There are lots of exciting companies working in the aging field, and it’s a great time to tell you about some of the more interesting ones. Most of these companies are a while away from human trials yet, but their innovations could possibly be truly game changing.
Atherosclerosis is the number one killer worldwide, and it currently has no totally effective solution. There are three ways in which current medicine tries to address it: Lifestyle changes, including diet and exercise; drugs that slow down the rate of cholesterol accumulation; and interventions such as stents and bypass surgery.
Chip Walter’s new book is titled “Immortality Inc.: Renegade Science, Silicon Valley Billions and the Quest to Live Forever.” It’s about the money, and the research, that’s seeking a way to extend human life indefinitely.
Chip Walter discusses “Immortality, Inc.” at Pittsburgh Arts & Lectures: 6 p.m. Thu., Jan. 16. Carnegie Library of Pittsburgh Main Branch, 4400 Forbes Ave., Oakland.
Sounds like science fiction, but Walter thinks breakthroughs are just around the corner.
What the reasons underlying these impairments are is yet unclear but scientists at the Center for Regenerative Therapies of TU Dresden (CRTD) wanted to investigate if increasing the number of stem cells in the brain would help in recovering cognitive functions, such as learning and memory, that are lost during ageing.”
Ein jeder wird es irgendwann erleben: Je älter wir werden, desto schwieriger wird es für unser Gehirn, neue Dinge zu lernen und sich an sie zu erinnern. Die Gründe hinter diesen Beeinträchtigungen sind oft unklar. Nun haben Wissenschaftler des Zentrums für Regenerative Therapien der TU Dresden (CRTD) untersucht, ob eine Erhöhung der Anzahl von Hirnstammzellen helfen würde, kognitive Funktionen wie Lernen und Gedächtnis wiederzuerlangen, die im Laufe des Alterns verloren gehen.
Die Forschungsgruppe von Prof. Federico Calegari hat dazu eine im eigenen Labor entwickelte Methode verwendet: Im Gehirn alter Mäuse stimulierten die Wissenschaftler den dort vorhandenen kleinen Pool neuronaler Stammzellen so, dass sich die Menge dieser Stammzellen und damit auch die Anzahl der aus ihnen erzeugten Gehirnzellen erhöhte. Das Team beobachtete, dass diese zusätzlichen Neuronen überleben und sogar neue Kontakte zu benachbarten Zellen knüpfen können. In einem nächsten Schritt untersuchten die Wissenschaftler eine wichtige Aufgabe des Gehirns, die ähnlich wie bei der Maus auch beim Menschen im Laufe des Alterns verloren geht: die Navigationsfähigkeit.
Es ist vom Alter abhängig, auf welche Art man sich in einer neuen Umgebung zurechtzufinden lernt. In der Jugend erstellt das Gehirn eine kognitive Landkarte und erinnert sich an diese. Diese Fähigkeit schwindet im Alter – statt mit der Landkarte im Kopf navigieren ältere Individuen anhand fester Abfolgen von Richtungswechseln, um ein bestimmtes Ziel zu erreichen. Die zuverlässigere Strategie von beiden ist jedoch die kognitive Landkarte, sprich: Die Strategie des jungen Gehirns.
Guardian of the Amazon! — Come hear the recent ideaXme (http://radioideaxme.com/) episode where we are joined by Ms. Nemonte Nenquimo, President of the Waorani Pastaza Organization, CONCONAWEP (Coordinating Council of the Waorani Nationality of Ecuador), following their recent landmark legal victory against the Ecuadorian government, leading to 500,000 acres of Amazon rainforest protected from oil drilling and timber companies (English voice over — Spanish audio link to be posted soon) — #Ideaxme #Amazon #Rainforest #Jungle #Ecuador #Waorani #Huaorani #Amerindian #Environment #Trees #Herbal #EthnoMedicine #Sustainability #Ayahuasca #ClimateChange #GretaThunberg #Health #Wellness #Longevity #Aging #IraPastor #Bioquark #Regenerage
Ira Pastor, ideaXme exponential health ambassador, interviews Ms. Nemonte Nenquimo, President of the Waorani Pastaza Organization (CONCONAWEP — Coordinating Council of the Waorani Nationality of Ecuador). This is an English language voice over of Ms Nenquimo’s audio interview.
Ira comments:
Today we have a fascinating guest joining us on the ideaXme show from a rather remote location, to discuss ethnomedicine, environmental conservation and protection, entheogens (the topic of bio-active plant substances for spiritual and religious practices), as well as the themes of bravery and perseverance.
Who Are the Waorani?
The Waorani (Huaorani) People, are a group of native Amerindians from the Amazonian Region of Ecuador. They comprise almost 4,000 inhabitants and primarily speak the Waorani language, a linguistic isolate that is not known to be related to any other language.
Their ancestral lands are located between the Curaray and Napo rivers, about 50 miles (80 km) south of the city of El Coca. These homelands—approximately 120 miles wide by 100 miles (from north to south) – are extensively threatened by oil exploration and illegal logging practices.
Over the last 40 years, the Waorani have shifted from a hunting and gathering society to live mostly in permanent forest settlements. However, an estimated five communities have rejected all contact with the outside world and continue to move into more isolated areas.
Findings from a recent research project, conducted by a Marshall University scientist and assistant professor in the Marshall University College of Science, with researchers in Texas, was recently published in the December issue of the prestigious online journal, Nature Communications.
Dr. Eugene Shakirov is studying the connection between ribosomes and telomeres in plants. Telomeres are the physical ends of chromosomes and they shorten with age in most cells. Accelerated shortening of telomeres is linked to age-related diseases and overly long telomeres are often linked to cancer.
Telomere length varies between individuals at birth and is known to predetermine cellular lifespan, but the genes establishing telomere length variations are largely unknown. The research being done by Shakirov, along with collaborators at the University of Texas at Austin, Texas A&M University, HudsonAlpha Institute for Biology and the Kazan Federal University in Russia focused on the study of the genetic and epigenetic causes of natural telomere length variation in Arabidopsis thaliana, a small flowering plant.
Scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, Calif., and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research.
The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists.
The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.
Seeking Delphi podcast host Mark Sackler is joined by panelists Liz Parrish, Aubrey de Grey, David Wood and co-moderator Keith Comito to discuss scenarios for getting to—and dealing with—a post aging future.
Telomerase defers the onset of telomere shortening and cellular senescence by adding telomeric repeat DNA to chromosome ends, and its activation contributes to carcinogenesis. Telomerase minimally consists of the telomerase reverse transcriptase (TERT) and the telomerase RNA (TR). However, how telomerase assembles is largely unknown. Here, we demonstrate that PES1 (Pescadillo), a protein overexpressed in many cancers, forms a complex with TERT and TR through direct interaction with TERT, regulating telomerase activity, telomere length maintenance, and senescence. PES1 does not interact with the previously reported telomerase components Reptin, Pontin, p23, and Hsp90. PES1 facilitates telomerase assembly by promoting direct interaction between TERT and TR without affecting TERT and TR levels. PES1 expression correlates positively with telomerase activity and negatively with senescence in patients with breast cancer. Thus, we identify a previously unknown telomerase complex, and targeting PES1 may open a new avenue for cancer therapy.
Telomerase is a ribonucleoprotein (RNP) enzyme that adds telomeric repeat DNA to chromosome ends (1–3). This prevents progressive shortening of telomeres caused by the failure of the DNA replication machinery to duplicate the very end of each chromosome. Once telomeres are shortened to a certain length, cells enter replicative senescence or, alternatively, undergo apoptosis, a major tumor-suppressive mechanism. Telomerase, which is required for de novo telomeric repeat DNA synthesis and telomere maintenance, is expressed in approximately 90% of cancer cells but undetectable in the majority of normal somatic cells (4–6). Thus, telomerase is thought to be a relevant factor in distinguishing cancer cells from normal cells and has become a target for cancer therapy.
Telomerase is minimally composed of the telomerase reverse transcriptase (TERT) and the telomerase RNA (TR). Studies have shown in vitro assembly of active telomerase by combining the purified RNA component with the TERT synthesized in rabbit reticulocyte extract (7–9). A few accessory proteins have been identified to associate with the active telomerase RNP complex. The molecular chaperones p23 and Hsp90 bind to human TERT (hTERT), and chemical inhibition of Hsp90 decreases telomerase activity (10, 11). However, determining whether Hsp90 is required for active telomerase assembly is difficult because chemical inhibition of a key chaperone in human cells potentially has pleiotropic and indirect effects. Assembly of human TR (hTR) and hTERT into catalytically active telomerase is facilitated by the adenosine triphosphatases Reptin and Pontin (12). Pontin knockdown (KD) reduces telomerase activity and hTR levels.
Scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, Calif., and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research.
The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists.
The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.
