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By Carl Zimmer

In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body.

Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease.

The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled.

A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions.

For some neuroscientists, new studies have changed the way they think about the brain.

One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test.

“It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.”

He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia.

Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too.

“I never imagined it would be such a striking result,” Dr. Sisodia said. “For someone with a background in molecular biology and neuroscience, this is like going into outer space.”

Following a string of similar experiments, he now suspects that just a few species in the gut — perhaps even one — influence the course of Alzheimer’s disease, perhaps by releasing chemical that alters how immune cells work in the brain.

He hasn’t found those microbes, let alone that chemical. But “there’s something’s in there,” he said. “And we have to figure out what it is.”

‘It was considered crazy’

Scientists have long known that microbes live inside us. In 1683, the Dutch scientist Antonie van Leeuwenhoek put plaque from his teeth under a microscope and discovered tiny creatures swimming about.

But the microbiome has stubbornly resisted scientific discovery. For generations, microbiologists only studied the species that they could grow in the lab. Most of our interior occupants can’t survive in petri dishes.

In the early 2000s, however, the science of the microbiome took a sudden leap forward when researchers figured out how to sequence DNA from these microbes. Researchers initially used this new technology to examine how the microbiome influences parts of our bodies rife with bacteria, such as the gut and the skin.

Few of them gave much thought to the brain — there didn’t seem to be much point. The brain is shielded from microbial invasion by the so-called blood-brain barrier. Normally, only small molecules pass through.

“As recently as 2011, it was considered crazy to look for associations between the microbiome and behavior,” said Rob Knight, a microbiologist at the University of California, San Diego.

He and his colleagues discovered some of the earliest hints of these links. Investigators took stool from mice with a genetic mutation that caused them to eat a lot and put on weight. They transferred the stool to mice that had been raised germ-free — that is, entirely without gut microbiomes — since birth.

After receiving this so-called fecal transplant, the germ-free mice got hungry, too, and put on weight.

Altering appetite isn’t the only thing that the microbiome can do to the brain, it turns out. Dr. Cryan and his colleagues, for example, have found that mice without microbiomes become loners, preferring to stay away from fellow rodents.

The scientists eventually discovered changes in the brains of these antisocial mice. One region, called the amygdala, is important for processing social emotions. In germ-free mice, the neurons in the amygdala make unusual sets of proteins, changing the connections they make with other cells.

Studies of humans revealed some surprising patterns, too. Children with autism have unusual patterns of microbial species in their stool. Differences in the gut bacteria of people with a host of other brain-based conditions also have been reported.

But none of these associations proves cause and effect. Finding an unusual microbiome in people with Alzheimer’s doesn’t mean that the bacteria drive the disease. It could be the reverse: People with Alzheimer’s disease often change their eating habits, for example, and that switch might favor different species of gut microbes.

Fecal transplants can help pin down these links. In his research on Alzheimer’s, Dr. Sisodia and his colleagues transferred stool from ordinary mice into the mice they had treated with antibiotics. Once their microbiomes were restored, the antibiotic-treated mice started developing protein clumps again.

“We’re extremely confident that it’s the bacteria that’s driving this,” he said. Other researchers have taken these experiments a step further by using human fecal transplants.

If you hold a mouse by its tail, it normally wriggles in an effort to escape. If you give it a fecal transplant from humans with major depression, you get a completely different result: The mice give up sooner, simply hanging motionless.

As intriguing as this sort of research can be, it has a major limitation. Because researchers are transferring hundreds of bacterial species at once, the experiments can’t reveal which in particular are responsible for changing the brain.

Now researchers are pinpointing individual strains that seem to have an effect.

To study autism, Dr. Mauro Costa-Mattioli and his colleagues at the Baylor College of Medicine in Houston investigated different kinds of mice, each of which display some symptoms of autism. A mutation in a gene called SHANK3 can cause mice to groom themselves repetitively and avoid contact with other mice, for example.

In another mouse strain, Dr. Costa-Mattioli found that feeding mothers a high-fat diet makes it more likely their pups will behave this way.

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After scientists unlocked the secrets of the human genome in 2003, there was immediate concern about how that knowledge might be abused in the wrong hands. Now, an East Bay entrepreneur wants to put that power in everyone’s hands.

Dr. Josiah Zayner has a PhD in biochemistry and worked for NASA, engineering organisms to help astronauts survive on Mars. But that wasn’t innovative enough for the young, self-described “Bio Hacker.”

“Normal scientists want to study, like, how fruit flies have sex or something, something that nobody really cares about,” said Dr. Zayner. “And what I want to study is, how do we make dragons or super-humans or something like that?”

Zayner wants others to do it as well. Out of a West Oakland apartment, he operates a company called The Odin that sells “gene-editing” kits; they come with all that’s necessary to create your own Genetically Modified Organism.

The kit teaches novice scientists how to inject tree frogs with a type of human growth enzyme that causes the frogs to double in size in about a month.

“It sounds ridiculous,” Dr. Zayner said, “but we’ve been doing gene therapy on human beings since the late 90’s, right? The stuff works, we know how to do it, I want to teach people that. I want people to see how it works.”

But at St. Mary’s College in Moraga, biology professor Vidya Chandrasekaran says there are ethical concerns about an untrained person using a live animal for experimentation.

“Using it in this manner, I’m not sure is the right way to approach biology,” she said.

Dr. Zayner frequently uses himself as a guinea pig. He once injected himself with a growth accelerator while live-streaming a talk at a bio conference. Dr. Chandrasekaran said that’s the kind of thing that occurs when people use science without accountability.

“It really matters whether the people who are doing these things understand the implications and the outcome of it,” she said.

But according to Dr. Zayner, new and powerful technologies are always feared at their beginnings. He pointed out that computers were once giant machines used only by business, government and universities.

“And if you ask yourself now, ‘Was it the correct thing to do to allow people to have access to computers?’, there’s nobody in the world who would say no,” he said.

“When you make a technology available to everybody, innovation happens.”

Whether gene-altering technology for the masses is the next innovation or a case of science gone mad is a question that only time will answer.

East Bay Biochemist Sells ‘Gene-Editing Kit’ For The Masses

Thank to Kebmodee for bringing this to the It’s Interesting community.

To determine whether someone is a psychopath, they have to score highly on tests like the Hare Psychopathy Checklist, answering questions about superficial charm, impulsive behaviour, and pathological lies.

But there could be a simpler test: yawning.

It’s hard not to yawn when someone else does, because yawning is so contagious. Even dogs can catch them. But according to a study from 2015, published in the journal Personality and Individual Differences, psychopaths aren’t so susceptible.

The researchers from Baylor University recruited 135 students and measured their personalities for psychopathic traits. They then subjected them to a contagious yawning experiment.

Those who scored highly on the psychopathic scale were much less likely to catch a yawn.

In previous research, yawning has been linked to empathy. For example, in one study, children with autism were less likely to catch yawns, possibly because they find it harder to read other people. Babies don’t catch yawns either, and won’t until they are at least 4 years old, when they have more emotional awareness.

The researchers suggest empathy could be at play in their experiment, as psychopaths tend to lack it.

This isn’t to say if someone doesn’t yawn when you do they must be a psychopath. It’s just an intriguing symptom of the people who struggle to connect with other people’s emotions.

Also, people can catch yawns to different degrees. For some, it’s just reading the word “yawn” is enough to set them off. So if you yawned the whole way through reading this article, you might be able to conclude that your empathy is pretty high.

https://www.thisisinsider.com/psychopaths-dont-catch-yawns-2018-10

by David Nield

Since the 1980s scientists have spotted a link between naval sonar systems and beaked whales seemingly killing themselves – by deliberately getting stranded on beaches. Now, researchers might have revealed the horrifying reason why.

In short, the sound pulses appear to scare the whales to death, acting like a shot of adrenaline might in a human, and causing deadly changes in their otherwise perfectly calibrated diving techniques.

By studying mass stranding events (MSEs) from recent history, the team found that beaked whales bring a sort of decompression sickness (also known as ‘the bends’ or ‘divers’ disease’) on themselves when they sense sonar. When panicked, their veins fill up with nitrogen gas bubbles, their brains suffer severe haemorrhaging, and other organs get damaged.

“In the presence of sonar they are stressed and swim vigorously away from the sound source, changing their diving pattern,” one of the researchers, Yara Bernaldo de Quiros from the University of Las Palmas de Gran Canaria in Spain, told AFP.

“The stress response, in other words, overrides the diving response, which makes the animals accumulate nitrogen.”

The end result is these poor creatures die in agony after getting the whale version of the bends – not something you would normally expect from whales that are so adept at navigating deep underwater.

Typically, these animals naturally lower their heart rate to reduce oxygen use and prevent nitrogen build-up when they plunge far below the surface. Tragically, it appears that a burst of sonar actually overrides these precautions.

The researchers weighed up the evidence from some 121 MSEs between the years 1960 and 2004, and particularly focussed on the autopsies of 10 dead whales stranded in the Canary Islands in 2002 after a nearby naval exercise.

It’s here that the decompression sickness effects were noticed, as they have been in other stranding events that the researchers looked at.

While the team notes that the effects of sonar on whales seem to “vary among individuals or populations”, and “predisposing factors may contribute to individual outcomes”, there does seem to be a common thread in terms of what happens to these unsuspecting mammals.

That’s especially true for Cuvier’s beaked whale (Ziphius cavirostris) – of the 121 MSEs we’ve mentioned, 61 involved Cuvier’s beaked whales, and the researchers say they appear particularly vulnerable to sonar.

There’s also a particular kind of sonar to be worried about: mid-frequency active sonar (MFAS), in the range of about 5 kilohertz.

Now the researchers behind the new report want to see the use of such sonar technology banned in areas where whales are known to live – such a ban has been in place in the Canary Islands since the 2002 incident.

“Up until then, the Canaries were a hotspot for this kind of atypical stranding,” de Quiros told AFP. “Since the moratorium, none have occurred.”

The research has been published in the Royal Society Journal Proceedings B.

https://www.sciencealert.com/this-is-the-horrifying-reason-why-sonar-makes-beaked-whales-beach-themselves

by SIDNEY FUSSELL

Walgreens is piloting a new line of “smart coolers”—fridges equipped with cameras that scan shoppers’ faces and make inferences on their age and gender. On January 14, the company announced its first trial at a store in Chicago in January, and plans to equip stores in New York and San Francisco with the tech.

Demographic information is key to retail shopping. Retailers want to know what people are buying, segmenting shoppers by gender, age, and income (to name a few characteristics) and then targeting them precisely. To that end, these smart coolers are a marvel.

If, for example, Pepsi launched an ad campaign targeting young women, it could use smart-cooler data to see if its campaign was working. These machines can draw all kinds of useful inferences: Maybe young men buy more Sprite if it’s displayed next to Mountain Dew. Maybe older women buy more ice cream on Thursday nights than any other day of the week. The tech also has “iris tracking” capabilities, meaning the company can collect data on which displayed items are the most looked at.

Crucially, the “Cooler Screens” system does not use facial recognition. Shoppers aren’t identified when the fridge cameras scan their face. Instead, the cameras analyze faces to make inferences about shoppers’ age and gender. First, the camera takes their picture, which an AI system will measure and analyze, say, the width of someone’s eyes, the distance between their lips and nose, and other micro measurements. From there, the system can estimate if the person who opened the door is, say, a woman in her early 20s or a male in his late 50s. It’s analysis, not recognition.

The distinction between the two is very important. In Illinois, facial recognition in public is outlawed under BIPA, the Biometric Privacy Act. For two years, Google and Facebook fought class-actions suits filed under the law, after plaintiffs claimed the companies obtained their facial data without their consent. Home-security cams with facial-recognition abilities, such as Nest or Amazon’s Ring, also have those features disabled in the state; even Google’s viral “art selfie” app is banned. The suit against Facebook was dismissed in January, but privacy advocates champion BIPA as a would-be template for a world where facial recognition is federally regulated.

Walgreens’s camera system makes note only of what shoppers picked up and basic information on their age and gender. Last year, a Canadian mall used cameras to track shoppers and make inferences about which demographics prefer which stores. Shoppers’ identities weren’t collected or stored, but the mall ended the pilot after widespread backlash.

The smart cooler is just one of dozens of tracking technologies emerging in retail. At Amazon Go stores, for example—which do not have cashiers or self-checkout stations—sensors make note of shoppers’ purchases and charge them to their Amazon account; the resulting data are part of the feedback loop the company uses to target ads at customers, making it more money.

https://www.theatlantic.com/technology/archive/2019/01/walgreens-tests-new-smart-coolers/581248/

Thanks to Kebmodee for bringing this to the It’s Interesting community.

by Debora MacKenzie

We may finally have found a long-elusive cause of Alzheimer’s disease: Porphyromonas gingivalis, the key bacteria in chronic gum disease. That’s bad, as gum disease affects around a third of all people. But the good news is that a drug that blocks the main toxins of P. gingivalis is entering major clinical trials this year, and research published this week shows it might stop and even reverse Alzheimer’s. There could even be a vaccine.

Alzheimer’s is one of the biggest mysteries in medicine. As populations have aged, dementia has skyrocketed to become the fifth biggest cause of death worldwide. Alzheimer’s constitutes some 70 per cent of these cases and yet, we don’t know what causes it. The disease often involves the accumulation of proteins called amyloid and tau in the brain, and the leading hypothesis has been that the disease arises from defective control of these two proteins. But research in recent years has revealed that people can have amyloid plaques without having dementia. So many efforts to treat Alzheimer’s by moderating these proteins have failed, and the hypothesis has now been seriously questioned.

Indeed, evidence has been growing that the function of amyloid proteins may be as a defence against bacteria, leading to a spate of recent studies looking at bacteria in Alzheimer’s, particularly those that cause gum disease, which is known to be a major risk factor for the condition.

Bacteria involved in gum disease and other illnesses have been found after death in the brains of people who had Alzheimer’s, but until now, it hasn’t been clear whether these bacteria caused the disease or simply got in via brain damage caused by the condition.

Gum disease link

Multiple research teams have been investigating P. gingivalis, and have so far found that it invades and inflames brain regions affected by Alzheimer’s; that gum infections can worsen symptoms in mice genetically engineered to have Alzheimer’s; and that it can cause Alzheimer’s-like brain inflammation, neural damage, and amyloid plaques in healthy mice.

“When science converges from multiple independent laboratories like this, it is very compelling,” says Casey Lynch of Cortexyme, a pharmaceutical firm in San Francisco, California.

In the new study, Cortexyme have now reported finding the toxic enzymes – called gingipains – that P. gingivalis uses to feed on human tissue in 96 per cent of the 54 Alzheimer’s brain samples they looked at, and found the bacteria themselves in all three Alzheimer’s brains whose DNA they examined.

“This is the first report showing P. gingivalis DNA in human brains, and the associated gingipains, co-lococalising with plaques,” says Sim Singhrao, of the University of Central Lancashire, UK. Her team previously found that P. gingivalis actively invades the brains of mice with gum infections. She adds that the new study is also the first to show that gingipains slice up tau protein in ways that could allow it to kill neurons, causing dementia.

The bacteria and its enzymes were found at higher levels in those who had experienced worse cognitive decline, and had more amyloid and tau accumulations. The team also found the bacteria in the spinal fluid of living people with Alzheimer’s, suggesting that this technique may provide a long-sought after method of diagnosing the disease.

When the team gave P. gingivalis gum disease to mice, it led to brain infection, amyloid production, tangles of tau protein, and neural damage in the regions and nerves normally affected by Alzheimer’s.

Cortexyme had previously developed molecules that block gingipains. Giving some of these to mice reduced their infections, halted amyloid production, lowered brain inflammation and even rescued damaged neurons.

The team found that an antibiotic that killed P. gingivalis did this too, but less effectively, and the bacteria rapidly developed resistance. They did not resist the gingipain blockers. “This provides hope of treating or preventing Alzheimer’s disease one day,” says Singhrao.

New treatment hope

Some brain samples from people without Alzheimer’s also had P. gingivalis and protein accumulations, but at lower levels. We already know that amyloid and tau can accumulate in the brain for 10 to 20 years before Alzheimer’s symptoms begin. This, say the researchers, shows P. gingivalis could be a cause of Alzheimer’s, but it is not a result.

Gum disease is far more common than Alzheimer’s. But “Alzheimer’s strikes people who accumulate gingipains and damage in the brain fast enough to develop symptoms during their lifetimes,” says Lynch. “We believe this is a universal hypothesis of pathogenesis.”

Cortexyme reported in October that the best of their gingipain blockers had passed initial safety tests in people, and entered the brain. It also seemed to improve participants with Alzheimer’s. Later this year the firm will launch a larger trial of the drug, looking for P. gingivalis in spinal fluid, and cognitive improvements, before and after.

They also plan to test it against gum disease itself. Efforts to fight that have led a team in Melbourne to develop a vaccine for P. gingivalis that started tests in 2018. A vaccine for gum disease would be welcome – but if it also stops Alzheimer’s the impact could be enormous.

Journal reference: Science Advances

https://www.newscientist.com/article/2191814-we-may-finally-know-what-causes-alzheimers-and-how-to-stop-it/


Coloured positron emission tomography (PET, centre) and computed tomography (CT, left) scans of the brain of a 62-year-old woman with Alzheimer’s disease.

By Pam Belluck

In dementia research, so many paths have led nowhere that any glimmer of optimism is noteworthy.

So some experts are heralding the results of a large new study, which found that people with hypertension who received intensive treatment to lower their blood pressure were less likely than those receiving standard blood pressure treatment to develop minor memory and thinking problems that often progress to dementia.

The study, published Monday in JAMA, is the first large, randomized clinical trial to find something that can help many older people reduce their risk of mild cognitive impairment — an early stage of faltering function and memory that is a frequent precursor to Alzheimer’s disease and other dementias.

The results apply only to those age 50 or older who have elevated blood pressure and who do not have diabetes or a history of stroke. But that’s a condition affecting a lot of people — more than 75 percent of people over 65 have hypertension, the study said. So millions might eventually benefit by reducing not only their risk of heart problems but of cognitive decline, too.

“It’s kind of remarkable that they found something,” said Dr. Kristine Yaffe, a professor of psychiatry and neurology at University of California San Francisco, who was not involved in the research. “I think it actually is very exciting because it tells us that by improving vascular health in a comprehensive way, we could actually have an effect on brain health.”

The research was part of a large cardiovascular study called Sprint, begun in 2010 and involving more than 9,000 racially and ethnically diverse people at 102 sites in the United States. The participants had hypertension, defined as a systolic blood pressure (the top number) from 130 to 180, without diabetes or a history of stroke.

These were people who could care for themselves, were able to walk and get themselves to doctors’ appointments, said the principal investigator, Dr. Jeff D. Williamson, chief of geriatric medicine and gerontology at Wake Forest School of Medicine.

The primary goal of the Sprint study was to see if people treated intensively enough that their blood pressure dropped below 120 would do better than people receiving standard treatment which brought their blood pressure just under 140. They did — so much so that in 2015, the trial was stopped because the intensively treated participants had significantly lower risk of cardiovascular events and death that it would have been unethical not to inform the standard group of the benefit of further lowering their blood pressure.

But the cognitive arm of the study, called Sprint Mind, continued to follow the participants for three more years even though they were no longer monitored for whether they continued with intensive blood pressure treatment. About 8,500 participants received at least one cognitive assessment.

The primary outcome researchers measured was whether patients developed “probable dementia.” Fewer patients did so in the group whose blood pressure was lowered to 120. But the difference — 149 people in the intensive-treatment group versus 176 people in the standard-treatment group — was not enough to be statistically significant.

But in the secondary outcome — developing mild cognitive impairment or MCI — results did show a statistically significant difference. In the intensive group, 287 people developed it, compared to 353 people in the standard group, giving the intensive treatment group a 19 percent lower risk of mild cognitive impairment, Dr. Williamson said.

Because dementia often develops over many years, Dr. Williamson said he believes that following the patients for longer would yield enough cases to definitively show whether intensive blood pressure treatment helps prevent dementia too. To find out, the Alzheimer’s Association said Monday it would fund two more years of the study.

“Sprint Mind 2.0 and the work leading up to it offers genuine, concrete hope,” Maria C. Carrillo, the association’s chief science officer, said in a statement. “MCI is a known risk factor for dementia, and everyone who experiences dementia passes through MCI. When you prevent new cases of MCI, you are preventing new cases of dementia.”

Dr. Yaffe said the study had several limitations and left many questions unanswered. It’s unclear how it applies to people with diabetes or other conditions that often accompany high blood pressure. And she said she would like to see data on the participants older than 80, since some studies have suggested that in people that age, hypertension might protect against dementia.

The researchers did not specify which type of medication people took, although Dr. Williamson said they plan to analyze by type to see if any of the drugs produced a stronger cognitive benefit. Side effects of the intensive treatment stopped being monitored after the main trial ended, but Dr. Williamson said the biggest negative effect was dehydration.

Dr. Williamson said the trial has changed how he treats patients, offering those with blood pressure over 130 the intensive treatment. “I’ll tell them it will give you a 19 percent lower chance of developing early memory loss,” he said.

Dr. Yaffe is more cautious about changing her approach. “I don’t think we’re ready to roll it out,” she said. “It’s not like I’m going to see a patient and say ‘Oh my gosh your blood pressure is 140; we need to go to 120.’ We really need to understand much more about how this might differ by your age, by the side effects, by maybe what else you have.”

Still, she said, “I do think the take-home message is that blood pressure and other measures of vascular health have a role in cognitive health,” she said. “And nothing else has worked.”