Lifeboat Foundation

Telomeres are the protective caps of our chromosomes and play a central role in the aging process. Shorter telomeres are associated with chronic diseases and high stress levels can contribute to their shortening. A new study now shows that if telomeres change in their length, that change is also reflected in our brain structure. This association was identified by a team of scientists including Lara Puhlmann and Pascal Vrtička from the Max Planck Institute for Cognitive Brain Sciences in Leipzig together with Elissa Epel from the University of California and Tania Singer from the Social Neuroscience Lab in Berlin as part of Singer’s ReSource Project.

Telomeres are protective caps at the ends of chromosomes that become shorter with each cell division. If they become so short that the genes they protect could be damaged, the cell stops dividing and renewing. Consequently, the cell is increasingly unable to perform its functions. This mechanism is one of the ways in which we age.

Telomere length is therefore regarded as a marker for the biological age of a person—in contrast to their chronological age. For two people of the same chronological age, the person with shorter telomeres has an increased risk of developing age-related diseases such as Alzheimer’s or cancer, and even a shorter life expectancy.

A recent review shows the current state of the industry with regards to using human pluripotent stem cells (hPSCs) to create cells that are useful for the study of, and therapies for, the human heart.

Pluripotent Stem Cells

Stem cells are the cells that form every other cell in the body, and adult humans naturally have native populations of stem cells to replace losses; the depletion of these reserves is stem cell exhaustion, which is one of the hallmarks of aging. To create stem cells from regular (somatic) cells, researchers use a technique called induced pluripotency, which creates induced pluripotent stem cells (iPSCs). However, purely naive, dedifferentiated pluripotent cells, which could create any cell in the body, are only of limited use and are not effective as a therapy. To form specific somatic cell lines, stem cells must first be differentiated into specific types.

Cells that become senescent irrevocably stop dividing under stress, spewing out a mix of inflammatory proteins that lead to chronic inflammation as more and more of the cells accumulate over time. Publishing in the September 24 edition of Cell Reports, researchers at the Buck Institute identified 44 specific senescence-associated proteins that are involved in blood clotting, marking the first time that cellular senescence has been associated with age-related blood clots.

“The incidence of venous thrombosis, which includes deep vein thrombosis and pulmonary embolism is extremely low until the age of 45, when it begins to rise rapidly. Over time it becomes a major risk factor for death. By 80, the condition affects five to six people per thousand individuals,” said Judith Campisi, PhD, Buck professor and senior co-author of the study. “Blood clots are also a serious side effect of chemotherapy, which sets off a cascade of senescence in those undergoing treatment. That’s why blood thinners, which carry their own risks, are often included in treatment protocols.”

Scientists in the Campisi lab and other labs around the world are working to develop senolytics, drugs which would clear senescent cells from the body, potentially providing treatment options for many age-related diseases that are either caused or linked to senescence. They include Alzheimer’s and Parkinson’s diseases, cardiovascular disease, osteoarthritis, macular degeneration, age-related cancers and sarcopenia, among others.

In this issue of Cell, Baar et al. show how FOXO4 protects senescent cell viability by keeping p53 sequestered in nuclear bodies, preventing it from inducing apoptosis. Disrupting this interaction with an all-D amino acid peptide (FOXO4-DRI) restores p53’s apoptotic role and ameliorates the consequences of senescence-associated loss of tissue homeostasis.

We’re continuing to release talks from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.

Dr. Kelsey Moody gave a detailed presentation on macular degeneration, discussing its origins in the lysosomes and how it progresses along with how his company, Ichor Therapeutics, is developing an exogenous enzyme treatment that may cure this crippling disease.

http://undoing-aging.org/videos/mike-west-presenting-at-undo…VDq1uEg-eQ

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We’re continuing to release talks from Ending Age-Related Diseases 2019, our highly successful two-day conference that featured talks from leading researchers and investors, bringing them together to discuss the future of aging and rejuvenation biotechnology.

In his talk, Reason of Repair Biotechnologies addressed the reasons why rejuvenation biotechnology is not proceeding as fast as it could be and discussed the ways in which his company is helping to expedite its development and release.

From the Errol Morris tv series First Person.

This episode features the eccentric Saul Kent, promoter of cryogenic immortality.