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Category: neuroscience

The world’s largest genetic study into chronic fatigue syndrome is to be launched in the UK after receiving £3.2m of funding from the Medical Research Council and National Institute for Health Research.

The research aims to shine a light on the debilitating long-term condition, about which little is known, by collecting DNA samples from 20,000 people who have CFS, also known as myalgic encephalomyelitis (ME).

CFS is believed to affect about 250,000 people in the UK and has been estimated to cost the economy billions of pounds each year. Individuals experience exhaustion that is not helped by rest, with one in four so severely affected they are unable to leave the house and, frequently, unable to leave their bed. Other symptoms include, pain, mental fogginess, light and noise sensitivities, as well as trouble with memory and sleep. No effective treatment exists.

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New research untangles the complex code the brain uses to distinguish between a vast array of smells, offering a scientific explanation for how it separates baby powder from bleach, lemon from orange, or freshly cut grass from freshly brewed coffee.

A single scent can trigger a complex chain of events in what’s known as the olfactory bulb, the brain’s control center for smell. To unravel the intricacies of that process, researchers in the U.S. and Italy turned to a technique known as optogenetics, which uses light to control neurons in the brain. In research on mice, they used light to trick the brain into thinking it smelled a particular scent, then studied brain activity to understand the role different neurons play in a mouse’s ability to recognize that scent. Their findings were published Thursday in Science.

When we encounter a certain smell, it stimulates a specific pattern of activity among tiny spheres known as glomeruli, which are found in the olfactory bulb. The odor plays across these glomeruli like a melody across piano keys: Just as a tune is made distinct by which keys are pressed and at what point in the melody, a scent is made distinct by which glomeruli are activated and in what order.

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“Despite their abundance, astrocytes have been relatively overlooked by neuroscientists,” says Mirko Santello, last author of the study. Yet these cells are extremely important to clear transmitters released by neurons. In their study the researchers were able to show that in familial migraine the astrocytes cannot remove excessive transmitters released by neurons. “The impairment in astrocytic glutamate uptake in the cingulate cortex strongly enhances cortical dendritic excitability and thus enhances firing of the neurons,” Santello says…

Migraine is a complicated disorder that affects part of the nervous system. “Our results provide a clear example of how astrocyte dysfunction produced by a genetic defect affects neuronal activity and sensitivity to head pain triggers,” explains Mirko Santello. The findings help to better understand migraine pathophysiology and suggest that the cingulate cortex may represent a critical hub in the disease. The demonstration of the link between dysfunction of astrocytes in the cingulate cortex and familial migraine could help in devising new migraine treatment strategies.

Neuroscientists of the University of Zurich shed a new light on the mechanisms responsible for familial migraine: They show that a genetic dysfunction in specific brain cells of the cingulate cortex area strongly influences head pain occurrence.

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In “2030: Beyond the Film” Director Johnny Boston discusses the futurist FM-2030, the Coronavirus Pandemic, and a range of urgent issues in the medical, philosophical, longevity & futurist space with leading voices.

In this episode, Boston talks with David A. Kekich on why Kekich believes working towards Biological Superlongevity should be the first goal of Transhumanists and futurists.

About David A. Kekich: (from Maximum Life Foundation)
David Kekich is President/CEO of Maximum Life Foundation that focuses on aging research. In 1999, he realized the inevitability that science will someday control the human aging process. He understood human beings will someday be able to enjoy very long health spans by studying aging research, the root cause of most deadly diseases. The problem? He was in a race against the clock. He was faced with the possibility of being part of the “last generation to suffer from heart disease, cancer, Alzheimer’s and other aging related diseases”. His solution was to further that aging research and hopefully move it forward by establishing the Maximum Life Foundation.

Maximum Life Foundation Website:

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About 2030 the film:
Johnny Boston was 10 years old when he first met FM-2030, a futurist who intended to live forever. But in 2000, after his body ceased to function, FM was cryonically preserved. 16 years later, an unexpected call places FM’s future in Johnny’s hands.

Directed By: Johnny Boston
See 2030:
Amazon:
https://www.amazon.com/2030-FM/dp/B08…

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The role genetics and gut bacteria play in human health has long been a fruitful source of scientific enquiry, but new research marks a significant step forward in unraveling this complex relationship. Its findings could transform our understanding and treatment of all manner of common diseases, including obesity, irritable bowel syndrome, and Alzheimer’s disease.

The international study, led by the University of Bristol and published today in Nature Microbiology, found specific changes in DNA — the chains of molecules comprising our genetic make-up — affected both the existence and amount of particular bacteria in the gut.

Lead author Dr David Hughes, Senior Research Associate in Applied Genetic Epidemiology, said: “Our findings represent a significant breakthrough in understanding how genetic variation affects gut bacteria. Moreover, it marks major progress in our ability to know whether changes in our gut bacteria actually cause, or are a consequence of, human disease.”

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A newly discovered Alzheimer’s gene may drive the first appearance of amyloid plaques in the brain, according to a study led by researchers at Columbia University Irving Medical Center.

Some variants of the gene, RBFOX1, appear to increase the concentration of protein fragments that make up these plaques and may contribute to the breakdown of critical connections between neurons, another early sign of the disease.

The finding could lead to new therapies that prevent Alzheimer’s and better ways of identifying people with the greatest risk of developing the disease.

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Summary: Findings reveal individual differences in the severity of depressive symptoms following a relationship breakdown are associated with changes in resting-state whole-brain dynamics.

Source: UPF Barcelona

During a person’s life, the experience of a stressful life event can lead to the development of depressive symptoms, even in a non-clinical population. For example, a relationship breakup is a fairly common event and is a powerful risk factor for quality of life, in addition to increasing the risk of a major depressive disorder.

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Summary: Chandelier cells have an unusual direct method of communication. Unlike other neurons, chandelier cells connect directly to the part of a target neuron that initiates a spike.

Source: CSHL

Within the intricate network of cells that make up the brain, chandelier cells stand out for their elaborate, branching structure. With an elegant shape similar to that of its namesake, a single chandelier cell reaches out to connect and communicate with more than 100 other neurons. Abnormalities in chandelier cells have been linked to epilepsy, autism, and schizophrenia, underscoring their critical role in keeping brain signaling in balance. However, these cells have been notoriously difficult to study as their numbers are few, so until recently, chandelier cells remained largely enigmatic.

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The expansion of the human brain during evolution, specifically of the neocortex, is linked to cognitive abilities such as reasoning and language. A certain gene called ARHGAP11B that is only found in humans triggers brain stem cells to form more stem cells, a prerequisite for a bigger brain. Past studies have shown that ARHGAP11B, when expressed in mice and ferrets to unphysiologically high levels, causes an expanded neocortex, but its relevance for primate evolution has been unclear.

Researchers at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, together with colleagues at the Central Institute for Experimental Animals (CIEA) in Kawasaki and the Keio University in Tokyo, both located in Japan, now show that this human-specific gene, when expressed to physiological levels, causes an enlarged in the common marmoset, a New World monkey. This suggests that the ARHGAP11B gene may have caused neocortex expansion during human evolution. The researchers published their findings in the journal Science.

The human neocortex, the evolutionarily youngest part of the cerebral cortex, is about three times bigger than that of the closest human relatives, chimpanzees, and its folding into wrinkles increased during evolution to fit inside the restricted space of the skull. A key question for scientists is how the human neocortex became so big. In a 2015 study, the research group of Wieland Huttner, a founding director of the MPI-CBG, found that under the influence of the human-specific gene ARHGAP11B, mouse embryos produced many more neural progenitor cells and could even undergo folding of their normally unfolded neocortex. The results suggested that the gene ARHGAP11B plays a key role in the evolutionary expansion of the human neocortex.

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