Suppose Smokey the Bear were to go on a tear and start setting forest fires instead of putting them out. That roughly describes the behavior of certain cells of our immune system that become increasingly irascible as we grow older. Instead of stamping out embers, they stoke the flames of chronic inflammation.
Biologists have long theorized that reducing this inflammation could slow the aging process and delay the onset of age-associated conditions, such as heart disease, Alzheimer’s disease, cancer and frailty, and perhaps even forestall the gradual loss of mental acuity that happens to nearly everyone.
Yet the question of what, exactly, causes particular cells of the immune system to kick into inflammatory overdrive has lacked a definitive answer.
This prompted a pair of neuroscientists to see if they could design an AI that could learn from few data points by borrowing principles from how we think the brain solves this problem. In a paper in Frontiers in Computational Neuroscience, they explained that the approach significantly boosts AI’s ability to learn new visual concepts from few examples.
“Our model provides a biologically plausible way for artificial neural networks to learn new visual concepts from a small number of examples,” Maximilian Riesenhuber, from Georgetown University Medical Center, said in a press release. “We can get computers to learn much better from few examples by leveraging prior learning in a way that we think mirrors what the brain is doing.”
Several decades of neuroscience research suggest that the brain’s ability to learn so quickly depends on its ability to use prior knowledge to understand new concepts based on little data. When it comes to visual understanding, this can rely on similarities of shape, structure, or color, but the brain can also leverage abstract visual concepts thought to be encoded in a brain region called the anterior temporal lobe (ATL).
The older we grow, the weaker our muscles get, riddling old age with frailty and physical disability. But this doesn’t only affect the individual, it also creates a significant burden on public healthcare. And yet, research efforts into the biological processes and biomarkers that define muscle aging have not yet defined the underlying causes.
Now, a team of scientists from lab of Johan Auwerx at EPFL’s School of Life Sciences looked at the issue through a different angle: the similarities between muscle aging and degenerative muscle diseases. They have discovered protein aggregates that deposit in skeletal muscles during natural aging, and that blocking this can prevent the detrimental features of muscle aging. The study is published in Cell Reports.
“During age-associated muscle diseases, such as inclusion body myositis (IBM), our cells struggle to maintain correct protein folding, leading these misfolded proteins to precipitate and forming toxic protein aggregates within the muscles,” explains Auwerx. “The most prominent component of these protein aggregates is beta-amyloid, just like in the amyloid plaques in the brains of patients with Alzheimer’s disease.”
Summary: Better glucose uptake compensates for age-related motor deterioration and extends lifespan in fruitflies.
Source: Tokyo Metropolitan University.
Researchers from Tokyo Metropolitan University have discovered that fruit flies with genetic modifications to enhance glucose uptake have significantly longer lifespans.
In a new study, German scientists have restored the ability to walk in mice that had been paralyzed after a complete spinal cord injury. The team created a “designer” signaling protein and injected it into the animals’ brains, stimulating their nerve cells to regenerate and share the recipe to make the protein.
Spinal cord injuries are among the most debilitating. Damaged nerve fibers (axons) may no longer be able to transmit signals between the brain and muscles, often resulting in paralysis to the lower limbs. Worse still, these axons cannot regenerate.
Researchers from Tokyo Metropolitan University have discovered that fruit flies with genetic modifications to enhance glucose uptake have significantly longer lifespans. Looking at the brain cells of aging flies, they found that better glucose uptake compensates for age-related deterioration in motor functions, and led to longer life. The effect was more pronounced when coupled with dietary restrictions. This suggests healthier eating plus improved glucose uptake in the brain might lead to enhanced lifespans.
The brain is a particularly power-hungry part of our bodies, consuming 20% of the oxygen we take in and 25% of the glucose. That’s why it’s so important that it can stay powered, using the glucose to produce adenosine triphosphate (ATP), the “energy courier” of the body. This chemical process, known as glycolysis, happens in both the intracellular fluid and a part of cells known as the mitochondria. But as we get older, our brain cells become less adept at making ATP, something that broadly correlates with less glucose availability. That might suggest that more food for more glucose might actually be a good thing. On the other hand, it is known that a healthier diet actually leads to longer life. Unraveling the mystery surrounding these two contradictory pieces of knowledge might lead to a better understanding of healthier, longer lifespans.
A team led by Associate Professor Kanae Ando studied this problem using Drosophila fruit flies. Firstly, they confirmed that brain cells in older flies tended to have lower levels of ATP, and lower uptake of glucose. They specifically tied this down to lower amounts of the enzymes needed for glycolysis. To counteract this effect, they genetically modified flies to produce more of a glucose-transporting protein called hGut3. Amazingly, this increase in glucose uptake was all that was required to significantly improve the amount of ATP in cells. More specifically, they found that more hGut3 led to less decrease in the production of the enzymes, counteracting the decline with age. Though this did not lead to an improvement in age-related damage to mitochondria, they also suffered less deterioration in locomotor functions.
“The results showed that rat cyborgs could be smoothly and successfully navigated by the human mind to complete a navigation task in a complex maze. Our experiments indicated that the cooperation through transmitting multidimensional information between two brains by computer-assisted BBI is promising.”
(2019)
Brain-machine interfaces (BMIs) provide a promising information channel between the biological brain and external devices and are applied in building brain-to-device control. Prior studies have explored the feasibility of establishing a brain-brain interface (BBI) across various brains via the combination of BMIs. However, using BBI to realize the efficient multidegree control of a living creature, such as a rat, to complete a navigation task in a complex environment has yet to be shown. In this study, we developed a BBI from the human brain to a rat implanted with microelectrodes (i.e., rat cyborg), which integrated electroencephalogram-based motor imagery and brain stimulation to realize human mind control of the rat’s continuous locomotion. Control instructions were transferred from continuous motor imagery decoding results with the proposed control models and were wirelessly sent to the rat cyborg through brain micro-electrical stimulation. The results showed that rat cyborgs could be smoothly and successfully navigated by the human mind to complete a navigation task in a complex maze. Our experiments indicated that the cooperation through transmitting multidimensional information between two brains by computer-assisted BBI is promising.
This last year has been not been one for the social calendar. It has left us all feeling more and more isolated with lockdown after lockdown and restricted travel options globally. It is something we need to actively work to overcome, for our own sakes and for those around us, it is as detrimental to our long term health as smoking, obesity or having an alcohol disorder. It increases the risk of many health conditions, and even alters gene expressions. If you want to know even more detail I break it down in this new video, and look out for those who are having a rougher time, pay it forward. Make this world a place you want to live in…
In Loneliness As Deadly As Smoking-How It Impacts Your Health & Longevity I will be talking about how social isolation, something becoming more and more apparent in many countries and cities across the globe, is a serious threat to health and longevity.
It’s effects on mental and physical health are amongst the most serious threats we face and as such it needs to be taken seriously. The studies I mention are linked below.
To see the video on the mother of all diseases, aging, follow this link:
And leave your thoughts, questions and suggestions for future topics in the comments.
Loneliness and Social Isolation as Risk Factors for Mortality: A Meta-Analytic Review. https://journals.sagepub.com/doi/10.1177/1745691614568352
Loneliness and social isolation as risk factors for coronary heart disease and stroke: systematic review and meta-analysis of longitudinal observational studies. https://heart.bmj.com/content/102/13/1009
Myeloid differentiation architecture of leukocyte transcriptome dynamics in perceived social isolation. https://www.pnas.org/content/112/49/15142
Summary: While 40% of people with primary progressive aphasia have underlying Alzheimer’s disease, a new study suggests they may not develop the memory problems associated with Alzheimer’s.
Source: AAN
Primary progressive aphasia is a rare neurodegenerative condition characterized by prominent language problems that worsen over time. About 40% of people with the condition have underlying Alzheimer’s disease. But a new study has found that people with the condition may not develop the memory problems associated with Alzheimer’s disease. The study is published in the January 132021, online issue of Neurology.
