+ buffering on neuronal function, and explore the role of mitochondria in neurotransmitter metabolism and local protein translation.

Enhanced Selenium Supplement Extends Lifespan and Delays Multi‐Organs Aging by Regulating the Sik1 Pathway Through Maintaining Calcium Homeostasis

In healthy aging strategies, nutritional supplements synergize with optimized dietary and lifestyle interventions by modulating aging-related molecular pathways.[ 8, 9 ] Notably, NMN exerts multi-organ anti-aging effects by elevating NAD+ levels to activate the SIRT1 pathway, thereby significantly enhancing mitochondrial function while reducing oxidative stress and DNA damage.[ 10 ] Similarly, curcumin delays aging and related diseases through pleiotropic mechanisms involving oxidative stress regulation, anti-inflammatory actions, telomere maintenance, and sirtuin protein modulation.[ 11 ] However, practical applications face significant challenges: bioactive compounds like resveratrol and curcumin suffer from limited bioavailability due to poor aqueous solubility and first-pass metabolism, while excessive supplementation of antioxidants such as vitamins C/E may disrupt reactive oxygen species (ROS) signaling homeostasis, potentially inducing cellular toxicity or even increasing hemorrhagic risk.[ 12-14 ] Future development of anti-aging supplements should focus on: 1) innovative formulation strategies to enhance bioavailability; 2) optimized dosing regimens to minimize toxicity; and 3) long-term clinical studies to validate efficacy.

Selenium, an essential trace element with diverse biological activities, plays a critical role in healthy aging.[ 15-17 ] ≈1 billion people worldwide are affected by selenium deficiency, which is closely linked to neurological disorders, cardiovascular abnormalities, malignancies, and immune dysfunction.[ 18-20 ] Substantial evidence supports the anti-aging effects of selenium through multiple mechanisms: 1) Selenomethionine (SeMet) effectively suppresses Fe2+/H2O2- or Aβ-induced free radical generation, demonstrating therapeutic potential for Alzheimer’s disease characterized by oxidative stress;[ 21 ] 2) Selenium supplementation elevates serum GPx3 levels, a selenoprotein predominantly localized in the basement membrane of renal proximal tubules, modulating mitochondrial quality control pathways to mitigate heavy metal-induced renal aging;[ 22 ] and 3) Our recent findings reveal that selenium supplementation significantly attenuates age-related muscle atrophy by preserving redox homeostasis and regulating muscle protein metabolism.[ 23 ] Recent clinical trials in patients with advanced non-small cell lung cancer (NSCLC) demonstrated that oral administration of selenium nanoparticles (SeNPs) as a dietary supplement (200 µg day−1) in combination with Bev+AP chemotherapy significantly enhanced therapeutic outcomes compared to chemotherapy alone. The SeNPs combination group showed remarkable tumor regression, with progression disease rates decreasing dramatically from 50% to 0% and partial response rates increasing to 83.3%, along with significantly improved objective response rate and disease control rate.[ 24 ] Importantly, this regimen maintained excellent safety profiles without triggering fluctuations in pro-inflammatory or immunosuppressive cytokines. These compelling findings not only establish SeNPs as a safe and effective adjuvant therapy for advanced NSCLC but also provide valuable clinical translation data for nano-selenium formulations in oncology. Despite selenium’s proven benefits in reducing oxidative damage, maintaining genomic stability, and delaying telomere shortening, its narrow therapeutic window, limited bioavailability, and specific mechanisms in multi-organ protection during natural aging require further investigation.

Nanodelivery carriers have emerged as a next-generation platform for gene and drug delivery, offering tunable physicochemical properties such as size, composition, and surface modifications.[ 25 ] Our team has developed organically-bridged mesoporous silica nanoparticles (MSNs) by incorporating functional diselenide bonds into the silica framework at the molecular level, addressing the critical challenge of poor biodegradability in conventional silica materials.[ 26 ] This nanocarrier exhibits unique dual redox-responsive properties, allowing for more precise maintenance of redox homeostasis compared to traditional antioxidants, aligning with the core goal of preserving organismal homeostasis in anti-aging research. Building on this breakthrough, a comprehensive research framework was established: first, this study constructed a natural aging mouse model with MSNs, disulfide-bridged MSNs (SMSNs), commercially available SeMet as controls and then compared the effects of diselenide-bridged MSNs (SeMSNs) on lifespan extension, frailty delay, and multi-organ anti-aging. Next, key pathways and targets were identified through multi-organ transcriptome sequencing, followed by in-depth mechanistic studies. Finally, clinical translation was integrated by analyzing the correlation between serum selenium levels and aging biomarkers in the elderly, and validating the clinical effects of SeMSNs using primary adipose precursor cells (APCs) models. This systematic approach provides a solid theoretical foundation and clinical evidence for the application of nano-selenium in anti-aging research.

No current theory of consciousness is scientific

A letter by distinguished scientists directed at Integrated Information Theory sought to discredit a leading theory of consciousness as pseudoscience. That, argues Erik Hoel, was a mistake.

Hoel contends that as no theory of consciousness is currently empirically testable, it’s impossible for any of these theories to be scientific.

Hoel is a neuroscientist, neurophilosopher, and fiction writer. He’s been a close collaborator of Giulio Tononi, and a Forbes 30 under 30 in science.

“Consciousness, according to IIT, might be more widespread than we think, but it is neither universal nor arbitrary,” writes Hoel.

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