Criticism of a recent video denouncing resveratrol.
Following Doctor Brad Stanfield’s latest ‘why I stopped video’, this last one about resveratrol and pterostilbene, many of you asked for my opinion, well here it is.
Continue reading “Why Dr. Brad Stanfield Needed to Apologize” »
Humans are distinguished from other species by several aspects of cognition. While much comparative evolutionary neuroscience has focused on the neocortex, increasing recognition of the cerebellum’s role in cognition and motor processing has inspired considerable new research. Comparative molecular studies, however, generally continue to focus on the neocortex. We sought to characterize potential genetic regulatory traits distinguishing the human cerebellum by undertaking genome-wide epigenetic profiling of the lateral cerebellum, and compared this to the prefrontal cortex of humans, chimpanzees, and rhesus macaque monkeys. We found that humans showed greater differential CpG methylation–an epigenetic modification of DNA that can reflect past or present gene expression–in the cerebellum than the prefrontal cortex, highlighting the importance of this structure in human brain evolution. Humans also specifically show methylation differences at genes involved in neurodevelopment, neuroinflammation, synaptic plasticity, and lipid metabolism. These differences are relevant for understanding processes specific to humans, such as extensive plasticity, as well as pronounced and prevalent neurodegenerative conditions associated with aging.
Citation: Guevara EE, Hopkins WD, Hof PR, Ely JJ, Bradley BJ, Sherwood CC (2021) Comparative analysis reveals distinctive epigenetic features of the human cerebellum. PLoS Genet 17: e1009506. https://doi.org/10.1371/journal.pgen.
Editor: Takashi Gojobori, National Institute of Genetics, JAPAN.
A handful of companies are trying vastly different approaches to spin animal studies into the next big anti-aging therapy.
While the mitochondrion has long fascinated biologists and the sheer diversity of druggable targets has made it attractive for potential drug development, there has been little success translatable to the clinic. Given the diversity of inborn errors of metabolism and mitochondrial diseases, mitochondrially mediated oxidative stress (myopathies, reperfusion injury, Parkinson’s disease, ageing) and the consequences of disturbed energetics (circulatory shock, diabetes, cancer), the potential for meaningful gain with novel drugs targeting mitochondrial mechanisms is huge both in terms of patient quality of life and health care costs. In this themed issue of the British Journal of Pharmacology, we highlight the key directions of the contemporary advances in the field of mitochondrial biology, emerging drug targets and new molecules which are close to clinical application. Authors’ contributions are diverse both in terms of species and organs in which the mitochondrially related studies are performed, and from the perspectives of mechanisms under study. Defined roles of mitochondria in disease are updated and previously unknown contributions to disease are described in terms of the interface between basic science and pathological relevance.
Getting older is a fact of life. As we age, we can grow bigger, smarter and stronger. But at a certain point, our bodies often start to slow down. The idea behind why we age and why our bodies slow down is that we start to lose the ability to make enough energy to support all the different functions that our body carries out.
Hazel H. Szeto, MD, PhD, is a medical doctor and a research scientist. She may have found the answer to reversing the aging process by restoring a person’s ability to make energy. Szeto presented her work last month at Experimental Biology 2021.
To better understand Szeto’s discovery, we must first understand how the body makes energy. We produce energy in the form of a small molecule called adenosine triphosphate, or ATP. When ATP is broken down, it releases energy that allows our bodies to do work, such as contracting the muscles in our arms and legs so we can lift a box. Mitochondria are small structures in the cells that make ATP from the food we eat.
Join Aubrey de Grey and Vitalik Buterin on our fireside chat where they discuss and answer questions at the intersection of longevity and web3.
The AMA is hosted by VitaDAO — VitaDAO is the world’s first decentralized intellectual property collective.
Continue reading “Longevity Meets Blockchain — AMA with Aubrey de Grey and Vitalik Buterin” »
Skin aging is a multifactorial process consisting of two distinct and independent mechanisms: intrinsic and extrinsic aging. Youthful skin retains its turgor, resilience and pliability, among others, due to its high content of water. Daily external injury, in addition to the normal process of aging, causes loss of moisture. The key molecule involved in skin moisture is hyaluronic acid (HA) that has unique capacity in retaining water. There are multiple sites for the control of HA synthesis, deposition, cell and protein association and degradation, reflecting the complexity of HA metabolism. The enzymes that synthesize or catabolize HA and HA receptors responsible for many of the functions of HA are all multigene families with distinct patterns of tissue expression. Understanding the metabolism of HA in the different layers of the skin and the interactions of HA with other skin components will facilitate the ability to modulate skin moisture in a rational manner.
Keywords: hyaluronic acid, hyaluronic acid synthases, hyaluronidases, CD44, RHAMM, skin aging.
Human skin aging is a complex biological process, not yet fully understood. It is the result of two biologically independent processes. The first is intrinsic or innate aging, an unpreventable process, which affects the skin in the same pattern as it affects all internal organs. The second is extrinsic aging, which is the result of exposure to external factors, mainly ultraviolet (UV) irradiation, that is also referred to as photoaging.1 Intrinsic skin aging is influenced by hormonal changes that occur with age,2 such as the gradual decreased production of sex hormones from the mid-twenties and the diminution of estrogens and progesterone associated with menopause. It is well established that the deficiency in estrogens and androgens results in collagen degradation, dryness, loss of elasticity, epidermal atrophy and wrinkling of the skin.3
A clinical-stage leader in immune-stimulatory vaccines for cancer announced the publication of its favorable long-term Overall Survival (OS) data from a Phase I trial evaluating a universal cancer vaccine candidate, UV1, in combination with checkpoint inhibitor ipilimumab, in patients with metastatic malignant melanoma.
UV1 is a peptide-based vaccine inducing a specific T cell response against the universal cancer antigen telomerase.
Published in the Frontiers in Immunology journal on May 11, 2021, Norway-based Ultimovacs ASA’s UV1 vaccine candidate achieved the primary endpoints of safety and tolerability.
Not sure how novel.
Paolo Garagnani and colleagues, in collaboration with several research groups in Italy and a research team led by Patrick Descombes at Nestlé Research in Lausanne, Switzerland, recruited 81 semi-supercentenarians (those aged 105 years or older) and supercentenarians (those aged 110 years or older) from across the Italian peninsula. They compared these with 36 healthy people matched from the same region who were an average age of 68 years old.
Continue reading “People Who Live Beyond 105 Have Better DNA Repair” »
Scientists at UC San Francisco are learning how immune cells naturally clear the body of defunct—or senescent—cells that contribute to aging and many chronic diseases. Understanding this process may open new ways of treating age-related chronic diseases with immunotherapy.
In a healthy state, these immune cells —known as invariant Natural Killer T (iNKT) cells—function as a surveillance system, eliminating cells the body senses as foreign, including senescent cells, which have irreparable DNA damage. But the iNKT cells become less active with age and other factors like obesity that contribute to chronic disease.
Finding ways to stimulate this natural surveillance system offers an alternative to senolytic therapies, which to date have been the primary approach to removing senescent cells. It could be a boon to a field that has struggled with how to systemically administer these senolytics without serious side effects.
