Our world’s population is an ageing one. By 2050, the number of people diagnosed with the form of dementia commonly known as Alzheimer’s disease could potentially be double than what it is today.
It’s little wonder that scientists are throwing their weight into searching for ways to understand and treat this debilitating neurological condition. And they’re succeeding!
Here are seven things we’ve learned about Alzheimer’s disease over the past year, inching us ever closer to a future where its worst effects are history.
1. We now have a good idea of what tau proteins look like
Tangled clumps of the protein called tau are commonly found in the brain cells of people who have died with Alzheimer’s.
While there are theories on how these tangles are related to the condition, there’s still a lot to confirm. Through a cutting edging imaging technique, we finally know what it looks like up close.
2. Bacteria seem to be playing some kind of role in Alzheimer’s development
As we learn more about the role of gut bacteria in potentially triggering neurological conditions such as Parkinson’s disease, we’re discovering our relationship with microbes is a complex one.
Brains from deceased Alzheimer’s patients found to contain more bacteria than those of controls might hint at some kind of inflammation response. If so, we might have a way to prevent it in some individuals.
3. An ultraprecise blood test could spot the condition decades ahead
The tragedy of Alzheimer’s is by the time it’s spotted, those with the condition are often already experiencing its effects.
A simple blood test could mean better care and prevention is put into action well ahead of time. One in the works detects variations in beta amyloid levels that also build-up as plaques in the brain.
Best of all, it could potentially detect the condition 30 years before symptoms appear. Watch this space!
4. Alzheimer’s patients lose access to memories, but not all is lost
Forgetting loved ones and significant life events has a deeply emotional impact not only on those with Alzheimer’s, but those close to them as well.
We now understand that those memories aren’t erased by the condition, and could even be accessed again with the right treatment.
One study on mice identified these isolated memories and managed to use a form of light therapy to repair the connections. Advances in brain implants that stimulate memory retrieval could also provide much needed relief for those with ailing memories.
5. Ultrasound with immunotherapy offers hope of future treatment
Part of the problem with treating Alzheimer’s is the brain is awfully protective of its contents. Getting materials into damaged areas requires crossing a formidable barrier.
Several years ago, scientists found tiny air bubbles made to jiggle with waves of ultrasound could make this barrier between blood vessels and the brain ‘leak’ enough to allow antibodies to cross and target the amyloid plaques that are thought to cause Alzheimer’s disease.
More recently, the same researchers found the technique could work better when antibodies for tau proteins were introduced as well. So far it’s only been shown in mice, but one day it might be an efficient treatment in humans.
6. Beta amyloid can move into the brain from other places around the body
New research is suggesting the beta amyloid that aggregates in the brains of people with Alzheimer’s could originate somewhere else in the body.
This finding could help us track down a starting point for the condition, opening the possibility that its origins lie somewhere outside of the brain.
7. A drug used to treat type 2 diabetes could also be used to treat Alzheimer’s
While the two conditions couldn’t seem to be more different, past research has found something of a relationship between Alzheimer’s and type 2 diabetes.
A drug used to treat diabetes found to also affect several receptors in the brain appears to stimulate nerve cells enough to help stave off further damage – at least in mice. It could join the list of potential Alzheimer’s treatments currently in the pipeline.
While it’s easy to get excited over so many significant discoveries, there’s little doubt that many could well become dead ends.
But that still leaves us with a lot of hope; bit by bit, we will learn enough about the disease to eventually see the worst of it as a treatable, if not preventable condition.
Novel vaccine technologies are critical to improving the public health response to infectious disease threats that continually emerge and re-emerge, according to scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH). In a perspective in The Journal of the American Medical Association, the experts highlight innovations that could significantly shorten the typical decades-long vaccine development timeline.
Historically, vaccines against viral diseases have used live-attenuated (weakened) viruses or inactivated whole viruses to induce protective immune responses. The development process often takes 15 to 20 years or more and requires virus cultivation, animal model testing, product formulation, immunogenicity testing and years of costly clinical trials. However, substantial technological advances of the past decade, such as synthetic vaccinology and platform manufacturing, can expedite the process and shorten manufacturing time, allowing clinical evaluation to begin sooner, according to the authors. Synthetic vaccinology uses information from viral gene sequencing to create DNA and mRNA molecules encoding viral proteins. Because this research does not require replicating “live” viruses, it does not need to be done in high-level containment facilities when developing vaccines for highly pathogenic viruses.
The perspective notes that once a vaccine platform is established, such as that for DNA or mRNA vaccines, potentially it can be applied to multiple pathogens, especially within virus classes or families. For example, NIAID’s Vaccine Research Center quickly developed a candidate DNA vaccine for Zika virus with the same platform used previously for a related flavivirus, West Nile virus. Platform technologies enable scientists to apply a standardized manufacturing process to multiple vaccines and create a collective database on their safety as well, which can shorten the preclinical development period to as little as several months, according to the authors. The perspective concludes that modern vaccine technology and improved surveillance in developing countries ultimately can help us better prepare for emerging infectious disease threats.
BS Graham et al. Novel vaccine technologies: essential components of an adequate response to emerging viral diseases. The Journal of the American Medical Association DOI: 10.1001/jama.2018.0345 (2018).
NIAID conducts and supports research — at NIH, throughout the United States, and worldwide — to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses.
If you often find yourself coming down with a cold after taking a flight, take note: by mapping the spread of a virus through an aeroplane cabin, researchers have found that your chances of getting the sniffles largely depend on how much you move about.
Based on influenza models, the new study shows you have an 80 percent chance of getting the flu off someone if you’re sitting in the row in front or the row behind, or within two seats to either side. Otherwise, your chance of infection drops all the way down to 3 percent.
But… that’s assuming you stay still. Move around the cabin, and you’re more likely to come into contact with a passenger or a crew member suffering from a cold. The advice seems to be, if you want to stay well by the end of your trip, try and limit the amount of walking around you do while up in the air.
“We found that direct disease transmission outside of the 1 metre [3.2 feet] area of an infected passenger is unlikely,” says one of the team, mathematician Howard Weiss from the Georgia Institute of Technology.
Very little research has actually looked at this question before. In this case, a team of 10 people flew on a total of 10 different transcontinental flights, armed with iPads to make observations about passenger and crew movements.
They backed up their observations by taking 229 samples from the air and surfaces on board the planes, looking for traces of 18 common respiratory viruses.
There’s one important limitation we should talk about: the researchers didn’t actually track the spread of flu or any other virus. Instead, they tracked passenger and crew movement, and then applied existing models of how flu spreads to this data.
“The simulations provide compelling evidence that for influenza, if you are not seated within a metre of an infected passenger, and you practice careful hand hygiene, then you are unlikely to get infected during flight,” Weiss told George Dvorsky at Gizmodo.
That was backed up by those 229 samples – not a fully comprehensive sweep of the planes, of course, but nevertheless there were no traces of bugs in any of them.
The research showed that around 40 percent of passengers never get up on these shorter, transcontinental flights. Another 40 percent get up at least once, and 20 percent get up two or more times.
You’re more than twice as likely to get up if you’re sat in the aisle than when you’re sat by the window, the study suggests. Meanwhile, the average time passengers spend away from their seats is 5 minutes.
A wandering member of the cabin crew can infect an average of 4.6 passengers on a flight, the research model also showed – so whether you’re working or travelling on a plane, it’s best to stay home if you’re ill.
As we’ve said, the research uses models of flu patterns rather than actually tracking the spread of bugs around a cabin, and the observations were also restricted to focus on shorter flights of up to 5 hours.
Those shorter flights mean smaller, single-aisle planes as well – and we already know they’re better at limiting the spread of infection.
All that said, this is still a useful and pretty rare look at the way sickness can make its way around an aeroplane, and particularly our movement habits.
We definitely need to understand more about why people get sick when they travel, and how those colds and coughs can spread, according to molecular biologist Edsel Maurice Salvaña, from the University of the Philippines Manila, who wasn’t involved in the study.
“The study team did a good job with mapping patient movements and going the extra step of testing for a panel of 18 respiratory viruses using highly sensitive nucleic acid testing,” Salvaña told Gizmodo.
So why is it that so many of us seem to pick up bugs when we’re on flights – is it just our imagination, or is there really an uptick in illness for travellers? Infections could be caught at the airport, suggest the researchers behind the study, or on other, longer connecting flights.
More detailed studies are going to be required before we can work out what’s really going on, but in the meantime your chances of getting a bug may not be as high as you thought – and you can minimise the risk by washing your hands, which protects against indirect transmission.
“Passengers and flight crews can eliminate this risk of indirect transmission by exercising hand hygiene and keeping their hands away from their nose and eyes,” says Weiss.
The research has been published in PNAS.
Process to set up Asia’s first rapid microbiological testing lab begins as GMSCL appoints agency to procure equipment
A rapid microbiological testing lab to assess drug quality in real time would soon be a reality as the Gujarat Medical Services Corporation Ltd (GMSCL) has finally selected an agency based on a tendering process to procure equipment and set up the lab. An amount of Rs.4.5 crore has also been allocated for the same by the Gujarat government.
Rapid microbiological testing facility will test 100 plus samples in a day and help detect pathogenic organisms in drugs which will help Indian manufacturers cater to the global regulatory requirements. French company bioMérieux has already signed an MoU with Gujarat Food and Drug Control Administration (FDCA) to help GMSCL set up lab which will bring turnaround time for drug testing from 14 days to just 4 hours.
Informed Gujarat FDCA Commissioner Dr H G Koshia, “Procurement of equipment is being done on war footing with the appointment of an agency. Further, manpower to run the lab has been recruited and once the equipment is installed it will become operational any time.”
Earlier this year, an MoU was signed between Dr H G Koshia, Commissioner FDCA and Nicolas Cartier, bioMérieux, corporate VP, industry unit, group portfolio and strategic planning in the presence of Vanrajsinh Vanzara, joint secretary, health and family welfare department, Gandhinagar and Arvind Kukrety, deputy drug controller, CDSCO Zonal office, Ahmedabad.
The partnership in the form of MoU will usher in knowledge, services and products to upgrade microbiological technology, environmental monitoring, sterility testing of raw material, in process testing and end product testing for filterable and non-filterable products.
It also includes detection and confirmation of specified micro organisms as per harmonized pharmacopoeia, trend analysis of microorganisms isolated from the environment and products, bio- burden testing of non-sterile products, antimicrobial efficacy testing, disinfection efficacy testing, preservative efficacy testing and challenge test among others.
As part of the strategic partnership, bioMérieux will conduct training programmes on microbiological testing technologies and applications for the pharmaceutical sector to cater to the regulatory requirements of domestic and export markets.
The French company has developed efficient, accurate and rapid methods for detection and enumeration of public health indicator organisms to cater to the needs of pharmaceutical and cosmetic sector.
Headquartered in Lyon, bioMérieux which operates in over 150 countries specializes in the field of in vitro diagnostics for clinical and industrial applications.
Our first few years of life play a crucial role in our brain’s wiring. New research suggests our experiences might also be influencing changes in our neurons at a genetic level.
A new study has discovered that when mice pups are neglected by their mother, it appears to trigger ‘jumping’ genes in their brain cells. This hints at similar processes in humans that could help explain the development of certain neurological disorders.
The ability for certain genes to copy themselves and migrate from one section to another is far from unknown. In fact, we’ve been studying them for more than half a century.
These sections of code – called transposons – can produce a mosaic of neighbouring cells that technically have slightly different genetic maps, even though they belong to the same individual.
“We are taught that our DNA is something stable and unchanging which makes us who we are, but in reality it’s much more dynamic,” explains geneticist Fred “Rusty” Gage from the Salk Institute in California.
“It turns out there are genes in your cells that are capable of copying themselves and moving around, which means that, in some ways, your DNA does change.”
The fact this happens in brain cells as they grow and divide is also well established. Sequences called long interspersed nuclear elements (LINEs) were seen changing positions in dividing hippocampus cells taken from rats more than a decade ago.
In recent years, a significant amount of attention has been devoted to understanding how external ‘epigenetic’ changes to our DNA can be the result of environmental conditions.
Some have even been considered as contributing factors behind the development of neurological conditions such as autism spectrum disorder.
But the effect of the environment on the transposons hasn’t been so scrutinised, possibly because we assume the genes we inherit simply don’t change their code all that easily.
“While we’ve known for a while that cells can acquire changes to their DNA, it’s been speculated that maybe it’s not a random process,” says the study’s first author Tracy Bedrosian.
“Maybe there are factors in the brain or in the environment that cause changes to happen more or less frequently.”
So together with two other researchers, Bedrosian and Gage investigated how a sequence called a LINE-1 retrotransposon copied and relocated itself in the dividing hippocampus cells of mice pups.
Specifically, they paid close attention to whether the pups’ environment made much of a difference to this gene-jumping process.
Rather than create a hostile environment for a sample of the young mice, the researchers watched how mothers raised their offspring over a period of two weeks.
They were then divided into groups based on how the mothers cared for their brood, detailing how they licked them, carried them around, nursed, and rested.
On analysing the hippocampus cells of the mice pups, they found a clear relationship between the kinds of care they received and the number of copies of LINE-1. The worse the care, the more times the gene copied itself and relocated.
Oddly, this didn’t occur for other types of transposon the researchers analysed, suggesting it was something specific to this sequence.
On closer inspection, they found epigenetic factors were primarily responsible. Unlike other transposons, copies of LINE-1 were tagged less with a methyl group, the signature of an epigenetic edit.
“This finding agrees with studies of childhood neglect that also show altered patterns of DNA methylation for other genes,” says Gage.
“That’s a hopeful thing, because once you understand a mechanism, you can begin to develop strategies for intervention.”
You can watch Gage dig into even more research details in the video clip below.
Exactly what this means for humans is a matter for future studies – but right now, it’s a sign that our childhood experiences could be powerful enough to have an effect right down to the level of our genes.
This research was published in Science.