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Common anti-seizure drug prevents Alzheimer’s plaques from forming

At the heart of the new discovery is amyloid precursor protein (APP), a protein that plays important roles in brain development and synaptic formation. Abnormal processing of APP can lead to the production of amyloid‑beta peptides, which play a central role in the development of Alzheimer’s disease. The scientists found that how APP is trafficked also controls whether a neuron forms amyloid-beta 42.

During the synaptic vesicle cycle — a fundamental process that underlies every thought, movement, memory or sensation — levetiracetam binds to a protein called SV2A. This interaction slows down a step in which neurons recycle synaptic vesicle components from the cell’s surface. By pausing this recycling process, the drug enables APP to remain on the cell’s surface longer, diverting it away from the pathway that produces toxic amyloid‑beta 42 proteins.

“In our 30s, 40s and 50s, our brains are generally able to steer proteins away from harmful pathways,” the author said. “As we age, that protective ability gradually weakens. This is not a statement of disease; this is just a part of aging. But in brains developing Alzheimer’s, too many neurons go astray, and that’s when you get amyloid-beta 42 production. And then it’s tau (or ‘tangles’), and then it’s dead cells, then dementia, then neuroinflammation — and then it’s too late.”

To effectively prevent Alzheimer’s symptoms, high-risk individuals would need to begin taking levetiracetam “very, very early,” the author said, possibly up to 20 years before the new FDA-approved Alzheimer’s disease test would even capture mildly elevated levels of amyloid-beta 42.

“You couldn’t take this when you already have dementia because the brain has already undergone a number of irreversible changes and a lot of cell death,” the author said.

Leveraging its status as an FDA-approved and widely used drug, the team mined existing human clinical data to investigate whether Alzheimer’s patients who took levetiracetam experienced slowed cognitive decline. They obtained clinical data from the National Alzheimer’s Coordinating Center and conducted a correlative analysis, finding that Alzheimer’s patients who took levetiracetam were associated with a significant delay from the diagnosis of cognitive decline to death compared to those taking lorazepam or no/other anti-epileptic drugs. ScienceMission sciencenewshighlights.


This Research Article uncovers an unexpected function of iron regulatory protein 1 in metabolic regulation

Kostas Pantopoulos & team find mice that lack IRP1 have altered energy metabolism and are protected against metabolic syndrome pathologies:

The figure shows liver in Irp1-/- mice fed a high-fat diet have reduced fat content; stained with oil red O. MetabolicSyndrome.


1Lady Davis Institute for Medical Research, Jewish General Hospital and Department of Medicine, McGill University, Montreal, Quebec, Canada.

2Department of Biochemistry, Microbiology & Immunology, University of Ottawa, Ottawa, Ontario, Canada.

3Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec, Canada.

New lab technique can reverse chemical process linked with Alzheimer’s disease

An Oregon State University scientist and a team of undergraduate students have uncovered real-time insights into a chemical process linked with Alzheimer’s disease, paving the way toward better drug designs. The researchers used a molecule measuring technique to observe in a laboratory setting how certain metals can promote the protein clumping that leads to the blocked neural pathways associated with Alzheimer’s. Led by Marilyn Rampersad Mackiewicz, associate professor of chemistry in the OSU College of Science, the research team also watched molecules known as chelators disrupt or reverse the clumping. The findings are published in ACS Omega.

Alzheimer’s disease is the most common form of dementia, a chronic condition of impaired cognitive function that affects large numbers of older adults and their loved ones. According to the Centers for Disease Control and Prevention, Alzheimer’s is the sixth-leading cause of death for people age 65 and older.

In Alzheimer’s patients, aggregations of amyloid-beta proteins interrupt brain cells’ ability to communicate with each other. The brain needs certain metals to work properly, but problems arise when the metals are present in unbalanced quantities.

Abstract: Birt-Hogg-Dubé syndrome is largely characterized by pulmonary cysts, but disease models for this lung phenotype are lacking

Here, Elizabeth P. Henske report mTORC1 hyperactivation in cystic lungs from patients and validate its role in lung cyst formation using a novel pre-clinical model:

The figure shows lung mesenchymal and epithelial cell differentiation.


1Division of Pulmonary, Critical Care and Sleep Medicine; Department of Internal Medicine; University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.

2The Saban Research Institute, Children’s Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, California, USA.

3Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA.

‘It seemed to defy the laws of physics’: The everlasting ‘memory crystals’ that could slash data centre emissions

In the face of rising emissions from data centres, researchers are turning to micro-explosions in glass, and using DNA to solve big data’s big problem.

FDA Greenlights Life Biosciences’ Human Study, Setting Up Pivotal Test for Aging Theory from Harvard’s David Sinclair

…Life Biosciences, a biotech company co-founded by Sinclair, received the FDA’s approval to begin a human trial testing its gene therapy based on the Information Theory of Aging. The gene therapy is designed to rewind the clock and restore the function of dying cells…

…Life Biosciences’ gene therapy has been under development for quite a while. In the 1990s, David Sinclair first contended that the deterioration and loss of epigenetic information—chemical tagging patterns on DNA that regulate which genes are turned on and off—plays an important role in driving aging. Sinclair subsequently dubbed this contention the Information Theory of Aging. Fast forward to the present day, and Life Biosciences has produced a gene therapy that delivers three proteins, which Sinclair’s laboratory helped establish, to reset epigenetic information to a more youthful state.

‘It’s extremely exciting,’ Sinclair told Endpoints News. ‘It’s been over 30 years to get to this point, and we’re about to learn if all of that work is going to come to fruition this year.’


The FDA has greenlighted Life Biosciences’ first human trial testing whether their gene therapy can confer a near-total rejuvenating reset of cells.

Virus-based therapy boosts anti-cancer immune responses to brain cancer

A team led by investigators has shown that a single injection of an oncolytic virus—a genetically modified virus that selectively infects and destroys cancer cells—can recruit immune cells to penetrate and persist deep within brain tumors. The research, which is published in Cell, provides details on how this therapy prolonged survival in patients with glioblastoma, the most common and malignant primary brain tumor, in a recent clinical trial.

The oncolytic virus used in the team’s trial is made from a herpes simplex virus genetically altered so it can only make copies of itself in glioblastoma cells and not normal healthy cells. The virus spreads to a glioblastoma cell, kills it, and then makes a copy of itself that spreads again to another glioblastoma cell. Infection of cells with the virus also triggers an immune response. In the phase 1 trial of 41 patients with recurrent glioblastoma, the oncolytic virus treatment extended survival compared to historically reported survival, especially among those with pre-existing viral antibodies.

In their Cell study, the investigators examined the extent of this immune response in clinical trial participants. Their analysis revealed that the treatment induced long-term infiltration of immune T cells into patients’ tumors. Closer proximity of cytotoxic T cells with dying brain tumor cells was associated with longer patient survival after treatment. The therapy also expanded pre-existing T cells in the brain. ScienceMission sciencenewshighlights.

RNA-binding proteins and ribonucleoproteins as determinants of immunity

RNA-binding proteins (RBPs) considerably expand the information content of the genome and can determine the lifespan, localization and function of RNA, thereby controlling when, where and how much protein is produced. There is a growing body of evidence that links RBPs to specialized functions of immune cells and they can also mediate cell-autonomous immunity to foreign RNA and to misfolded self-RNAs. This Review examines how RBPs regulate the biogenesis and fate of mRNAs to mediate immune cell function and cell-autonomous immunity and their roles in immunodeficiency, autoimmunity and chronic inflammation.

The Secret to Fighting Alzheimer’s May Be Hiding in Your Muscles

The study’s findings suggest that the key to combating Alzheimer’s disease may lie not only in the brain but also in our muscles. Alzheimer’s disease (AD) is a progressive condition marked by memory loss and declining cognitive function, and there is still no cure. Among the many factors that inf

Atom-sized gates could transform DNA sequencing and neuromorphic computing

Scientists have taken a major step toward mimicking nature’s tiniest gateways by creating ultra-small pores that rival the dimensions of biological ion channels—just a few atoms wide. The breakthrough opens new possibilities for single-molecule sensing, neuromorphic computing, and studying how matter behaves in spaces barely larger than atoms.

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