A team at Harvard has identified molecules that restore protective caps on the tips of our chromosomes that regulate cells ageing.
Circa 2019 face_with_colon_three
Multipotent cells are critical to regenerative medicine and its associated deployment strategies. Localizing an abundant source of autologous, adult stem cells circumvents the immunological prohibitions of allogeneity and ethical dilemmas of embryologic stem cells, respectively. Classically, these cells have been described as mesenchymal stem cells (MSCs). In this chapter, we characterize adipose tissue as a unique source of MSCs because of its ubiquity, redundancy, and procurability. Specifically, lipoaspirates can be minimally processed to provide a heterogenous, cell-dense isolate – the stromal vascular fraction (SVF) – composed of terminally differentiated vessel-associated cell lines as well as putative progenitor cells. These cells have been cultured and expanded, giving rise to a dynamic cell line termed adipose-derived stromal cells (ASCs). SVF and ASC cell isolates are often administered by standard clinical routes including parenteral, topical application, and local injection in the clinical translational studies of cardiovascular ischemia, neurological injury, rheumatologic and orthopedic disease as well as advanced wound care and tissue engineering. These clinical applications raise safety concerns specific to administration, sequestration, and tumor growth augmentation. Further studies SVF and ASC cells are necessary to realize their potential in a regenerative medicine capacity.
Various stem cell sources are being explored to treat diabetes since the proof-of-concept for cell therapy was laid down by transplanting cadaveric islets as a part of Edmonton protocol in 2000. Human embryonic stem (hES) cells derived pancreatic progenitors have got US-FDA approval to be used in clinical trials to treat type 1 diabetes mellitus (T1DM). However, these progenitors more closely resemble their foetal counterparts and thus whether they will provide long-term regeneration of adult human pancreas remains to be demonstrated. In addition to lifestyle changes and administration of insulin sensitizers, regeneration of islets from endogenous pancreatic stem cells may benefit T2DM patients. The true identity of pancreatic stem cells, whether these exist or not, whether regeneration involves reduplication of existing islets or ductal epithelial cells transdifferentiate, remains a highly controversial area. We have recently demonstrated that a novel population of very small embryonic-like stem cells (VSELs) is involved during regeneration of adult mouse pancreas after partial-pancreatectomy. VSELs (pluripotent stem cells in adult organs) should be appreciated as an alternative for regenerative medicine as these are autologous (thus immune rejection issues do not exist) with no associated risk of teratoma formation. T2DM is a result of VSELs dysfunction with age and uncontrolled proliferation of VSELs possibly results in pancreatic cancer. Extensive brainstorming and financial support are required to exploit the potential of endogenous VSELs to regenerate the pancreas in a patient with diabetes.
Diabetes is one of the major non-communicable diseases in the world with majority of patients belonging to India, China and USA. Along with associated complications like heart disease and stroke, diabetes results in increased morbidity and mortality and it is expected that by the year 2025, India alone will have more than 70 million diabetics1,2. Diabetes is a metabolic disorder associated with progressive loss or dysfunction of β-cells of pancreas. Onset of type 1 diabetes mellitus (T1DM) occurs when the β-cell mass is reduced to less than 20 per cent due to autoimmune effect, whereas the declining β-cell mass is unable to meet the age-related increased insulin demands of the body in type 2 (T2DM) as a result of insulin resistance and in due course the β-cells are lost by apoptosis. Thus, in both T1 and T2DM, restoration of a functional β-cell mass constitutes the central goal of diabetes therapy.
A bit of transhuman fiction. It doesn’t take long.
What would it be like to live forever? Writer Richard Dooling explores this question in this fictional piece from Esquire.
Originally published May 1999. Published on KurzweilAI.net May 22, 2001.
1994
As people get older, they often feel less energetic, mobile or active. This may be due in part to a decline in mitochondria, the tiny powerhouses inside of our cells, which provide energy and regulate metabolism. In fact, mitochondria decline with age not only in humans, but in many species. Why they do so is not well understood. Scientists at the Max Planck Institute for Biology of Ageing in Cologne set out to understand how mitochondrial function is diminished with age and to find factors that prevent this process. They found that communication between mitochondria and other parts of the cell plays a key role.
For their studies, the scientists used the simple roundworm, Caenorhabditis elegans, an important model system for aging research. Over half the genes of this animal are similar to those found in humans, and their mitochondria also decline with age. From their research, the scientists found a nuclear protein called NFYB-1 that switches on and off genes affecting mitochondrial activity, and which itself goes down during aging. In mutant worms lacking this protein, mitochondria don’t work as well and worms don’t live as long.
Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. “We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity,” says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains.
A pre-print study reveals that young blood plasma given to older mice reduced aging by an average of 54% across multiple tissues; and had an impact on other signs of aging, such as cellular senescence, fat accumulation, and behavioural measures.
“We’ve wondered if it might be possible to simply rewind the aging clock without inducing pluripotency,” said Vittorio Sebastiano, assistant professor at Stanford University and senior author of the Nature Communications article. “Now we’ve found that tightly controlling the exposure to these proteins can promote rejuvenation in multiple human cell types, including stem cells. This has profound implications for regeneration and restoration of cell functionality of aged tissues.”
MOUNTAIN VIEW, Calif., March 25, 2020 /PRNewswire/ — A study published in the respected Nature Communications journal highlights the promise of technology being developed by Turn Biotechnologies to treat age-related health conditions.
The study by researchers at the Stanford University School of Medicine found that old human cells can be induced into a more youthful and vigorous state when they are exposed to a rejuvenating treatment that triggers the limited expression of a group of proteins known as Yamanaka factors, which are important to embryonic development.
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In the human world, if you make it up to 90 years old or more, you’re considered to have remarkable longevity. But in the animal world, 90 years old is still considered a baby’s age. Some of these creatures have been around for so long that nowadays they’re considered living fossils since dinosaurs are their direct relatives.
Bright Side is encouraging you to take a look at some creatures that have been on Earth way longer than the human species and some of them were born when the Age of Discovery had not even started. And there’s a surprising bonus waiting for you at the end of the article!
An international team of scientists, led by University of Helsinki reported that vitamin B3, niacin, has therapeutic effects in progressive muscle disease. Niacin delayed disease progression in patients with mitochondrial myopathy, a progressive disease with no previous curative treatments.
Vitamin B3 forms have recently emerged as potent boosters of energy metabolism in rodents. These vitamins are precursors for NAD+, a molecular switch of metabolism between fasting and growth modes.
As fasting has been shown promote health and longevity in for example mice, a variety of “NAD boosters” are being developed. However, whether actual NAD+ deficiency exists in human disease, and whether NAD+ boosters could have curative effects in patients with degenerative diseases, has remained elusive.
