Lifeboat Foundation

Daniel Dennett explores the first steps towards a unified theory of information, through common threads in the convergence of evolution, learning, and engineering.
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A team of scientists is using the tools offered by the HBP’s digital research infrastructure EBRAINS to address one of the oldest enigmas in neuroscience: the dichotomy of brain structure and function.

Every human brain is different. But even with structural differences, individual brains function in a similar way. In other words, there are functional brains based on completely different configurations. At the same time, a structural change may cause loss of function in one brain, but have no consequences in another individual. Or a drug cocktail may be efficient for one patient, and have no effects for another.

The study population comprised 6,245,282 older adults (age ≥65 years) who had medical encounters with healthcare organizations between 2/2/2020–5/30/2021 and had no prior diagnosis of Alzheimer’s disease. The population was divided into two cohorts: 1) COVID-19 cohort (n = 410,748)— contracted COVID-19 between 2/2/2020–5/30/2021; 2) non-COVID-19 cohort (n = 5,834,534)— had no documented COVID-19 but had medical encounters with healthcare organizations between 2/2/2020–5/30/2021. The status of Alzheimer’s disease and COVID-19 were based on the International Classification of Diseases (ICD-10) diagnosis codes and laboratory tests (details in the Supplementary Material).

We examined risks for new diagnosis of Alzheimer’s disease in COVID-19 and non-COVID-19 cohorts in all older adults, three age groups (65–74, 75–84, ≥85), and three racial/ethnic groups (Black, White, and Hispanic). Cohorts were propensity-score matched (1:1 using a nearest neighbor greedy matching) for demographics, adverse socioeconomical determinants of health including problems with education, occupational exposure, physical, social and psychosocial environment, and known risk factors for Alzheimer’s disease [13] (details in the Supplementary Material). Kaplan-Meier analysis was used to estimate the probability of new diagnosis of Alzheimer’s disease within 360 days after the COVID-19 diagnosis. Cox’s proportional hazards model was used to compare matched cohorts using hazard ratios and 95% confidence intervals. All statistical tests were conducted within the TriNetX Advanced Analytics Platform at significance set at p < 0.05 (2-sided).

(Medical Xpress)—A team of researchers at the Max Planck Institute has found what they believe is the DNA mutation that led to a change in function of a gene in humans that sparked the growth of a larger neocortex. In their paper published in the journal Science Advances, the team describes how they engineered a gene found only in humans, Denisovans and Neanderthals to look like a precursor to reveal its neuroproliferative effect.

A year ago, another team of researchers found the human gene that most in the field believe was a major factor in allowing the human brain to grow bigger, allowing for more complex processing. In this new effort, the researchers have found what they believe was the DNA change that arose in that gene.

To pinpoint that change, the researchers engineered the unique ARHGAP11B gene to make it more similar to the ARHGAP11A gene, which researchers believe was a predecessor gene—they swapped a single nucleotide (out of 55 possibilities) for another and in so doing, found the ARHGAP11B gene lost its neuroproliferative abilities. This, the team claims, shows that it was a single mutation that allowed humans to grow bigger brains. Such a mutation, they note, was not likely due to natural selection, but was more likely a simple mistake that occurred as a brain cell was splitting. Because it conferred an advantage (the ability to grow higher than normal amounts of brain cells) the mutation was retained through subsequent generations. They also point out that such a mutation would have resulted specifically in a larger neocortex—a portion of the cortex that has been associated with hearing and sight.

When the right gene is expressed in the right manner in the right population of stem cells, the developing mouse brain can exhibit primate-like features. In a paper publishing August 7th in the Open Access journal PLOS Biology, researchers at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) succeeded in mimicking the sustained expression of the transcription factor Pax6 as seen in the developing human brain, in mouse cortical progenitor cells. This altered the behavior of these cells to one that is akin to that of progenitors in the developing primate neocortex. Consequently, the mouse progenitors generated more neurons — a prerequisite for a bigger brain.

The neocortex consists of different types of progenitors, but one particular class, the basal progenitors, behave differently in small-brained animals such as mice than in large-brained animals such as humans. In humans, basal progenitors can undergo multiple rounds of cell division, thereby substantially increasing neuron number and ultimately the size of the neocortex. In mice, these progenitors typically undergo only one round of cell division, thus limiting the number of neurons produced. A potential cause underlying this difference in the proliferative capacity of basal progenitors could be the differential expression of Pax6 between species. Mouse basal progenitors, in contrast to human, do not express Pax6. “We were very curious to see what would happen if we were to change the expression pattern of Pax6 in developing mouse brain to mimic that observed in large-brained animals”, says Fong Kuan Wong, a PhD student in the lab of Wieland Huttner and first author of the study.

To this end, another PhD student in the lab, Ji-Feng Fei, generated a novel transgenic mouse line. This line provided the basis for altering the expression of Pax6 in the cortical stem cell lineage such that it would be sustained in basal progenitors. The researchers then introduced the Pax6 gene into the stem cells of these mice. Strikingly, sustaining Pax6 expression in mouse basal progenitors increased their capacity to undergo multiple rounds of cell division, as typically observed in primates. This not only expanded the size of the basal progenitor population in a way somewhat reminiscent to what is seen in large-brained animals. It also resulted in an increase in cortical neurons, notably those in the top layer, another characteristic feature of an expanded neocortex.

About 99 percent of human genes are shared with chimpanzees. Only the small remainder sets us apart. However, we have one important difference: The brain of humans is three times as big as the chimpanzee brain.

During evolution our genome must have changed in order to trigger such brain growth. Wieland Huttner, Director and Research Group Leader a the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), and his team identified for the first time a gene that is only present in humans and contributes to the reproduction of basal brain stem cells, triggering a folding of the neocortex. The researchers isolated different subpopulations of human brain stem cells and precisely identified, which genes are active in which cell type. In doing so, they noticed the gene ARHGAP11B: it is only found in humans and in our closest relatives, the Neanderthals and Denisova-Humans, but not in chimpanzees. This gene manages to trigger brain stem cells to form a bigger pool of stem cells. In that way, during brain development more neurons can arise and the cerebrum can expand. The cerebrum is responsible for cognitive functions like speaking and thinking.

Wieland Huttner’s researchers developed a method that isolates and identifies special subpopulations of brain stem cells from the developing human cerebrum. No one has managed to do this so far. The scientists first isolated different stem and progenitor cell types from fetal mice and human cerebrum tissue. In contrast to the big and folded human brain, the brain of mice is small and smooth. After the isolation, the researchers compared the genes that are active in the various cell types and were able to identify 56 genes that are only present in humans and which play a role in brain development. “We noticed that the gene ARHGAP11B is especially active in basal brain stem cells. These cells are really important for the expansion of the neocortex during evolution,” says Marta Florio, PhD student in Wieland Huttner’s lab, who carried out the main part of the study.