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The researchers turned to a group of molecules called acylcarnitines, which are associated with declining cognition and breaking down or metabolizing fats and proteins for energy. To test if high acylcarnitine levels in the blood could predict who’s at risk of developing Alzheimer’s, the researchers used data from a large-scale study called the Alzheimer’s Disease Neuroimaging Initiative.

“It was fascinating,” the author said. “Dividing research participants into groups based on their specific acylcarnitine levels highlighted people with more severe Alzheimer’s disease and others with fewer symptoms.” This led the researchers to define a bioenergetic clock based on acylcarnitines—how old a person’s metabolism acts, compared to actual age. Higher bioenergetic age is linked to higher acylcarnitine levels, worsened Alzheimer’s pathology, cognitive decline and brain atrophy.

The researchers also quantified cognitive decline using a common test called the mini-mental state examination, on which a score below 24 out of 30 points indicates impairment. They found that people with low acylcarnitine levels to begin with declined more slowly, losing about 0.5 points less per year than people with high acylcarnitine levels. The benefit is on par with the Alzheimer’s drug lecanemab.

To some degree, a person’s bioenergetic clock ticks forward at a rate determined by their genetics, but having a healthy lifestyle—for example, eating a plant-based diet and exercising —can help keep acylcarnitine levels low, which means a younger bioenergetic age, the author explained.

They went on to identify a subgroup of participants, about 30% of the Alzheimer’s Disease Neuroimaging Initiative, with older bioenergetic age but favorable genetic background. These individuals may benefit more from early lifestyle interventions designed to decrease their bioenergetic age and potentially delay or prevent the onset of Alzheimer’s.

Moving forward, the senior author hopes to home in on the lifestyle interventions most effective for lowering bioenergetic age. For example, eating a low-carb diet may help maintain metabolic health, but just how low would carbohydrate consumption have to be for a person to see benefits?


Like people, bacteria get invaded by viruses. In bacteria, the viral invaders are called bacteriophages, derived from the Greek word for bacteria-eaters, or in shortened form, “phages.” Scientists have sought to learn how the single-cell organisms survive phage infection in a bid to further understand human immunity and develop ways to combat diseases.

Now, Johns Hopkins Medicine scientists say they have shed new light on how bacteria protect themselves from certain phage invaders—by seizing genetic material from weakened, dormant phages and using it to “vaccinate” themselves to elicit an immune response.

In their experiments, the scientists say Streptococcus pyogenes bacteria (which cause ) take advantage of a class of phages known as temperate phages, which can either kill cells or become dormant. The bacteria steal from temperate phages during this dormant period and form a biological “memory” of the invader that their offspring inherit as the bacteria multiply. Equipped with these memories, the new population can recognize these viruses and fight them off.

A drug-resistant type of bacteria that has adapted to health care settings evolved in the past several years to weaponize an antimicrobial genetic tool, eliminating its cousins and replacing them as the dominant strain. University of Pittsburgh School of Medicine scientists made the discovery when combing through local hospital data—and then confirmed that it was a global phenomenon.

The finding, published in Nature Microbiology, may be the impetus for new approaches in developing therapeutics against some of the world’s deadliest . It also validates a new use for a system developed at Pitt and UPMC that couples genomic sequencing with computer algorithms to rapidly detect infectious disease outbreaks.

“Our lab has a front row seat to the parade of pathogens that move through the ,” said senior author Daria Van Tyne, Ph.D., associate professor of medicine in Pitt’s Division of Infectious Diseases. “And when we took a step back and zoomed out, it quickly became apparent that big changes were afoot with one of the world’s more difficult-to-treat bacteria.”

Memory engrams are formed through experience-dependent plasticity of neural circuits, but their detailed architectures remain unresolved. Using three-dimensional electron microscopy, we performed nanoscale reconstructions of the hippocampal CA3-CA1 pathway after chemogenetic labeling of cellular ensembles recruited during associative learning. Neurons with a remote history of activity coinciding with memory acquisition showed no strong preference for wiring with each other. Instead, their connectomes expanded through multisynaptic boutons independently of the coactivation state of postsynaptic partners. The rewiring of ensembles representing an initial engram was accompanied by input-specific, spatially restricted upscaling of individual synapses, as well as remodeling of mitochondria, smooth endoplasmic reticulum, and interactions with astrocytes.

Long non-coding RNAs (long ncRNAs,) are a type of RNA, generally defined as transcripts more than 200 nucleotides that are not translated into protein.

Long non-coding transcripts are found in many species.

LncRNAs are extensively reported to be involved in transcriptional regulation, and epigenetic regulation.

Long non coding RNA has been proven to be associated with multiple diseases, such as cardiovascular diseases, rheumatic diseases, cancer etc.

More detailed information ons are provided in the link below.

As the race between U.S. and Chinese biotech companies heats up, the competition is particularly fierce in one field: CRISPR gene editing.

China has rapidly emerged as a global leader in CRISPR research. While much of the initial focus in the industry was on the use of the technology to develop cancer treatments, Chinese biotech firms have since moved to apply it to test therapies for rare diseases, including sickle cell disease and inherited eye disorders.

In many areas, Chinese companies have been more aggressive, pushing into diseases that their U.S. counterparts have shied away from, including in Duchenne muscular dystrophy and herpes virus. That willingness has raised eyebrows among some executives and academics in the U.S., while exciting others who fear the American regulators and companies have been too conservative.

Glioblastoma (GBM) is a highly aggressive and malignant brain tumor with a poor prognosis. Treatment options are limited, and the development of effective therapeutics is a major challenge. Here are some current and emerging therapeutic strategies for GBM:

Current Therapies 1. Surgery: Surgical resection is the primary treatment for GBM, aiming to remove as much of the tumor as possible. 2. Radiation Therapy: Radiation therapy is used to kill remaining tumor cells after surgery. 3. Temozolomide (TMZ): TMZ is a chemotherapy drug that is used to treat GBM, often in combination with radiation therapy. 4. Bevacizumab (Avastin): Bevacizumab is a monoclonal antibody that targets vascular endothelial growth factor (VEGF) to inhibit angiogenesis.

Emerging Therapies 1. Immunotherapy: Immunotherapies, such as checkpoint inhibitors (e.g., PD-1/PD-L1 inhibitors) and cancer vaccines, aim to stimulate the immune system to attack GBM cells. 2. Targeted Therapies: Targeted therapies focus on specific molecular pathways involved in GBM, such as the PI3K/AKT/mTOR pathway. 3. Gene Therapy: Gene therapies aim to introduce genes that can help kill GBM cells or inhibit tumor growth. 4. Oncolytic Viruses: Oncolytic viruses are engineered to selectively infect and kill GBM cells. 5. CAR-T Cell Therapy: CAR-T cell therapy involves genetically modifying T cells to recognize and attack GBM cells. 6. Small Molecule Inhibitors: Small molecule inhibitors target specific proteins involved in GBM, such as EGFR, PDGFR, and BRAF.

Researchers have corrected a disease-causing gene mutation with a single infusion carrying a treatment that precisely targeted the errant gene.

This was the first time a mutated gene has been restored to normal.

The small study of nine patients announced Monday by the company Beam Therapeutics of Cambridge, Mass., involved fixing a spelling error involving the four base sequences — G, A, C and T — in DNA. The effect was to change an incorrect DNA letter to the right one. The result was a normal gene that functioned as it should, potentially halting liver and lung damage of patients with a rare disorder.


The small study in patients with a rare disorder that causes liver and lung damage showed the potential for precisely targeted infusions.