Lifeboat Foundation

A groundbreaking scientific discovery changes what we know about dying.

The BACE1 enzyme has a rate-limiting role in the amyloidogenic pathway (see Glossary) and has been extensively studied for its neuronal functions[1]. Since 2000, intensive efforts have focused on developing small-molecule BACE1 inhibitors to reduce amyloid β (Aβ) production in Alzheimer’s disease (AD) brains. However, human clinical trials involving most BACE1 inhibitors were stopped at Phase 2/3 due to limited therapeutic benefits[2]. BACE1 inhibitors act by reducing Aβ-related pathologies in AD brains, that is, they are used to treat the symptoms rather than the underlying disease.

Summary: Researchers engineered cells containing customized adhesion molecules that bind to specific cell partners in predictable ways to form complex multicellular entities. The discovery is a major step toward building new tissue and organs.

Source: UCSF

Researchers at UC San Francisco (UCSF) have engineered molecules that act like “cellular glue,” allowing them to direct in precise fashion how cells bond with each other. The discovery represents a major step toward building tissues and organs, a long-sought goal of regenerative medicine.

Achieving a long-sought goal of regenerative medicine.

Researchers from the University of California, San Francisco, (UCSF) engineered molecules that function as “cellular glue,” enabling them to precisely direct how cells bond with each other. This is a significant step toward regenerative medicine’s long-term goal of creating new tissues and organs, according to a press release.

Adhesive molecules are naturally present in the body and keep the tens of trillions of cells together in organized patterns. They build neural networks, develop structures, and direct immune cells to specific areas of the body. Adhesion also makes cell communication easier to maintain the body functioning as a self-regulating whole.

Mayo Clinic researchers found a noncellular substance suggested improvement in restoring muscle function and bladder control in preclinical models. The teams of Atta Behfar, M.D., Ph.D. and Emanuel Trabuco, M.D., led this research in a collaboration between Mayo Clinic Departments of Cardiovascular Medicine and Obstetrics and Gynecology. The paper is published in NPJ Regenerative Medicine.

“Surgical treatment for stress urinary incontinence, a condition afflicting 25 million women, has significantly declined over concerns about negative side effects,” says Dr. Trabuco. “This has led many women to delay therapy and suffer needlessly. We hope to develop a minimally invasive, noncellular, exosome-based approach to muscle regeneration for urinary incontinence that not only targets the underlying cause of the condition but also avoids the problem with invasive surgical options presently available.”

The research team used regenerative purified exosome product, known as PEP, derived from platelets to deliver messages into the cells of preclinical models. Exosomes are extracellular vesicles that are like a delivery service moving cargo from one cell to another, with instructions for targeting exact tissues that need repair. The study suggests that the use of purified exosome product alleviates stress urinary incontinence from musculoskeletal breakdown in animals. The team did not detect any infection or off-target toxicity with application of PEP.

For people ages 75 and older, age-related changes in general health and in the heart and blood vessels require consideration and likely modifications in how heart attacks and heart disease are treated, according to a new American Heart Association scientific statement published today in the Association’s flagship, peer-reviewed journal Circulation.

The new statement, “Management of acute coronary syndrome (ACS) in the older adult population,” highlights recent evidence to help clinicians better care for patients over age 75. According to the statement, 30–40% of people hospitalized with ACS are age 75 or older. ACS includes heart attack and unstable angina (heart-related chest pain).

The statement is an update of a 2007 American Heart Association statement on the treatment of heart attacks in the elderly.

Northwestern University researchers have discovered a previously unknown mechanism that drives aging.

In a new study, researchers used artificial intelligence to analyze data from a wide variety of tissues, collected from humans, mice, rats and killifish. They discovered that the length of genes can explain most molecular-level changes that occur during aging.

All cells must balance the activity of long and short genes. The researchers found that longer genes are linked to longer lifespans, and shorter genes are linked to shorter lifespans. They also found that aging genes change their activity according to length. More specifically, aging is accompanied by a shift in activity toward short genes. This causes the gene activity in cells to become unbalanced.

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Northwestern University researchers have discovered a previously unknown mechanism that drives aging.

In a new study, researchers used artificial intelligence to analyze data from a wide variety of tissues, collected from humans, mice, rats and killifish. They discovered that the length of genes can explain most molecular-level changes that occur during aging.

Continue reading “Aging is driven by unbalanced genes” »