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Category: biotech/medical

CRISPR-Based Screen Reveals Possible Anti-Tau Mechanism

This screening platform washed cells with a broad range of retroviruses to determine which ones affect tau. In follow-up testing, the gene CUL5 was singled out as being crucial for tau degradation. Mitochondrial function was also found to be a key part of preventing tau pathology.

Using an ingenious CRISPR-based screening technique, scientists have found a protein that tags tau for degradation and is more strongly expressed in tau-resilient neurons [1].

Some neurons are more equal than others

The accumulation of tau protein fibrils in neurons is a hallmark of Alzheimer’s and several other diseases [2]. Scientists have long noticed that even in the brains of people who died of Alzheimer’s, some neurons are markedly healthier than others, suggesting that neurons differ in how they handle tau and that these differences may explain selective vulnerability in tauopathies [3].

Epistasis study uncovers genetic interactions linked to heart disease

Euan Ashley’s lab explores the intricate interactions of gene variants. Tiny “typos,” or genetic mutations, can sneak into segments of DNA. Many of these are harmless, but some can cause health problems. Two or more genes can team up and change the outcome of a physical or molecular trait. This phenomenon, known as epistasis, occurs through complex interactions between genes that are functionally related—such as those that support protein creation.

Identifying these group dynamics provides crucial clues to how genetic diseases manifest and should be treated. But they’re not easily detected and often fly under the radar.

To help root out these connections, Ashley, MB ChB, DPhil, professor of genetics and of biomedical data science, and a team of scientists, including co-corresponding author Bin Yu, Ph.D., a professor of statistics and of electrical engineering and computer sciences at the University of California, Berkeley, have developed computational techniques to identify and understand the hidden ways epistasis influences inherited diseases.

Maternal microbiome compound may hold key to preventing liver disease

Children born to mothers who consume a high-fat, high-sugar diet during pregnancy and breastfeeding face a higher risk of developing fatty liver disease later in life.

New research from the University of Oklahoma suggests that risk may be reduced. A recent study has found that supplementing pregnant and lactating mice with a naturally occurring compound produced by healthy gut bacteria significantly lowered rates of fatty liver disease in their offspring as they aged.

The research is published in the journal eBioMedicine.

The Successor to CRISPR May Be Even More World Changing

When Feng Zhang was in his early 30s, he used a set of genes found in bacteria called CRISPR to pioneer a new kind of gene editing tool in human cells. Today, the MIT biochemist is studying a different set of microbial genes called TIGR. And they may be the key to developing CRISPR’s successor. For this SciShow Field Trips video, we traveled to Zhang’s lab to learn about what may be the next generation of gene editing.

High-risk EPN models present the immunotherapeutic target GD2 and are sensitive to GD2–CAR T cell therapy in vitro and in vivo

Research Letter: CAR T cells targeting the glycoprotein GD2 show potent antitumor efficacy in high-risk ependymoma models.

Antonio Carlos Tallon-Cobos & team establish a new ependymoma model for preclinical research and demonstrate a promising immunotherapeutic approach for this largely aggressive pediatric brain cancer.

1Princess Máxima Center for pediatric oncology, Utrecht, Netherlands.

2Hopp Children’s Cancer Center Heidelberg (KiTZ), Heidelberg, Germany.

3Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ) and German Consortium (DKTK), Heidelberg, Germany.

Immunotherapy could prevent the loss of neurons in Parkinson’s disease

Parkinson’s disease is characterized by the progressive loss of dopaminergic neurons in a specific brain region known as the substantia nigra. This neuronal degeneration is closely linked to inflammatory processes mediated by microglia, the immune cells of the central nervous system. However, the precise mechanisms that trigger this destructive process are still not fully understood.

Now, in an article published in npj Parkinson’s Disease, researchers from the Institut de Neurociències of the Universitat Autònoma de Barcelona (INc-UAB) and the UAB Department of Biochemistry and Molecular Biology report that brain tissue from Parkinson’s disease patients contains a higher proportion of reactive microglia, meaning cells that are primed to respond. But most importantly, these reactive microglial cells also show an increased density of receptors known as Fc gamma on their membranes.

Study maps 30 rheumatoid arthritis biopsies, linking joint scarring to treatment resistance

Rheumatoid arthritis (RA) is a common autoimmune disease where the body’s immune system mistakenly attacks the lining of its own joints, causing chronic pain, swelling, and stiffness. While there have been remarkable advancements in the treatment of RA with an array of therapies that target inflammation, a large subset of patients (approximately 6–28%) continue to experience difficult-to-manage symptoms of disease even after receiving multiple lines of treatment.

There is a critical need to identify new therapeutic approaches for patients who are refractory to existing treatment options.

By looking closely at the biology of joint tissue, researchers at the Mass General Brigham Department of Medicine conducted a study, published in Nature Immunology, focusing on discovering why some people with rheumatoid arthritis don’t respond well to standard treatments. The paper is titled “Spatial patterning of fibroblast TGFβ signaling underlies treatment resistance in rheumatoid arthritis.”

Scientists Uncover a Hidden Early Stage of Alzheimer’s That They Can Stop

The researchers suggested that higher concentrations of charged ions weaken the interaction between tau proteins and heparin, making cluster formation more difficult. This occurs because charged molecules such as tau and heparin become less able to interact due to electrostatic “screening,” which effectively masks their charges from one another.

A New Direction for Treating Neurodegenerative Disease

These results point toward a different strategy for developing therapies. Rather than attempting to break apart fully formed tau fibrils, future treatments could focus on blocking the reversible precursor stage before irreversible damage takes place. This approach could have implications beyond Alzheimer’s disease, potentially influencing research into other neurodegenerative disorders, including Parkinson’s disease.

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