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Nowhere is that clearer than in Africa, which has the world’s lowest share of people using the internet, under 25%. The cohort of 800 million offline people spread across the continent’s 54 countries is younger and growing faster than most, but incomes are lower and a larger share of residents live in rural areas that are tough to wire for internet access—or, for that matter, electricity. Now, however, a handful of phone purveyors are trying in greater earnest to nudge internet-ready upgrades into African markets, with models designed with an eye toward rural priorities (first those of rural India, where they’re already hits), rather than battered thirdhand flip phones from the heyday of the Spice Girls.


About half of humanity don’t have internet access, and a lot of those people are in Africa. Enter a $20 device with smartphone brains and a five-day battery.

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“Do we have a chance of ever understanding brain function without brain simulations?” So asked the Human Brain Project (HBP), the brainchild of Henry Markram, in a new paper in the prestigious journal Neuron.

The key, the team argued, is to consider brain simulators in the vein of calculus for Newton’s laws—not as specific ideas of how the brain works, but rather as a programming language that can execute many candidate neural models, or programs, now and in the future. When viewed not as a vanity project, but rather as the way forward to understand—and eventually imitate—higher brain functions, the response to brain simulation is a resounding yes.

Because of the brain’s complexity and chaotic nature, the authors argue, rather than reining in simulation efforts, we need to ramp up and develop multiple “brain-simulation engines” with varying levels of detail.

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Researchers at Amsterdam’s UMC have identified a rare gene that halves people’s chances of developing dementia in old age.

People with the genetic variant, which occurs in around 1% of the population, are also more likely to live longer. The researchers studied 16 different sample populations in Europe and North America, including a number of people over the age of 100, for the study published in the journal Acta Neuropathologica.

The discovery could potentially be used to treat Alzheimer’s disease and other degenerative illnesses such as frontotemporal and Lewy body dementia.

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Why didn’t it tell the world? Drug companies frequently have been pilloried for not fully disclosing negative side effects of their drugs. What happens when the opposite is the case?

A team of researchers inside Pfizer made a startling find in 2015: The company’s blockbuster rheumatoid arthritis therapy Enbrel, a powerful anti-inflammatory drug, appeared to reduce the risk of Alzheimer’s disease by 64 percent.

The results were from an analysis of hundreds of thousands of insurance claims. Verifying that the drug would actually have that effect in people would require a costly clinical trial — and after several years of internal discussion, Pfizer opted against further investigation and chose not to make the data public, the company confirmed.

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A group of Spanish researchers, including Dr. Maria Blasco and others at the CNIO, have published a new study that examines the consequences of short telomeres and telomerase deficiency on the brain [1].

This study addresses an aspect of telomere attrition, one of the primary hallmarks of aging. Telomeres are repeating sequences of DNA (TTAGGG) that can can reach a length of 15,000 base pairs and appear at the ends of chromosomes, acting as protective caps. They prevent damage, stop chromosomes from fusing with each other, and prevent chromosomes from losing base pair sequences at their end during cell replication.

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The past year or so has seen an energetic debate over whether or not new neurons are generated in the adult human brain, a process known as neurogenesis. This process is well known and well studied in mice, and thought to be very important in the resilience and maintenance of brain tissue. The human data has always been limited, however, due to the challenges inherent in working with brain tissue in living people, and it was assumed was that the mouse data was representative of the state of neurogenesis in other mammals. In this environment, the publication of a careful study that seemed to rule out the existence of neurogenesis in adult humans produced some upheaval, and spurred many other teams to assess the human brain with greater rigor than was previously the case.

So far, all of the following studies published so far do in fact show evidence of adult neurogenesis in humans. This is the better of the two outcomes, as the regenerative medicine community has based a great deal of work on the prospect of being able to upregulate neurogenesis in order to better repair injuries to the central nervous system, or partially reverse the decline of cognitive function in the aging brain. The study here is particularly reassuring, as it shows that even in very late life there are signs that new neurons are being generated in the brain.

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