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Proteins are the building blocks of life. Formed of chains of amino acids, folded up into complex shapes, their 3D structure largely determines their function. Once you know how a protein folds up, you can start to understand how it works, and how to change its behaviour

Although DNA provides the instructions for making the chain of amino acids, predicting how they interact to form a 3D shape was more tricky and, until recently, scientists had only deciphered a fraction of the 200m or so proteins known to science

Although previous work had indirectly suggested that changing mitochondrial function affected lifespan, “this is the first clear demonstration [that it] extends mouse lifespan,” Miller added.

well known that mitochondria are linked to health. Some evidence suggests that inhibiting mitochondrial function can be harmful—as in the case of diabetes or obesity—but earlier data from nematodes and fruit flies also suggest a link to lifespan increase. The latest findings are a step toward untangling one of the current debates in the field—whether inhibiting mitochondrial function is detrimental or beneficial,

The average lifespan of BXD mice range from 1 year to almost 2.5 years. The researchers were able to link 3 genes to longevity variability, including mitochondrial ribosomal protein S5 (Mrps5), which encodes a protein integral to mitochondrial protein synthesis. They found that BXD strains with 50 percent less Mrps5 expression lived about 250 days longer than BXD mice with more robust Mrps5 expression.

If, as expected in the next few weeks, regulators give those vaccines the green light, the technology and the precision approach to vaccine design could turn out to be the pandemic’s silver linings: scientific breakthroughs that could begin to change the trajectory of the virus this winter and also pave the way for highly effective vaccines and treatments for other diseases.

Vaccine development typically takes years, even decades. The progress of the last 11 months shifts the paradigm for what’s possible, creating a new model for vaccine development and a toolset for a world that will have to fight more never-before-seen viruses in years to come.

Long before the pandemic, Graham worked with colleagues there and in academia to create a particularly accurate 3-D version of the spiky proteins that protrude from the surface of coronaviruses — an innovation that was rejected for publication by scientific journals five times because reviewers questioned its relevance.

Working at a breakneck pace, a team of hundreds of scientists has identified 50 drugs that may be effective treatments for people infected with the coronavirus.

Many of the candidate drugs are already approved to treat diseases, such as cancer, that would seem to have nothing to do with Covid-19, the illness caused by the coronavirus.

If the research effort succeeds, it will be a significant scientific achievement: an antiviral identified in just months to treat a virus that no one knew existed until January.

The idea that dietary restriction can be used as a tool to increase lifespan has been a centrepiece of ageing research for decades. But the mechanisms by which dietary restriction might act, and the specific nutritional components involved, remain unclear.

Both dietary protein restriction (which results in low levels of leucine and other BCAAs) and inhibition of mTOR can extend lifespan in animals

Flies that carry a mutation in this residue have lower mTOR activity than do controls. They are also longer-lived, and are protected against the negative lifespan-shortening effects of a high-protein diet.

Researchers identify gene that helps prevent brain disease: Protein 'proofreading' errors lead to neurodegenerative disease

Without normal levels of Ankrd16, these nerve cells, located in the cerebellum, incorrectly activate the amino acid serine, which is then improperly incorporated into proteins and causes protein aggregation.

Elevating the level of Ankrd16 protects these cells from dying, while removing Ankrd16 from other neurons in mice with a proofreading deficiency caused widespread buildup of abnormal proteins and ultimately neuronal death.

have found evidence linking problems in the lymphatic and glymphatic systems to Alzheimer’s. In a study on mice, they showed that glymphatic dysfunction contributes to the buildup in the brain of amyloid beta, a protein that plays a key role in the disease.

several colleagues examined postmortem tissue from 79 human brains. They focused on aquaporin-4, a key protein in glymphatic vessels. In the brains of people with Alzheimer’s, this protein was jumbled; in those without the disease, the protein was well organized. This suggests that glymphatic breakdowns may play a role in the disease

The vessels have also been implicated in autoimmune disease. Researchers knew that the immune system has limited access to the brain. But at the same time, the immune system kept tabs on the brain’s status; no one knew exactly how. Some researchers theorize that the glymphatic system could be the conduit and that in diseases such as multiple sclerosis — where the body’s immune system attacks certain brain cells — the communication may go awry.

Healthy adults built up Alzheimer’s-associated proteins in their cerebral spinal fluid when prevented from getting slow-wave sleep, the deepest stage of sleep, researchers report July 10 in Brain. Just one night of deep-sleep disruption was enough to increase the amount of amyloid-beta, a protein that clumps into brain cell‒killing plaques in people with Alzheimer’s. People in the study who slept poorly for a week also had more of a protein called tau in their spinal fluid than they did when well rested. Tau snarls itself into tangles inside brain cells of people with the disease.

A longitudinal study, published Thursday in the journal Diabetologia, followed 5,189 people over 10 years and found that people with high blood sugar had a faster rate of cognitive decline than those with normal blood sugar

In other words, the higher the blood sugar, the faster the cognitive decline.

“Currently, dementia is not curable, which makes it very important to study risk factors.”

Molybdenum cofactor (Moco) is a compound that is little known but is essential for life.

Molybdenum cofactor (Moco) is a compound that is little known but is essential for life.

Children born without the ability to synthesize Moco die young.

Puzzle-solving science, according to Kuhn, can therefore trigger a scientific revolution as scientists struggle to explain these anomalies and develop a novel basic theory to incorporate them into the existing body of knowledge. After an extended period of upheaval, in which followers of the new theory storm the bastions of accepted dogma, the old paradigm is gradually replaced.

biology is heading towards a similar scientific revolution that may shatter one of its most central paradigms. The discovery of a few small proteins with anomalous behaviour is about to overcome a central tenet of molecular biology: that information flows unidirectionally from the gene to the protein to the phenotype. It started with the discovery that prions, a class of small proteins that can exist in different forms, cause a range of highly debilitating diseases. This sparked further research

Scientific revolutions are still rare in biology, given that the field, unlike astronomy or physics, is relatively young.

British researchers discovered that a new variant was sweeping through their country.

tended to become more common in its new homes as well

Alpha disables the first line of immune defense in our bodies, giving the variant more time to multiply.

The cells of octopus suckers are decorated with a mixture of tiny detector proteins. Each type of sensor responds to a distinct chemical cue, giving the animals an extraordinarily refined palate that can inform how their agile arms react, jettisoning an object as useless or dangerous, or nabbing it for a snack.

Though humans have nothing quite comparable in their anatomy, being an octopus might be roughly akin to exploring the world with eight giant, sucker-studded tongues

The internal architecture of an octopus is as labyrinthine as it is bizarre. Nestled inside each body are three hearts, a parrot-like beak and, arguably, nine “brains”

Sixty years after scientists described the chemical code of life — an interweaving double helix called DNA — researchers have found four-stranded DNA is also lurking in human cells.

they form in regions of deoxyribonucleic acid (DNA) that are full of guanine, one of the DNA molecule's four building blocks

Scientists had shown in the past that such quadruplex DNA could form in test tubes and had even been found in the cells of ciliated protozoa, or single-celled organisms with hairlike appendages. Also there were hints of its existence in human cells, though no direct proof, Lipps said.

Some have argued that it’s a way to save energy. Others have suggested that slumber provides an opportunity to clear away the brain’s cellular waste. Still others have proposed that sleep simply forces animals to lie still, letting them hide from predators.

It turns out, for example, that neurons can prune their synapses — at least in a dish.

Dr. Diering and his colleagues then searched for the molecular trigger for this change. They found that hundreds of proteins increase or decrease inside of synapses during the night. But one protein in particular, called Homer1A, stood out.

Scientists at Stanford University and the J. Craig Venter Institute have developed the first software simulation of an entire organism, a humble single-cell bacterium that lives in the human genital and respiratory tracts.

the work was a giant step toward developing computerized laboratories that could carry out many thousands of experiments much faster than is possible now, helping scientists penetrate the mysteries of diseases like cancer and Alzheimer’s.

cancer is not a one-gene problem; it’s a many-thousands-of-factors problem.”

At the center of your brain, a clump of nerves—called the suprachiasmatic nucleus—oversees your body’s clock: the circadian rhythm. It determines when you feel sleepy and when you feel bright-eyed. It controls your blood pressure, your body temperature, and your sense of time. It turns your body into a finely tuned machine.

Your sleep-wake cycle is regulated by a protein called PER. The protein level rises and falls each day, peaking in the evening and plummeting at night. When PER levels are low, your blood pressure drops, heart rate slows, and thinking becomes foggier. You get sleepy. If you follow a diligent sleep routine—waking up the same time every day—your body learns to increase your PER levels in time for your alarm. About an hour before you’re supposed to wake up, PER levels rise (along with your body temperature and blood pressure). To prepare for the stress of waking, your body releases a cocktail of stress hormones, like cortisol. Gradually, your sleep becomes lighter and lighter.  And that’s why you wake up before your alarm. Your body hates your alarm clock. It’s jarring. It’s stressful. And it ruins all that hard work. It defeats the purpose of gradually waking up. So, to avoid being interrupted, your body does something amazing: It starts increasing PER and stress hormones earlier in the night. Your body gets a head start so the waking process isn’t cut short. It’s so precise that your eyelids open minutes—maybe even seconds—before the alarm goes off.

if you don’t wake before your alarm, you probably aren’t getting enough sleep—or you aren’t sleeping on a consistent schedule

“What we think we found is a new way that disruption of sleep contributes to the pathology that can disrupt the cementing of memories,” says Bryce Mander, a post doctoral fellow at University of California, Berkeley, and lead author of the paper. The findings also resolve one of the puzzling questions in Alzheimer’s disease: why buildup of amyloid starts initially in areas of the brain that don’t have anything to do with memory. Mander and Walker’s team found that the protein does deposit, however, in areas of the brain that generate the wave patterns of deep sleep.

The relationship between sleep and amyloid is likely a two-way street, they say, in which the more amyloid that builds up, the worse the sleep, and the more disrupted the sleep, the more amyloid that gets deposited. Other studies have shown that deep sleep can cement memories as well as clear away amyloid. Not getting enough deep sleep, then, perpetuates the poor memory cycle.

When the team studied 26 cognitively normal older adults, they found that higher amounts of amyloid, the protein responsible for the hallmark plaques found in Alzheimer’s disease, were linked with more disrupted deep sleep patterns.

Where do memories come from?

For quite some time the science of memories seemed focused on one pathway, but now there is new research indicating that this is only part of a larger story

There’s a kind of fashion about memory – like many mental models constructed for difficult concepts, the signs of the times inform how the current models approach the inquiry.