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Longevity escape velocity

In the life extension movement, longevity escape velocity (sometimes referred to as Actuarial escape velocity[1]) is a hypothetical situation in which life expectancy is extended longer than the time that is passing. For example, in a given year in which longevity escape velocity would be maintained, technological advances would increase life expectancy more than the year that just went by.

Life expectancy increases slightly every year as treatment strategies and technologies improve. At present, more than one year of research is required for each additional year of expected life. Longevity escape velocity occurs when this ratio reverses, so that life expectancy increases faster than one year per one year of research, as long as that rate of advance is sustainable.[2][3][4]

The concept was first publicly proposed by David Gobel, co-founder of the Methuselah Foundation (MF). The idea has been championed by biogerontologist Aubrey de Grey[5] (the other co-founder of the MF), and futurist Ray Kurzweil,[6] who named one of his books, Fantastic Voyage: Live Long Enough to Live Forever, after the concept. These two claim that by putting further pressure on science and medicine to focus research on increasing limits of aging, rather than continuing along at its current pace, more lives will be saved in the future, even if the benefit is not immediately apparent.[2].

Study Finds New Key To Longevity — And It’s In The Gut

Having a healthy gut should always be a priority when dealing with any health-related issues. It’s connected to various problems like IBS, asthma, thyroid disorders, and even diabetes. A new study, however, is giving us another reason to promote gut health—and we’re excited about it.

Using mice, an international research team has discovered a specific microorganism living in the gut that may affect the aging process.

A molecular map of the brain’s decision-making area

Researchers at Karolinska Institutet have come one step closer toward understanding how the part of our brain that is central for decision-making and the development of addiction is organized on a molecular level. In mouse models and with methods used for mapping cell types and brain tissue, the researchers were able to visualize the organization of different opioid-islands in striatum. Their spatiomolecular map, published in the journal Cell Reports, may further our understanding of the brain’s reward-system.

Striatum is the inner part of the brain that among other things regulates rewards, motivation, impulses and motor function. It is considered central to decision-making and the development of various addictions.

In this study, the researchers created a molecular 3D-map of the nerve cells targeted by opioids, such as morphine and heroin, and showed how they are organized in . It is an important step toward understanding how the brain’s network governing motivation and drug addiction is organized. In the study, the researchers described a spatiomolecular code that can be used to divide striatum into different subregions.

Human Brain-Like Functions Emerge in Neuromorphic Metallic Nanowire Network

An international joint research team led by NIMS succeeded in fabricating a neuromorphic network composed of numerous metallic nanowires. Using this network, the team was able to generate electrical characteristics similar to those associated with higher-order brain functions unique to humans, such as memorization, learning, forgetting, becoming alert and returning to calm. The team then clarified the mechanisms that induced these electrical characteristics.

The development of artificial intelligence (AI) techniques has been rapidly advancing in recent years and has begun impacting our lives in various ways. Although AI processes information in a manner similar to the human brain, the mechanisms by which human brains operate are still largely unknown. Fundamental brain components, such as neurons and the junctions between them (synapses), have been studied in detail. However, many questions concerning the brain as a collective whole need to be answered. For example, we still do not fully understand how the brain performs such functions as memorization, learning, and forgetting, and how the brain becomes alert and returns to calm. In addition, live brains are difficult to manipulate in experimental research. For these reasons, the brain remains a mysterious organ.

Evolutionary Changes in Brain Potentially Make us More Prone to Anxiety

Neurochemicals such as serotonin and dopamine play crucial roles in cognitive and emotional functions of our brain. Vesicular monoamine transporter 1 (VMAT1) is one of the genes responsible for transporting neurotransmitters and regulating neuronal signaling. A research team led by Tohoku University has reconstructed ancestral VMAT1 proteins, revealing the functional changes in neurotransmitter uptake of VMAT1 throughout the course of human evolution.

Human bodies are made up of millions of cells. Each individual contains a specific set of instruction of codes that make up all of a living thing’s genetic material. These instructions are known as genomes. PhD candidate Daiki Sato and Professor Masakado Kawata of the Graduate School of Life Sciences at Tohoku University, and two of the authors involved in the current study, previously discovered VMAT1 to be one of the genes that had evolved throughout human lineage.

VMAT 1 contains two human-specific mutations, or where the genomes changed, with the change being represented as 130Glu to 130Gly and from 136Asn to 136Thr. Previous studies have shown that having the new 130Gly/136Thr variant decreases the uptake of neurotransmitters and is associated with higher depression and/or anxiety. In this study, Sato, Kawata and their colleagues revealed the evolutionary changes in neurotransmitter uptake of VMAT1 by reconstructing ancestral VMAT1 proteins. First they applied a fluorescent substrate to visualize and quantify the neurotransmitter uptake of each genotype. The ancestral (130Glu/136Asn) VMAT1 protein exhibited an increased uptake of neurotransmitters compared to a derived (130Gly/136Thr) genotype. Given that the derived (130Gly/136Thr) genotype is shown to be associated with depression and/or anxiety in modern human populations. “This results of our study reveal that our ancestors may have been able to withstand higher levels of anxiety or depression,” noted the authors.


In this study, Sato, Kawata and their colleagues revealed the evolutionary changes in neurotransmitter uptake of VMAT1 by reconstructing ancestral VMAT1 proteins. First they applied a fluorescent substrate to visualize and quantify the neurotransmitter uptake of each genotype. The ancestral (130Glu/136Asn) VMAT1 protein exhibited an increased uptake of neurotransmitters compared to a derived (130Gly/136Thr) genotype. Given that the derived (130Gly/136Thr) genotype is shown to be associated with depression and/or anxiety in modern human populations. “This results of our study reveal that our ancestors may have been able to withstand higher levels of anxiety or depression,” noted the authors.

The researcher’s next step is to identify the neurological and behavioral consequences of the mutations in mice to clarify how the variants contributed to our brain evolution. “This would be the striking evidence that links evolution of our genome and brain,” said the authors. The researchers hope that this finding provides insights into our diverse psychological traits including psychiatric disorders.

Researchers identify immune-suppressing target in glioblastoma

Researchers at The University of Texas MD Anderson Cancer Center have identified a tenacious subset of immune macrophages that thwart treatment of glioblastoma with anti-PD-1 checkpoint blockade, elevating a new potential target for treating the almost uniformly lethal brain tumor.

Their findings, reported in Nature Medicine, identify macrophages that express high levels of CD73, a surface enzyme that’s a vital piece of an immunosuppressive molecular pathway. The strong presence of the CD73 macrophages was unique to among five analyzed by the researchers.

“By studying the immune microenvironments across tumor types, we’ve identified a rational combination therapy for glioblastoma,” says first author Sangeeta Goswami, M.D., Ph.D., assistant professor of Genitourinary Medical Oncology.

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