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Category: biotech/medical – Page 37

Alzheimer’s disease pathogenesis: standing at the crossroad of lipid metabolism and immune response

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by macroscopic features such as cortical atrophy, narrowing of the gyri, widening of the sulci, and enlargement of the ventricles. At the cellular level, the pathological characteristics include the extracellular aggregation of β-amyloid (Aβ) forming senile plaques, and the intracellular accumulation of hyperphosphorylated tau proteins forming neurofibrillary tangles. AD leads to the progressive decline of cognitive, behavioral, and social abilities, with no effective treatment available currently. The pathophysiology of AD is complex, involving mechanisms such as immune dysregulation and lipid metabolism alterations. Immune cells, such as microglia, can identify and clear pathological aggregates like Aβ early in the disease.

A more realistic look at DNA in action

The background

Most biochemistry labs that study DNA isolate it within a water-based solution that allows scientists to manipulate DNA without interacting with other molecules. They also tend to use heat to separate strands, heating the DNA to over 150 degrees Fahrenheit, a temperature a cell would never naturally reach. By contrast, in a living cell DNA lives in a very crowded environment, and special proteins attach to DNA to mechanically unwind the double helix and then pry it apart.

New Insights Into How Neural Stem Cells Age

Researchers publishing in Aging Cell have used single-cell transcriptomics to discover new insights into how neural stem cells (NSCs) change with aging.

Adults do generate neurons

The adult brain does generate new neurons [1], particularly in the hippocampus, the part of the brain responsible for memory formation [2]. Neurogenesis is limited to very specific niches, however, and does not occur across the entire brain [3]. This is accomplished by NSCs, cells that can differentiate into neural progenitors (NPs), which can themselves differentiate into both neurons and astrocytes and have less ability to proliferate [4]. Astrocytes are helper cells that support neurons’ connections and metabolism [5].

Study finds protein droplets shield fragile DNA from repair errors

When DNA breaks inside the cell, it can spell disaster, especially if the damage occurs in areas of the genome that are difficult to repair. Now, scientists Irene Chiolo and Chiara Merigliano at the USC Dornsife College of Letters, Arts and Sciences have discovered that a protein called Nup98, long known for helping traffic molecules in and out of the cell’s nucleus, plays another surprising role: guiding the cell’s most delicate repairs and reducing the risk of genetic mistakes that can lead to cancer. Their findings were published in Molecular Cell.

With support from the National Institutes of Health, the National Science Foundation, and the American Cancer Society, the researchers revealed that Nup98 forms droplet-like structures deep inside the nucleus. These “condensates” act as protective bubbles around broken strands of DNA in areas called heterochromatin—zones where the genetic material is so tightly packed that making accurate repairs is especially challenging.

Heterochromatin—a major focus of Chiolo’s research—is filled with repeated DNA sequences, making it easy for the cell to confuse one stretch for another. Nup98’s droplets help lift the damaged section out of that dense zone and create a safer space where it can be repaired accurately, reducing the chance of genetic mix-ups that could lead to cancer.

How artificial retinas could cure blindness | Dante Muratore | TEDxRoma

In this TEDx talk, Dante Muratore shows the transformative potential of brain-computer interfaces. He explains how they can be used to help patients suffering from neurodegenerative diseases, focusing on an artificial retina he and his team are developing to cure blindness in patients with macular degeneration and retinitis pigmentosa. He also describes how brain-computer interfaces will change what it means to be human in the future and challenges us to think deeply about the use we want to make of this technology in society.

Professor of Bioelectronics at Delft University of Technology, where he leads the Smart Brain Interfaces group. His research group explores hardware and system solutions for brain-computer interfaces capable of interacting with the nervous system. The group is working, in collaboration with leading universities in the field, on a microchip to be implanted in the retina to improve the lives of people affected by retinitis pigmentosa and degenerative maculopathy.

This talk was given at a TEDx event using the TED conference format but independently organized by a local community.

Artificial intelligence in prostate cancer

Artificial intelligence (A.I.) has recently become a buzzword in so many aspects of our lives, but it has been used to some degree in health care for a while. One area of health care where A.I. has made significant strides is the diagnosis and treatment of prostate cancer.

“We are just at the tip of the iceberg of utilizing A.I. for prostate cancer,” says Dr. David D. Yang, a radiation oncologist with Harvard-affiliated Brigham and Women’s Hospital and Dana-Farber Cancer Institute. “So far, it has been shown to help improve the care for men with prostate cancer in limited, yet effective ways.”

Pausing cell death can change space travel, human aging: Study

Dr Keith Siew, one of the study authors, says, “Nobody really likes talking about death, even cell death, which is perhaps why the physiology of death is so poorly understood. And in a way necrosis is death. If enough cells die, then tissues die, then we die. The question is what would happen if we could pause or stop necrosis.”

“Necrosis remains one of the last frontiers in medicine – a common thread across aging, disease, space biology, and scientific progress itself,” adds Dr Carina Kern, lead author of the study.

Necrosis occurs when cells are overwhelmed by injury, infection, or stress. The process floods cells with calcium, disrupting vital functions and causing the cell to rupture. This sudden collapse spills toxic molecules into surrounding tissue, triggering inflammation and accelerating damage.

Sickle cell disease induces chromatin introversion and ferroptosis in CD8+ T cells to suppress anti-tumor immunity

How sickle cell disease suppresses antitumor immunity.

Sickle cell disease (SCD) have a higher risk of developing certain cancers than the general population, but the mechanisms driving this increased risk remain unclear.

SCD inhibits CD8+ T cell function in the tumor microenvironment, potentially affecting cancer immunotherapy.

The researchers reveal that SCD alters the 3D genome architecture of CD8+ T cells, triggering ferroptosis and impairing antitumor response resulting in reduced expression of anti-ferroptotic genes, including SLC7A11 and hydrogen sulfide (H2S) biogenesis genes, thereby increasing susceptibility to ferroptosis.

They also demonstrate that hydrogen sulfide treatment rescued SLC7A11 expression, mitigated ferroptosis and enhanced immune and anti-tumor responses, thereby offering new avenues for precision immunotherapy in patients with inherited disorders. https://sciencemission.com/Sickle-cell-disease

Sickle cell disease (SCD) inhibits CD8+ T cell function in the tumor microenvironment, potentially affecting cancer immunotherapy. Zhao, Hu, Deng, et al. reveal that SCD alters the 3D genome architecture of CD8+ T cells, triggering ferroptosis and impairing anti-tumor responses, which can be reversed by hydrogen sulfide treatment, offering new avenues for precision immunotherapy in patients with inherited disorders.

Continue reading “Sickle cell disease induces chromatin introversion and ferroptosis in CD8+ T cells to suppress anti-tumor immunity” | >