Toggle light / dark theme

James Kirkland: Senolytics have a 20% chance of success

One of the hallmarks of aging, cellular senescence is what happens when aging cells do not die in the usual way (a process known as apoptosis) and start to accumulate in our bodies. The accumulation of these “senescent” cells is implicated in diseases including dementias, atherosclerosis, cancers, diabetes and arthritis. But senescence is not just part of the aging process – it tends to occur in individuals who develop frailty and multiple illnesses, and this can occur at any point during life.

In 2015, a team of researchers at the Mayo Clinic, led by Dr James L Kirkland, published a seminal paper in Aging Cell that introduced a new class of drugs called senolytics. Based on the idea that removing senescent cells may enhance human healthspan, these drugs were identified based on their ability to selectively target and eliminate those cells.

Longevity. Technology: Since the discovery of the first senolytics, hundreds of others have since been identified or created, and senotherapeutics is now one of the hottest areas in longevity, with a host of clinical trials under way and companies pursuing senolytic therapies for a range of age-related conditions. But what does the man who started it all think about the therapeutic field he helped create? In the first of two articles, we bring you Dr Kirkland’s unique perspective on the world of senolytics.

Groundbreaking Research Exposes Immune System’s “Off Button”

Scientists have discovered what turns off the molecular alarm system that plays a critical role in our immune response.

The antibacterial superhero MR1 (MHC class I-related molecule) is a protein found in every cell of the human body that functions as a molecular alarm system, alerting powerful cells of our immune system, our white blood cells, when cancer or bacterial infection is present.

While prior groundbreaking research revealed the cellular machinery that MR1 depends on to activate, nothing was understood about how the MR1 alarm is “turned off” until now.

UC study: Decreased proteins, not amyloid plaques, tied to Alzheimer’s disease

New research from the University of Cincinnati bolsters a hypothesis that Alzheimer’s disease is caused by a decline in levels of a specific protein, contrary to a prevailing theory that has been recently called into question.

UC researchers led by Alberto Espay, MD, and Andrea Sturchio, MD, in collaboration with the Karolinska Institute in Sweden, published the research on Oct. 4 in the Journal of Alzheimer’s Disease.

The research is focused on a protein called amyloid-beta. The protein normally carries out its functions in the brain in a form that is soluble, meaning dissolvable in water, but it sometimes hardens into clumps, known as amyloid plaques.

X·terroir

The advanced Computer Vision and Artificial Intelligence technologies in X·TERROIR allow enologists to make optimal decisions about the wine destination of grapes.

X·TERROIR technology makes possible cost-effective phenotypic profiling of every vine in the vineyard. This is an exponential increase over what is possible with current technology. The more information that Enologists have to work their magic… the more quality and value they can extract from the vineyard.

Transcript:

To the naked eye, this vineyard looks homogeneous. One might assume that a vineyard like this will produce grapes that are fairly uniform in aromatic profile.
The reality is very different.

The grapes from this vine, will produce a different wine than the vines that are only 50 meters away. Plant genomics, varying soil types, cultural interventions, micro-climate, and even disease result in a substantial variety of aromatic expressions in a single vineyard.

So the grapes that this vine will produce will embody the unique complexity of the aromatic expressions of the soil, climate, and cultural interventions of its own micro-terroir.

A Universal Cancer Treatment?

Himanshu Brahmbhatt was staring at the results of a clinical trial that looked too good to be true. A co-founder and CEO of EnGeneIC, a biopharmaceutical company, Brahmbhatt was running a small trial that was testing a fundamentally different approach to fighting cancer. Patients in the group had grim prospects. They had exhausted all other options. With nothing left to lose and not expecting any miracles, they enrolled in the trial. They wanted to give it one more chance. Now their scans showed their tumors had stopped progressing. Even more remarkable was they didn’t have the same type of tumors. They had malignancies affecting different organs—lungs, bladders, colons, pancreases—and yet, they uniformly did well.

“These people were facing death,” Brahmbhatt says. “Then we started seeing that they were actually succeeding. You could see in the scan that the tumor has stopped growing. It was a feeling of such extreme internal joy that it’s very difficult to describe.”

The results may have appeared miraculous, but they were anything but. They stemmed from fundamental research into cell division that forms the basis of the EnGeneIC process. A longtime advisor to the company, Bruce Stillman, professor of biochemistry and president and CEO of Cold Spring Harbor Laboratory, has been studying the process of DNA replication, which plays a key role in cell division and cancer progression.

Ancestral Heritage and Cancer: New Connection Discovered

Two groundbreaking studies recently published in the journals Nature and Genome Medicine found genetic signatures that explain ethnic disparities in the severity of prostate cancer, notably in Sub-Saharan Africa.

By genetically analyzing prostate cancer tumors from Australian, Brazilian, and South African donors, the team developed a new prostate cancer taxonomy (classification scheme) and cancer drivers that not only distinguish patients based on their genetic ancestry but also predict which cancers are likely to become life-threatening, a task that is currently difficult.

“Our understanding of prostate cancer has been severely limited by a research focus on Western populations,” said senior author Professor Vanessa Hayes, genomicist and Petre Chair of Prostate Cancer Research at the University of Sydney’s Charles Perkins Centre and Faculty of Medicine and Health in Australia. “Being of African descent, or from Africa, more than doubles a man’s risk for lethal prostate cancer. While genomics holds a critical key to unraveling contributing genetic and non-genetic factors, data for Africa has till now, been lacking.”

Discovery of a New Rare Blood Type Could Save The Lives of Future Newborns

The devastating loss of a pair of newborns has provided critical insights into a rare set of blood types spotted for the first time in humans 40 years ago.

By unravelling the molecular identity of the relatively new blood type known as the Er system, a new study could hopefully prevent such tragedies in the future.

“This work demonstrates that even after all the research conducted to date, the simple red blood cell can still surprise us,” says University of Bristol cell biologist Ash Toye.

Second Stem Cell Type Discovered in Mouse Brain

Summary: A newly discovered second stem cell population in the mouse brain is responsible for the production of new neurons in the olfactory bulb of adult mice.

Source: Heidelburg University.

In the brain of adult mammals, neural stem cells ensure that new nerve cells, i.e. neurons, are constantly formed. This process, known as adult neurogenesis, helps mice maintain their sense of smell.

Omega-3’s Linked to Improved Brain Structure and Cognition at Midlife

Summary: Boosting omega-3 fatty acid intake helps to preserve brain health and improve cognition in middle age, a new study reports. For those with the Alzheimer’s associated APOE4 gene, omega-3 fatty acid intake was associated with greater hippocampal volume and less small vessel disease.

Source: UT San Antonio.

Eating cold-water fish and other sources of omega-3 fatty acids may preserve brain health and enhance cognition in middle age, new evidence indicates.

Lab-grown ‘mini-brains’ suggest COVID-19 virus can infect human brain cells

A multidisciplinary team from two Johns Hopkins University institutions, including neurotoxicologists and virologists from the Bloomberg School of Public Health and infectious disease specialists from the school of medicine, has found that organoids (tiny tissue cultures made from human cells that simulate whole organs) known as “mini-brains” can be infected by the SARS-CoV-2 virus that causes COVID-19.

The results, which suggest that the virus can infect human cells, were published online June 26, 2020, in the journal ALTEX: Alternatives to Animal Experimentation.

Early reports from Wuhan, China, the origin of the COVID-19 pandemic, have suggested that 36% of patients with the disease show , but it has been unclear whether or not the virus infects human brain cells. In their study, the Johns Hopkins researchers demonstrated that certain human neurons express a receptor, ACE2, which is the same one that the SARS-CoV-2 virus uses to enter the lungs. Therefore, they surmised, ACE2 also might provide access to the brain.

/* */