Lifeboat Foundation

https://paper.li/e-1437691924#/ https://www.nature.com/articles/s41591-019-0375-9

The hippocampus is one of the most affected areas in Alzheimer’s disease (AD). Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life. This process, called adult hippocampal neurogenesis (AHN), confers an unparalleled degree of plasticity to the entire hippocampal circuitry^3,4. Nonetheless, direct evidence of AHN in humans has remained elusive. Thus, determining whether new neurons are continuously incorporated into the human dentate gyrus (DG) during physiological and pathological aging is a crucial question with outstanding therapeutic potential. By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the DG of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages of AHN. In sharp contrast, the number and maturation of these neurons progressively declined as AD advanced. These results demonstrate the persistence of AHN during both physiological and pathological aging in humans and provide evidence for impaired neurogenesis as a potentially relevant mechanism underlying memory deficits in AD that might be amenable to novel therapeutic strategies.

A new review discusses how neutrophils release toxic substances into the body under inflammatory conditions, detailing one of the ways in which chronic inflammation causes long-term damage.

Casting a deadly NET

As we age, we suffer from the ever-increasing chronic inflammation known as inflammaging. This persistent, smoldering background of low-grade inflammation harms wound healing and promotes multiple age-related diseases. Senescent cells, a weakened immune system, and chronic infections are all proposed to contribute to inflammaging.

Continue reading “Chronic Inflammation Leads to Toxic NET Buildup” »

The presence of senescent cells has been implicated in a wide range of age-related diseases and even conditions such as T1 diabetes. Today, we want to draw your attention to a new publication that explores the relationship between senescent cells and intervertebral disc degeneration (IDD).

It was already known that senescent cells increase during the progression of IDD, but it was not known if they were a driver or a consequence of IDD.

The findings, published on February 18, 2019 in the journal Nature Medicine, highlight a novel CRISPR/Cas9 genome-editing therapy that can suppress the accelerated aging observed in mice with Hutchinson-Gilford progeria syndrome, a rare genetic disorder that also afflicts humans. This treatment provides important insight into the molecular pathways involved in accelerated aging, as well as how to reduce toxic proteins via gene therapy.

“Aging is a complex process in which cells start to lose their functionality, so it is critical for us to find effective ways to study the molecular drivers of aging,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and senior author of the paper. “Progeria is an ideal aging model because it allows us to devise an intervention, refine it and test it again quickly.”

With an early onset and fast progression, progeria is one of the most severe forms of a group of degenerative disorders caused by a mutation in the LMNA gene. Both mice and humans with progeria show many signs of aging, including DNA damage, cardiac dysfunction and dramatically shortened life span. The LMNA gene normally produces two similar proteins inside a cell: lamin A and lamin C. Progeria shifts the production of lamin A to progerin. Progerin is a shortened, toxic form of lamin A that accumulates with age and is exacerbated in those with progeria.

On July 11-12th, we return to the Cooper Union in New York City for our second annual Ending Age-Related Diseases conference, which focuses on the progress in aging research as well as the business side of biotech.

We will be bringing you the latest aging research, investment, and business knowledge from some of the top experts in the industry. We will be packing two days full of talks and discussion panels featuring the people who are developing the technologies that could change the way we regard and treat aging forever.

We are currently offering reduced ticket prices until March 31st, after which the price increases to the regular $400 cost. If you would like to take advantage of this special offer, head on over to our event ticket page to secure your place now.

Continue reading “Ending Age-Related Diseases Conference: March Update” »

A Harvard-led team is the first to demonstrate the ability to use low-power light to trigger stem cells inside the body to regenerate tissue, an advance they reported in Science Translational Medicine. The research, led by Wyss Institute Core Faculty member David Mooney, Ph.D., lays the foundation for a host of clinical applications in restorative dentistry and regenerative medicine more broadly, such as wound healing, bone regeneration, and more.

Earlier this year, we hosted the Ending Age-Related Diseases 2018 conference at the Cooper Union, New York City. This conference was designed to bring together the best in the aging research and biotech investment worlds and saw a range of industry experts sharing their insights.

Joe Betts Lacroix of Y Combinator and Vium discusses the different ways in which entrepreneurs can focus on overcoming the diseases of aging, namely direct, indirect, and money-first approaches, and the strengths and weakness of each.

Joe was the primary technical founder of hardware/software startup OQO, which entered the Guinness Book of World Records for building the smallest fully featured PC. His experience spans from biotech research to electronics design. Very experienced in invention, prosecution and monetization of intellectual property, he has over 80 patents granted and pending in fields ranging from biophysics and safety systems to antennas, thermal systems, user interfaces, and analog electronics. He has written numerous peer-reviewed publications in fields such as biophysics, genetics, electronics, and robotics. Joe holds a Harvard A.B., an MIT S.M. and a Caltech research fellowship.

A new publication from researchers at the University of Colorado Boulder shows how gut bacteria increase the risk of cardiovascular disease by contributing to the stiffening of the blood vessels during aging. This study is the first to demonstrate that changes to the gut microbiome promote vascular aging and harm health [1].

The researchers treated groups of young and old mice with a range of antibiotics that are known to kill gut bacteria. Following this, they examined the vascular systems of the mice, particularly the lining of the blood vessels (endothelium) and the stiffness in their large arteries. Additionally, the researchers measured a number of biomarkers, including free radicals, antioxidants, pro-inflammatory cytokines, and nitric oxide in the blood.

After 3–4 weeks of treatment, the researchers once again measured the biomarkers and looked at the vascular system. There was no change in the young group of mice; however, the old mice saw significant improvement in both vascular health and biomarkers. The researchers note that the treatment had suppressed the microbiome of the aged mice and, in doing so, improved their health. Therefore, they concluded that something in the microbiome of old mice was contributing to vascular aging.