Lifeboat Foundation: Safeguarding Humanity
Toggle light / dark theme

Blog

Category: biotech/medical – Page 2812

While billions have now been spent on researching dementia in its various forms, progress is still limited and the underlying triggers are still not clear. The majority of research over the past 30 years has revolved around targeting the amyloid plaques that build up in the disease, but this has resulted in limited success. Is it time to focus resources on other hypotheses instead?

The real problem with tackling these conditions is the sheer complexity of the brain and biology. Research is usually a trial and error process filled with intelligent guesswork, but this means it can often take a great deal of time to establish what’s actually going wrong. The cause or effect conundrum is a significant roadblock in research and working out which aspects drive a disease and which are a result of another malfunction can take serious resources and time. When researchers first began analysing Alzheimer’s patients, perhaps the most obvious feature was the now famous amyloid plaque, but while amyloid may seem like a clear culprit because it’s so clearly out of place, it could easily be a smokescreen; the reason why it appears at all may be far more relevant than the plaque itself.

Read more

A medication called modafinil is commonly used to treat people who experience narcolepsy, but it’s suspected that the vast majority of those who use the drug are taking it for another purpose that isn’t medically authorised: as a general cognitive enhancer for tasks such as studying or meeting a deadline.

Now a comprehensive review of the medication has looked at this ‘off licence’ use of the drug by healthy, non-sleep-deprived subjects to determine whether modafinil is safe – and to confirm whether the belief that it acts as a general-purpose ‘smart drug’ is grounded in reality.

According to researchers from the University of Oxford in the UK and Harvard Medical School in the US, modafinil delivers on both counts, constituting what’s thought to be the first safe smart drug that can provide demonstrable cognitive and concentration benefits. Brainpower in a pill, in other words.

Read more

If cancer is predominantly a random process, then why don’t organisms with thousands of times more cells suffer more from cancer? Large species like whales and elephants generally live longer, not shorter lives, so how are they protected against the threat of cancer?

While we have a great deal more to learn when it comes to cancer biology, the general belief is that it arises first from mutation. It’s becoming clear it’s actually an incredibly complicated process, requiring a range of variable factors such as mutation, epigenetic alteration and local environment change (like inflammation). While some students may have spent sleepless nights wondering how many mutated cells they contain after learning the fallibility of our replication mechanisms, the reality is that with such an error rate we should all be ridden with cancer in childhood — but we’re not. Our canine companions sadly often succumb around their 1st decade, but humans are actually comparatively good at dealing with cancer. We live a relatively long time in the mammal kingdom for our size and even in a modern environment, it’s predominantly an age-related disease.

While evolution may have honed replication accuracy, life itself requires ‘imperfection’ to evolve. We needed those occasional errors in germ cells to allow evolution. If keeping the odd error is either preferable or essentially not worth the energy tackling when you’re dealing with tens of trillions of cells, then clearly there is more to the story than mutation. In order to maintain a multi-cellular organism for a long enough period, considering that errors are essentially inevitable, other mechanisms must be in place to remove or quarantine problematic cells.

Read more

Scientists at Ohio State University say they’ve grown the first near-complete human brain in a lab.

The brain organoid, if licensed for commercial lab use, could help speed research for neurological diseases and disorders, like Alzheimer’s and autism, Rene Anand, an Ohio State professor who worked on the project, said in a statement Tuesday.

“We will have a more precise prediction of efficacy of therapy and possible side effects before we do clinical trials,” Anand told The Huffington Post via email, explaining how his model is a more ethical alternative to trials that use rodent specimens. Anand said reducing the use of animals improves research as they’re “not as likely to predict clinical outcomes as human brain models.”

Read more

Cancer requires extensive and fast division in order to become a serious threat, but this feature also renders it vulnerable, allowing certain growth pathways to be targeted. A new drug candidate has emerged which exploits this weakness, overstimulating proteins required for growth — tipping cellular stress in virulent cancer cells over the edge.

“No prior drug has been previously developed or proposed that actually stimulates an oncogene to promote therapy. Our prototype drug works in multiple types of cancers and encourages us that this could be a more general addition to the cancer drug arsenal.”

Many types of cancer require specific mutations in genes related to growth, and one particular target is the steroid receptor coactivator (SRC) family of oncogenes. These lie at the centre of signalling pathways used to grow rapidly, and conventional research has focused on inhibiting them to prevent tumour growth. Instead of inhibiting, this new strategy aims to upregulate their activity, overstimulating them to an extent that destroys the host cell. In their search for a suitable molecule which might cause such stimulation, researchers stumbled across a compound labeled MCB-613.

Read more