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Let’s not just cure cancer: let’s cure aging One of the most exciting areas of modern scientific research is the investigation of the causes and cures for aging. Not individual diseases like cancer and heart disease, but the processes which make us elderly and frail, and which thereby make us more susceptible to these diseases.

Australian researchers have uncovered a new form of antimicrobial resistance (AMR), undetectable using traditional laboratory testing methods, in a discovery set to challenge existing efforts to monitor and tackle one of the world’s greatest health threats.

AMR is expected to claim 10 million lives a year by 2050, with scientists racing to understand and get ahead of the diminishing benefits of antibiotics.

Now, a team led by Dr. Timothy Barnett, Head of the Strep A Pathogenesis and Diagnostics team at the Wesfarmers Centre of Vaccines and Infectious Diseases, based at Telethon Kids Institute in Perth, Western Australia, has unearthed a critical clue to the way some bacteria are managing to dodge antibiotics—a finding expected to be the tip of the iceberg.

Short version: One treated rat is sill alive and equivalent to a 110 year old human.


In this video we review the latest updates from Dr Katcher’s Lifespan trials and NEEL clinical trials.
NTZ Newsletter.
https://www.ntzplural.com/newsletter.
NEEL website.
https://www.neel.bio.

Renue By Science 10% of all products: https://tinyurl.com/4yrf4tv3

If you enjoyed this video, you might like my book: https://ageless.link/

I saw a Twitter thread about Bryan Johnson’s ‘Blueprint’, claiming that he’d made himself biologically younger with a highly optimised combination of diet, supplements and exercise. What could that mean? And should we all start chugging 25 pills a day to start on the Blueprint ourselves? Probably not…but the biology behind it is surprisingly interesting.

*Chapters*

00:00 A tweet goes viral.

“Let’s see how things go.”

So psychiatrists often say to one another after a patient has been diagnosed with the first disorder—not because the diagnosis is not correct, but because psychiatrists know that have a tendency to change over the years.

In fact, 47% of psychiatric patients are diagnosed with a different diagnose within 10 years of receiving their first diagnosis.

After statins, the next leading class of medications for managing cholesterol are PCSK9 inhibitors. These highly effective agents help the body pull excess cholesterol from the blood, but unlike statins, which are available as oral agents, PCSK9 inhibitors can only be administered as injections, creating barriers to their use.

Longevity. Technology: Having high cholesterol can increase the risk of heart and circulatory diseases such as heart attack, stroke and vascular dementia, but a new study from investigators at University Hospitals (UH) and Case Western Reserve University School of Medicine details an orally administered small-molecule drug that reduces PCSK9 levels and lowers cholesterol in animal models by 70%. Published in Cell Reports, the findings represent a previously unrecognised strategy for managing cholesterol and may also impact cancer treatments.

Cardiovascular disease ranking as the world’s number one killer, so it’s no surprise that a significant amount of research into potential therapeutic options is ongoing; just last week we looked at Cyclarity’s rationally-designed cyclodextrin molecules that remove arterial plaque by clearing the non-degradable oxidised cholesterol and which can be used in conjunction with statins for a broad-spectrum approach. Our report into Cyclarity’s new platform comes out next week, so stay tuned!

Year 2020 Stroke victims could eventually get dmt infusions where they can recover quickly after a stroke.


N, N-dimethyltryptamine (DMT) is an endogenous ligand of the Sigma 1 receptor (Sig-1R) with documented in vitro cytoprotective properties against hypoxia. Our aim was to demonstrate the in vivo neuroprotective effect of DMT following ischemia-reperfusion injury in the rat brain.

Transient middle cerebral occlusion (MCAO) was induced for 60 min in male Wistar rats using the filament occlusion model under general anaesthesia. Before the removal of the filament the treatment group (n = 10) received an intra-peritoneal (IP) bolus of 1 mg/kg-body weight (bw) DMT dissolved in 1 ml 7% ethanol/saline vehicle, followed by a maintenance dose of 2 mg/Kg-bw/h delivered over 24 h via osmotic minipumps. Controls (n = 10) received a vehicle bolus only. A third group (n = 10) received a Sig-1R antagonist (BD1063, 1 mg/kg-bw bolus +2 mg/kg-bw/h maintenance) in parallel with the DMT. Lesion volume was measured by MRI 24 h following the MCAO. Shortly after imaging the animals were terminated, and the native brains and sera were removed. Four rats were perfusion fixed. Functional recovery was studied in two separate group of pre-trained animals (n = 8–8) using the staircase method for 30 days.

Research from the Babraham Institute has developed a method to “time jump” human skin cells by 30 years, turning back the aging clock for cells without losing their specialized function. Work by researchers in the Institute’s Epigenetics research program has been able to partly restore the function of older cells, as well as rejuvenating the molecular measures of biological age. The research is published today in the journal eLife, and while this topic is still at an early stage of exploration, it could revolutionize regenerative medicine.

What is regenerative medicine?

As we age, our cells’ ability to function declines and the accumulates marks of aging. Regenerative biology aims to repair or replace cells including old ones. One of the most important tools in regenerative biology is our ability to create “induced” stem cells. The process is a result of several steps, each erasing some of the marks that make cells specialized. In theory, these stem cells have the potential to become any cell type, but scientists aren’t yet able to reliably recreate the conditions to re-differentiate stem cells into all cell types.

Scientists have found a new drug treatment that can slow the progression of neurodegenerative disease in mice. The breakthrough research may offer fresh hope in tackling currently untreatable conditions such as Alzheimer’s disease.

The study—led by researchers at the University of Glasgow’s new Advanced Research Center (ARC) and published today in Science Signaling —found that by using a novel , which selectively activates a brain protein called the M1-receptor, the lifespan of mice suffering from neurodegeneration could be extended. The M1-receptor is a key brain protein, involved in memory and learning in people, and is an important potential target for neurodegenerative disease treatment.

Currently, Alzheimer’s disease is the most common form of neurodegenerative disease, affecting more then 850,000 people in the U.K. and over 55 million worldwide. The study demonstrates how many of the features of human Alzheimer’s disease, including memory loss and inflammation of the brain, could be treated in mice when they were given the new drug, known as a positive allosteric modulator (M1-PAM). The breakthrough described in this study indicates that, beyond treating symptoms, M1-PAMs may also be able to slow the overall progression of the disease.

Basically this is one of the cure all options for thousands of brain disorders.


Researchers in Portugal have discovered a new collaborative mechanism that unveils how neural stem cells sense injury and communicate for tissue repair, moving science closer to boosting neuron regeneration after brain damage.

Stroke and traumatic brain injury can permanently damage neurons and, depending on injury site, patients may experience long-term impairments of critical motor or cognitive functions. For this reason, the brain has a reserve of special cells—known as neural stem cells—that can partially activate after tissue damage.

However, though many stem cells begin the process of regeneration, complete activation only happens in a few, meaning only a small number of fresh neurons are created. Fewer still survive to re-populate the damaged site. Instead, the area is typically filled by glia, a common non-neural support cell, which acts as the “glue” of the nervous system.