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Scientists reverse Alzheimer’s in mice using nanoparticles

A research team co-led by the Institute for Bioengineering of Catalonia (IBEC) and West China Hospital Sichuan University (WCHSU), working with partners in the UK, has demonstrated a nanotechnology strategy that reverses Alzheimer’s disease in mice.

Unlike traditional nanomedicine, which relies on nanoparticles as carriers for therapeutic molecules, this approach employs nanoparticles that are bioactive in their own right: “supramolecular drugs.” The work has been published in Signal Transduction and Targeted Therapy.

Instead of targeting neurons directly, the therapy restores the proper function of the blood-brain barrier (BBB), the vascular gatekeeper that regulates the brain’s environment. By repairing this critical interface, the researchers achieved a reversal of Alzheimer’s pathology in animal models.

Epigenetic shifts link maternal infection during pregnancy to higher risk of offspring developing schizophrenia

The health of mothers during pregnancy has long been known to play a role in the lifelong mental and physical health of offspring. Recent studies have found that contracting an infection during pregnancy can increase the risk that offspring will develop some neurodevelopmental disorders, conditions that are associated with the atypical maturation of some parts of the brain.

An infection is an invasion of pathogens, such as bacteria, viruses, fungi or parasites, which can then multiply and colonize host tissues. Findings suggest that when an expecting mother contracts an infection, her immune system can respond to it in ways that could impact the development of the fetus.

Researchers at University of Manchester and Manchester Metropolitan University recently carried out a study aimed at further investigating the processes through which maternal infections during pregnancy could increase the risk that offspring will develop schizophrenia later in life. Schizophrenia is a typically debilitating mental health condition characterized by hallucinations, false beliefs about oneself or the world (e.g., delusions) and cognitive impairments.

Synaptic changes in the brains of patients with frontotemporal dementia can be modeled in the laboratory

Neurons produced from frontotemporal dementia patients’ skin biopsies using modern stem cell technology recapitulate the synaptic loss and dysfunction detected in the patients’ brains, a new study from the University of Eastern Finland shows.

Frontotemporal dementia is a progressive neurodegenerative disease affecting the frontal and temporal lobes of the brain. The most common symptoms are , difficulties in understanding or producing speech, problems in movement, and psychiatric symptoms.

Often, has no identified genetic cause, but especially in Finnish patients, hexanucleotide repeat expansion in the C9orf72 gene is a common genetic cause, present in about half of the familial cases and in 20% of the sporadic cases where there is no family history of the disease.

Map of bacterial gene interactions uncovers targets for future antibiotics

Despite rapid advances in reading the genetic code of living organisms, scientists still face a major challenge today—knowing a gene’s sequence does not automatically reveal what it does. Even in simple, well-studied bacteria like Escherichia coli (better known as E. coli), about one-quarter of the genes have no known function. Traditional approaches—turning off one gene at a time and studying the effects—are slow, laborious, and sometimes inconclusive due to gene redundancy.

Researchers from the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine) and collaborators from the University of California, Berkeley (UC Berkeley) have developed a new technique called Dual transposon sequencing (Dual Tn-seq), which allows for rapid identification of genetic interactions. It maps how bacterial genes work together, revealing vulnerabilities that could be targeted by future antibiotics.

“This is like mapping the social network for ,” said Assistant Professor Chris Sham Lok To from the Infectious Diseases Translational Research Program and the Department of Microbiology and Immunology, NUS Medicine, who led the study. “We can now see which genes depend on each other, and which pairs of genes bacteria can’t live without. That’s exactly the insight we need for next-generation antibiotics.”

The AI Safety Expert: These Are The Only 5 Jobs That Will Remain In 2030! — Dr. Roman Yampolskiy

WARNING: AI could end humanity, and we’re completely unprepared. Dr. Roman Yampolskiy reveals how AI will take 99% of jobs, why Sam Altman is ignoring safety, and how we’re heading toward global collapse…or even World War III.

Dr. Roman Yampolskiy is a leading voice in AI safety and a Professor of Computer Science and Engineering. He coined the term “AI safety” in 2010 and has published over 100 papers on the dangers of AI. He is also the author of books such as, ‘Considerations on the AI Endgame: Ethics, Risks and Computational Frameworks’

He explains:
⬛How AI could release a deadly virus.
⬛Why these 5 jobs might be the only ones left.
⬛How superintelligence will dominate humans.
⬛Why ‘superintelligence’ could trigger a global collapse by 2027
⬛How AI could be worse than nuclear weapons.
⬛Why we’re almost certainly living in a simulation.

00:00 Intro.
02:28 How to Stop AI From Killing Everyone.
04:35 What’s the Probability Something Goes Wrong?
04:57 How Long Have You Been Working on AI Safety?
08:15 What Is AI?
09:54 Prediction for 2027
11:38 What Jobs Will Actually Exist?
14:27 Can AI Really Take All Jobs?
18:49 What Happens When All Jobs Are Taken?
20:32 Is There a Good Argument Against AI Replacing Humans?
22:04 Prediction for 2030
23:58 What Happens by 2045?
25:37 Will We Just Find New Careers and Ways to Live?
28:51 Is Anything More Important Than AI Safety Right Now?
30:07 Can’t We Just Unplug It?
31:32 Do We Just Go With It?
37:20 What Is Most Likely to Cause Human Extinction?
39:45 No One Knows What’s Going On Inside AI
41:30 Ads.
42:32 Thoughts on OpenAI and Sam Altman.
46:24 What Will the World Look Like in 2100?
46:56 What Can Be Done About the AI Doom Narrative?
53:55 Should People Be Protesting?
56:10 Are We Living in a Simulation?
1:01:45 How Certain Are You We’re in a Simulation?
1:07:45 Can We Live Forever?
1:12:20 Bitcoin.
1:14:03 What Should I Do Differently After This Conversation?
1:15:07 Are You Religious?
1:17:11 Do These Conversations Make People Feel Good?
1:20:10 What Do Your Strongest Critics Say?
1:21:36 Closing Statements.
1:22:08 If You Had One Button, What Would You Pick?
1:23:36 Are We Moving Toward Mass Unemployment?
1:24:37 Most Important Characteristics.

Follow Dr Roman:
X — https://bit.ly/41C7f70
Google Scholar — https://bit.ly/4gaGE72

You can purchase Dr Roman’s book, ‘Considerations on the AI Endgame: Ethics, Risks and Computational Frameworks’, here: https://amzn.to/4g4Jpa5

Neuroscientists can now predict dementia from the way you breathe in your sleep

Scientists have discovered that disrupted breathing during sleep, particularly conditions like sleep apnea, creates a measurable cascade of brain changes that predicts cognitive decline with startling accuracy.

Recent research analyzing over one million health records found that people with sleep-disordered breathing face between 1.3 and 5.11 times higher risk of developing various forms of dementia, depending on the specific condition.

The most dramatic finding: those with documented sleep breathing problems showed dementia risk ratios that peaked above five-fold for certain neurodegenerative diseases.

Biomaterials and cell-based therapy post spinal cord injury

Spinal cord injury (SCI) imposes a significant physical, social, and economic burden on millions of patients and their families worldwide. Although medical and surgical care improvements have decreased mortality rates, sustained recovery remains constrained. Cell-based therapies offer a promising strategy for neuroprotection and neuro-regeneration post-SCI. This article reviews the most promising preclinical approaches, encompassing the transplantation of embryonic stem cells (ESCs), mesenchymal stem cells (MSCs), neural stem cells (NSCs), oligodendrocyte progenitor cells (OPCs), Schwann cells (SCs), and olfactory ensheathing cells (OECs), along with the activation of endogenous pluripotency cell banking strategies. We also outline key ancillary strategies to enhance graft cell viability and differentiation, such as trophic factor assistance, engineered biomaterials for supportive scaffolds, and innovative methods for a synergistic effect in treatment, including promoting neuronal regeneration and reducing glial scars. We highlight the key aspects of SCI pathophysiology, the fundamental biology of cell treatments, and the advantages and limitations of each approach.

There are several approaches to treating spinal cord injuries that show great promise: Cellular therapies, which utilize a range of cells such as embryonic, neural, and mesenchymal stem cells, along with astrocytes, Schwann cells, olfactory ensheathing cells, and reprogrammed cells; The use of innovative biomaterials, including hydrogels, collagen, polycaprolactone fibers, and advanced 3D-printing technologies, provides valuable support for tissue repair.

Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy

Cellular senescence has gradually been recognized as a key process, which not only inhibits the occurrence of early tumors but also promotes advanced malignant progression through secretory and immunomodulatory functions. Initially, cellular senescence manifested as irreversible cell cycle arrest, but now it encompasses a broader phenotype regulated by the p53-p21CIP1 and p16INK4A-Rb pathways. Although secretory phenotypes related to aging can recruit immune effectors to clear new tumor cells, persistent senescent cell populations often trigger chronic inflammation, promoting immune escape and fibrosis. In this review, we first discuss the molecular underpinnings of cellular senescence, highlighting its induction pathways and diverse physiological or pathological roles. We then examine the composition of the tumor microenvironment, where senescent cells accumulate and secrete pro-inflammatory cytokines, reshaping immune surveillance and extracellular matrix architecture. Against this backdrop, we explore how aging clocks refine our understanding of individual susceptibility to malignancy by distinguishing biological from chronological aging. We also present current therapeutic prospects, including senolytic agents targeting senescent stromal cells that promote tumor growth, and the utilization of aging clock metrics to tailor immunotherapies more effectively for older patients. Finally, we consider the major challenges facing clinical translation, from standardizing multi-omics data pipelines to clarifying the ethical implications of measuring biological age. By bridging senescence biology with geroscience and cutting-edge oncology, we posit that aging clocks may catalyze a transformation in cancer care, enabling more personalized, effective, and age-conscious treatment strategies.

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