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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 , and whether NAD+ boosters could have curative effects in patients with degenerative diseases, has remained elusive.

Ira Pastor, ideaXme life sciences ambassador, interviews Dr. Mark Wolff, Morton Amsterdam Dean, and Professor, Division of Restorative Dentistry, at the University of Pennsylvania, School of Dental Medicine.

Ira Pastor Comments:

So as frequent listeners of the ideaXme show know, we spend a lot of time talking about the theme of “healthy aging”, and the reality that aging, and related biological changes associated with aging, occur across all of the body’s cells, tissues, and organs, and these changes affect all structure and function of the body, including the teeth and gums, and as such, oral health is the focus of our show today.

The underlying processes of biological aging can dramatically affect oral health and many of the specific changes that occur over time in our bodies as we age (such as cells renewing at a slower rate, tissues become thinner and less elastic, bones become less dense and strong, our immune system become weaker, such that infection can occur more quickly and wound healing takes longer), can have major impact in the oral cavity (affecting tissue and bone in the mouth), as well as trickle down effects on the rest of the body.

Oral health problems in older adults include, but are not limited to: untreated tooth decay, gum disease, tooth loss, oral cancer, as well as exacerbated chronic disease associated with various co-morbid conditions and physiologic changes associated with aging (e.g., hypertension, diabetes mellitus).

Dr. Mark Wolff:

Researchers at the RIKEN Center for Biosystems Dynamics Research (BDR) in Japan have identified changes in the aging brain related to blood circulation. Published in the scientific journal Brain, the study found that natural age-related enlargement of the ventricles—a condition called ventriculomegaly—was associated with a lag in blood drainage from a specific deep region of the brain. The lag can be detected easily with MRI, making it a potential biomarker for predicting ventriculomegaly and the aging brain, which can then be treated quickly.

Ventriculomegaly is an abnormal condition in which fluid accumulates in the ventricles of the without properly draining, making them enlarged. Although ventricular enlargement within normal range is not itself considered a disease, when left unchecked it can lead to ventriculomegaly and dementia resulting from normal pressure hydrocephalus. In their study, the team found that ventriculomegaly was associated with changes in circulation of the brain. “We found an age-related perfusion timing shift in the brain’s venous systems whose lifespan profile was very similar to, but slightly preceded that of ventricular enlargement,” explains first author Toshihiko Aso.

After blood circulates through the brain providing necessary oxygen, the deoxygenated blood must return to the heart though our veins. This happens through two pathways, one draining blood from regions close to the surface of the brain, and the other from areas deep in the brain. By using MRI to measure changes in , the team at BDR recently found that as we age, the time it takes for blood to drain through these two pathways becomes out of sync. The result is a time lag between the deep drainage and the surface pathway, which increases with age.

Scientists at Sanford Burnham Prebys Medical Discovery Institute and Loma Linda University Health have demonstrated the promise of applying magnetic resonance imaging (MRI) to predict the efficacy of using human neural stem cells to treat a brain injury—a first-ever “biomarker” for regenerative medicine that could help personalize stem cell treatments for neurological disorders and improve efficacy. The researchers expect to test the findings in a clinical trial evaluating the stem cell therapy in newborns who experience a brain injury during birth called perinatal hypoxic-ischemic brain injury (HII). The study was published in Cell Reports.

“In order for stem cell therapies to benefit patients, we need to be thoughtful and scientific about who receives these treatments,” says Evan Y. Snyder, M.D., Ph.D., professor and director of the Center for Stem Cells and Regenerative Medicine at Sanford Burnham Prebys, and corresponding study author. “I am hopeful that MRI, which is already used during the course of care for these newborns, will help ensure that infants who experience HII get the best, most appropriate treatment possible. In the future, MRI could help guide the use of stem cells to treat—or in some instances, not treat—additional disorders such as spinal cord injury and stroke.”

Scientists now understand that, in many instances, human neural stem cells are therapeutic because they can protect living cells—in contrast to “re-animating” or replacing nerve cells that are already dead. As a result, understanding the health of brain tissue prior to a is critical to the treatment’s potential success. Tools that help predict the efficacy of neural stem cell therapy could increase the success of clinical trials, which are ongoing in people with Parkinson’s disease, spinal cord injury and additional neurological conditions, while also sparing people who will not respond to treatment from an invasive procedure that offers false hope.

An interdisciplinary team of researchers at the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at UCLA has developed a first-of-its-kind roadmap of how human skeletal muscle develops, including the formation of muscle stem cells.

The study, published in the peer-reviewed journal Cell Stem Cell, identified various cell types present in skeletal muscle tissues, from all the way to adulthood. Focusing on muscle progenitor cells, which contribute to muscle formation before birth, and muscle stem cells, which contribute to muscle formation after birth and to regeneration from injury throughout life, the group mapped out how the cells’ gene networks—which genes are active and inactive—change as the cells mature.

The roadmap is critical for researchers who aim to develop muscle stem cells in the lab that can be used in regenerative cell therapies for devastating muscle diseases, including muscular dystrophies, and sarcopenia, the age-related loss of muscle mass and strength.

If you are interested in age reversal, and you haven’t read Dr David Sinclair (Harvard Medical School) yet, then I’d recommend this research paper.

“Excitingly, new studies show that age-related epigenetic changes can be reversed with interventions such as cyclic expression of the Yamanaka reprogramming factors. This review presents a summary of epigenetic changes that occur in aging, highlights studies indicating that epigenetic changes may contribute to the aging process and outlines the current state of research into interventions to reprogram age-related epigenetic changes.”


The aging process results in significant epigenetic changes at all levels of chromatin and DNA organization. These include reduced global heterochromatin, nucleosome remodeling and loss, changes in histone marks, global DNA hypomethylation with CpG island hypermethylation, and the relocalization of chromatin modifying factors. Exactly how and why these changes occur is not fully understood, but evidence that these epigenetic changes affect longevity and may cause aging, is growing. Excitingly, new studies show that age-related epigenetic changes can be reversed with interventions such as cyclic expression of the Yamanaka reprogramming factors. This review presents a summary of epigenetic changes that occur in aging, highlights studies indicating that epigenetic changes may contribute to the aging process and outlines the current state of research into interventions to reprogram age-related epigenetic changes.

The term “epigenetics” is thrown around a lot. Originally, it was coined to describe heritable changes that were non-mendelian, but use of the term has evolved. These days, “epigenetics” more generally refers to all non-genomic information storage in cells including gene networks, chromatin structure and post-translational modifications to histones. With aging, there are distinct changes across the epigenome from DNA modifications to alterations in global chromatin organization. But key questions remain unanswered: How and why do these changes occur? Do these changes drive disease and aging? Are they reversible?

Genomic organization is determined by the complex structure of chromatin ( Figure 1 ). The basic unit of chromatin is the nucleosome, which is made up of 147 DNA base pairs wrapped around an octamer of histone proteins. This octamer usually comprises two copies each of H2A, H2B, H3 and H4 (Luger et al. 1997; Hansen 2002). Within nucleosomes, both histones and the DNA itself are subject to a range of chemical modifications that affect the chromatin structure and ultimately the expression of genes. Chromatin falls into one of two major subtypes: euchromatin, in which the chromatin is open and transcriptionally active and heterochromatin, in which the chromatin is tightly closed and transcriptionally silent (Wallrath 1998; Grewal and Moazed 2003). Regulating the epigenetic network are factors that modify chromatin including DNA- and histone-modifying enzymes, transcription factors, and the more recently identified noncoding RNAs (ncRNAs).

Neuroplasticity is the brain’s ability to change under the influence of experience and activities. Several aspects of neuroplasticity are noteworthy: neurogenesis (development of new nerve cells) and synaptogenesis (development of new contacts between nerve cells) among them. Neuroplasticity used to be thought of as a limited phenomenon, mostly restricted to the early years of life. More recently it has been demonstrated that neuroplasticity continues throughout life, even in advanced age. This provides the conceptual basis for a wide range of therapeutic efforts aiming to slow the detrimental effects of aging on the brain and to treat various brain disorders.

What are the factors influencing neuroplasticity? The question is compelling both as a scientific challenge and because of the therapeutic promise of neuroplasticity once we know how to control and harness it. Among such factors, the environmental factors influencing neuroplasticity are particularly intriguing. It turns out that a strong relationship exists between what people do with their brains and how their brains age.

Both anecdotal observations and formal research suggest that education confers a protective effect against dementia. Highly educated people are less likely to succumb to its effects. Robert Katzman was the first to note that the prevalence of dementia, including Alzheimer’s disease, is lower in people with advanced education. The MacArthur Foundation Research Network on Successful Aging sponsored a study of the predictors of cognitive change in older persons. Education emerged as by far the most powerful predictor of cognitive vigor in old age.