Increase In Brain Size Research Articles

Heterochronies and allometries in the evolution of the hominid cranium: a morphometric approach using classical anthropometric variables.

This article studies the evolutionary change of allometries in the relative size of the two main cranial modules (neurocranium and splanchnocranium) in the five living hominid species and a diverse sample of extinct hominins. We use six standard craniometric variables as proxies for the length, width and height of each cranial module. Factor analysis and two-block partial least squares (2B-PLS) show that the great apes and modern humans share a pervasive negative ontogenetic allometry in the neurocranium and a positive one in the splanchnocranium. This developmental constraint makes it possible to interpret the cranial heterochronies in terms of ontogenetic scaling processes (i.e., extensions or truncations of the ancestral ontogenetic trajectory) and lateral transpositions (i.e., parallel translations of the entire trajectory starting from a different shape for a given cranial size). We hypothesize that ontogenetic scaling is the main evolutionary modality in the australopithecines while in the species of Homo it is also necessary to apply transpositions. Both types of processes are coordinated in Homo, which result in an evolutionary trend toward an increase in brain size and in the degree of paedomorphosis from the earliest habilines.

Pattern and rate in the Plio-Pleistocene evolution of modern human brain size

Fourteen studies of brain size evolution in Plio-Pleistocene hominins published over the past fifty years show substantial long-term increase in endocranial volume (ECV) for the broad lineage leading to modern humans. The median generation-to-generation step rate for a consensus time series of ECV values, h0 = 0.15 standard deviations per generation, is almost identical to the median step rate observed in modern biological field studies. When specimens are aggregated in a series of 100 k.y. time bins to reflect the precision of their geological ages, temporal scaling identifies four successive phases of stasis and change that are significantly different from random. Phase I from about 3.2 to 2.0 million years before present is an initial phase of relative stasis. Phase II from 2.0 to 1.5 m.y. is a phase of directional brain size increase. Phase III from 1.5 to 0.7 m.y. is a second phase of stasis. Finally, Phase IV from about 0.7 m.y. to 10 k.y. is a second phase of directional increase. The tempo (rate) and the mode (stasis, random, or directional change) of an evolutionary time series are related to each other, and both are related to the time scale appropriate for analysis.

The Evolution of Language‐Related Long Association Pathways: A Comparative Study Between Humans and Rhesus Macaques

The human brain stands out from other primates for its large size. After the split with our last common ancestor (LCA) with chimpanzees—our closest living relative—, the hominin brain expanded threefold, and the frontal and parietal operculum underwent substantial morphological reorganization, likely reflecting language acquisition in our species. The increase of brain size was not homogeneous: the inferior frontal and the parietal areas had a disproportionally large expansion while the occipital lobe retained its absolute size. These evolutionary changes are even more pronounced when human brains are compared to those of Old World monkeys. However, the amount of change in long association pathways within these highly modified regions is not well understood.This study aims to identify differences and similarities in homologous pathways of the human language network in the macaque brain. We hypothesize that language‐related pathways projecting to/from the inferior frontal and parietal areas will exhibit substantial reorganization in humans.Using state‐of‐the‐art, publicly available diffusion MRI data of a healthy (in vivo) adult human (MGH‐USC) [1] and 6 ex vivo rhesus macaque (Oxford University, PRIME‐DE) [2] brains, we reconstructed and virtually dissected in DSI Studio three association pathways: the arcuate fasciculus (AF), the frontal aslant tract (FAT), and the parietal‐projecting portion of the extreme capsule (pEmC). We show that the course and terminal projections of the FAT (inferior frontal and supplementary motor area) and the pEmC (superior parietal lobule and frontal cortical areas) are highly evolutionarily preserved in both species despite their crucial role in language in humans. In stark contrast, the AF underwent a major modification in its posterior segment, as previously reported.Our results suggest that evolutionary changes in the regional volumetric morphology of the brain do not necessarily imply similarly large changes in the relative volumes and trajectories of underlying white matter pathways. In addition, the current results suggest that the structural basis of human language functions already existed, at least to some extent, in the LCA with macaques. Functional and behavioral studies are needed to understand the role of this white matter network in both species.

Expression of the Human Serotonin 5-HT7 Receptor Rescues Phenotype Profile and Restores Dysregulated Biomarkers in a Drosophila melanogaster Glioma Model.

Gliomas are the most common primary brain tumors in adults. Significant progress has been made in recent years in identifying the molecular alterations involved in gliomas. Among them, an amplification/overexpression of the EGFR (Epidermal Growth Factor Receptor) proto-oncogene and its associated signaling pathways have been widely described. However, current treatments remain ineffective for glioblastomas, the most severe forms. Thus, the identification of other pharmacological targets could open new therapeutic avenues. We used a glioma model in Drosophila melanogaster that results from the overexpression of constitutively active forms of EGFR and PI3K specifically in glial cells. We observed hyperproliferation of glial cells that leads to an increase in brain size and lethality at the third instar larval stage. After expression of the human serotonin 5-HT7 receptor in this glioma model, we observed a decrease in larval lethality associated with the presence of surviving adults and a return to a normal morphology of brain for some Drosophila. Those phenotypic changes are accompanied by the normalization of certain metabolic biomarkers measured by High-Resolution Magic Angle Spinning NMR (HR-MAS NMR). The 5-HT7R expression in glioma also restores some epigenetic modifications and characteristic markers of the signaling pathways associated with tumor growth. This study demonstrates the role of the serotonin 5-HT7 receptor as a tumor suppressor gene which is in agreement with transcriptomic analysis obtained on human glioblastomas.

Role of IL-17 in Morphogenesis and Dissemination of Cryptococcus neoformans during Murine Infection.

Cryptococcus neoformans is a pathogenic yeast that can form Titan cells in the lungs, which are fungal cells of abnormally large size. The factors that regulate Titan cell formation in vivo are still unknown, although an increased proportion of these fungal cells of infected mice correlates with induction of Th2-type responses. Here, we focused on the role played by the cytokine IL-17 in the formation of cryptococcal Titan cells using Il17a−/− knockout mice. We found that after 9 days of infection, there was a lower proportion of Titan cells in Il17a−/− mice compared to the fungal cells found in wild-type animals. Dissemination to the brain occurred earlier in Il17a−/− mice, which correlated with the lower proportion of Titan cells in the lungs. Furthermore, knockout-infected mice increased brain size more than WT mice. We also determined the profile of cytokines accumulated in the brain, and we found significant differences between both mouse strains. We found that in Il17a−/−, there was a modest increase in the concentrations of the Th1 cytokine TNF-α. To validate if the increase in this cytokine had any role in cryptococcal morphogenesis, we injected wild-type mice with TNF-α t and observed that fungal cell size was significantly reduced in mice treated with this cytokine. Our results suggest a compensatory production of cytokines in Il17a−/− mice that influences both cryptococcal morphology and dissemination.

A new early Miocene archaic dolphin (Odontoceti, Cetacea) from New Zealand, and brain evolution of the Odontoceti

ABSTRACT The major increase in cetacean brain size happened in the middle Miocene, about 15 million years ago, and involved the modern oceanic dolphin lineage Delphinoidea. In this paper, we describe a new specimen of an archaic dolphin, aff. Prosqualodon davidis, from the Gee Greensand, near Oamaru, New Zealand. The specimen is from the early Miocene, approximately 23–19–18 Ma, and includes an incomplete cranium, endocast, teeth, and some postcranial elements. Comparison of the median sulcus among previously reported endocasts and brains of the Cetacea suggests that the cerebrum was expanded incipiently in the Odontoceti from the early Miocene in the Eurhinodelphinidae + Delphinoidea lineage. Conversely, the olfactory fossa has been reduced in Odontoceti, and completely lost in at least two clades (Delphinoidea and Platanista gangetica), because olfaction was most likely no longer an essential sense for animals spending their life in water. Reduction and loss of the olfactory fossa saved energy, which may be related to the expansion of the cerebrum and cortex in an Odontoceti lineage that led to modern oceanic dolphins. The early Miocene appears to have been a transitional period for archaic and modern-type odontocetes, which were possibly and partly separated by these differences.

Endosomal trafficking defects alter neural progenitor proliferation and cause microcephaly

Primary microcephaly and megalencephaly are severe brain malformations defined by reduced and increased brain size, respectively. Whether these two pathologies arise from related alterations at the molecular level is unclear. Microcephaly has been largely associated with centrosomal defects, leading to cell death. Here, we investigate the consequences of WDR81 loss of function, which causes severe microcephaly in patients. We show that WDR81 regulates endosomal trafficking of EGFR and that loss of function leads to reduced MAP kinase pathway activation. Mouse radial glial progenitor cells knocked-out for WDR81 exhibit reduced proliferation rate, subsequently leading to reduced brain size. These proliferation defects are rescued in vivo by expressing a megalencephaly-causing mutant form of Cyclin D2. Our results identify the endosomal machinery as an important regulator of proliferation rates and brain growth, demonstrating that microcephaly and megalencephaly can be caused by opposite effects on the proliferation rate of radial glial progenitors.

Interpopulational variation in human brain size: implications for hominin cognitive phylogeny

Throughout the hominin lineage brain size is believed to have increased threefold – increase which, it is argued by some researchers, results in the enhanced brain power that distinguishes humans from any other living being. However, as we demonstrate in this article this supposed increase is the result of comparing the species mean of contemporary humans with other great apes and fossil hominins. This method obscures both interpopulational variation among modern humans, and the fact that the putative increases in the mean are the result of an increase in the upper limit in some populations, which has the result of obscuring the relative stasis in the lower limit over the last 600k years. For example, populations such as Aboriginal Australians have a range that is more different from Danes than it is from that of Asian H. erectus over the last 600ka. Yet Aboriginal Australians, whose unique anatomy seems to be related to the climatic conditions of Australia, possess all of the socio-cognitive traits characteristic of all other modern-day populations – yet they seemed not to have undergone increase in brain size to the degree that many other populations have. In this instance brain size seems to be unrelated to cognition. In this article we present a statistical analysis of interpopulational variation in contemporary humans and why such an analysis is crucial for our understanding of hominin cognitive, social and technological evolution. We also suggest how such variation may add to our understanding of hominin ontogeny or life history. Additionally, we develop a model based on humanity’s unique form of embodied social cognition that results from our upright bipedal posture and hand morphology. This model is then used to explain the results of our statistical analysis and the possible factors underpinning the human emergence.

The human FOXM1 homolog promotes basal progenitor cell proliferation and cortical folding in mouse.

Cortical expansion and folding are key processes in human brain development and evolution and are considered to be principal elements of intellectual ability. How cortical folding has evolved and is induced during embryo development is not well understood. Here, we show that the expression of human FOXM1 promotes basal progenitor cell proliferation and induces cortical thickening and folding in mice. Human-specific protein sequences further promote the generation of basal progenitor cells. Human FOXM1 increases the proliferation of neural progenitors by binding to the Lin28a promoter and increasing Lin28a expression. Furthermore, overexpression of LIN28A rescues the proliferation of human FOXM1 knockout neural progenitor cells. Together, our findings demonstrate that a human gene can increase the number of basal progenitor cells in mice, leading to brain size increase and gyrification, and may thus contribute to evolutionary brain development and cortical expansion.

Relative Brain Size and Cognitive Equivalence in Fishes

Scientists have long struggled to establish how larger brains translate into higher cognitive performance across species. While absolute brain size often yields high predictive power of performance, its positive correlation with body size warrants some level of correction. It is expected that larger brains are needed to control larger bodies without any changes in cognitive performance. Potentially, the mean value of intraspecific brain-body slopes provides the best available estimate for an interspecific correction factor. For example, in primates, including humans, an increase in body size translates into an increase in brain size without changes in cognitive performance. Here, we provide the first evaluation of this hypothesis for another clade, teleost fishes. First, we obtained a mean intraspecific brain-body regression slope of 0.46 (albeit with a relatively large range of 0.26–0.79) from a dataset of 51 species, with at least 10 wild adult specimens per species. This mean intraspecific slope value (0.46) is similar to that of the encephalisation quotient reported for teleosts (0.5), which can be used to predict mean cognitive performance in fishes. Importantly, such a mean value (0.46) is much higher than in endothermic vertebrate species (≤0.3). Second, we used wild-caught adult cleaner fish Labroides dimidiatus as a case study to test whether variation in individual cognitive performance can be explained by body size. We first obtained the brain-body regression slope for this species from two different datasets, which gave slope values of 0.58 (MRI scan data) and 0.47 (dissection data). Then, we used another dataset involving 69 adult cleaners different from those tested for their brain-body slope. We found that cognitive performance from four different tasks that estimated their learning, numerical, and inhibitory control abilities was not significantly associated with body size. These results suggest that the intraspecific brain-body slope captures cognitive equivalence for this species. That is, individuals that are on the brain-body regression line are cognitively equal. While rather preliminary, our results suggest that fish and mammalian brain organisations are fundamentally different, resulting in different intra- and interspecific slopes of cognitive equivalence.

Anatomical Variation, Hominins, Species, and Self-Domestication

The evolution of hominins, members of the zoological tribe Hominini, has been a much-studied topic, and the construction of phylogenetic trees has been the key method in molecular evolutionary studies. How scientists determine the phylogenetic trees are governed by the assumptions they place on the construction of similarities and differences in morphological traits, the differences in the number of base pairs in the genomes, and the number of similar gene clusters that code for traits (haplotypes) or are error sequences (SNPs). Among the several methods employed for the construction of a phylogenetic tree, mathematical methods (utilized for sorting data, including fabrication of algorithms) are the most significant ones; also, the nature of population structuring plays an important role in the evolutionary process. In this paper, I will not only describe the drawbacks of current assumptions in hominin evolution during the Middle Pleistocene era (based on fossil evidence) but also the aspects of brain evolution and the self-domestication of our species. The evolution of the brain is usually associated with an increase in neurons and other types of cells associated with signal processing (connectivity) and memory. Assessing actual neuron counts in fossils is challenging; moreover, new research has shown decreased neuron numbers in the neocortex and demonstrated large counts in the cerebellum, leading to a decreased focus on brain size. The idea of increased brain size in the Pleistocene era without a substantial increase in the evidence of cognitive activity in complex behavior residues might be explained by increased myelination to provide additional insulation in Ice Age conditions and faster transition of signals due to increased competition for reduced food supplies. Other cold-adaptation features can also be noted. Such a model can provide a new approach to assess the apparent brain size reduction in the Upper Paleolithic period.

The pattern of brain-size change in the early evolution of cetaceans.

Most authors have identified two rapid increases in relative brain size (encephalization quotient, EQ) in cetacean evolution: first at the origin of the modern suborders (odontocetes and mysticetes) around the Eocene-Oligocene transition, and a second at the origin of the delphinoid odontocetes during the middle Miocene. We explore how methods used to estimate brain and body mass alter this perceived timing and rate of cetacean EQ evolution. We provide new data on modern mammals (mysticetes, odontocetes, and terrestrial artiodactyls) and show that brain mass and endocranial volume scale allometrically, and that endocranial volume is not a direct proxy for brain mass. We demonstrate that inconsistencies in the methods used to estimate body size across the Eocene-Oligocene boundary have caused a spurious pattern in earlier relative brain size studies. Instead, we employ a single method, using occipital condyle width as a skeletal proxy for body mass using a new dataset of extant cetaceans, to clarify this pattern. We suggest that cetacean relative brain size is most accurately portrayed using EQs based on the scaling coefficients as observed in the closely related terrestrial artiodactyls. Finally, we include additional data for an Eocene whale, raising the sample size of Eocene archaeocetes to seven. Our analysis of fossil cetacean EQ is different from previous works which had shown that a sudden increase in EQ coincided with the origin of odontocetes at the Eocene-Oligocene boundary. Instead, our data show that brain size increased at the origin of basilosaurids, 5 million years before the Eocene-Oligocene transition, and we do not observe a significant increase in relative brain size at the origin of odontocetes.

Genes underlying the evolution of tetrapod testes size

BackgroundTestes vary widely in mass relative to body mass across species, but we know very little about which genes underlie and contribute to such variation. This is partly because evidence for which genes are implicated in testis size variation tends to come from investigations involving just one or a few species. Contemporary comparative phylogenetic methods provide an opportunity to test candidate genes for their role in phenotypic change at a macro-evolutionary scale—across species and over millions of years. Previous attempts to detect genotype-phenotype associations across species have been limited in that they can only detect where genes have driven directional selection (e.g. brain size increase).ResultsHere, we introduce an approach that uses rates of evolutionary change to overcome this limitation to test whether any of twelve candidate genes have driven testis size evolution across tetrapod vertebrates—regardless of directionality. We do this by seeking a relationship between the rates of genetic and phenotypic evolution. Our results reveal five genes (Alkbh5, Dmrtb1, Pld6, Nlrp3, Sp4) that each have played unique and complex roles in tetrapod testis size diversity. In all five genes, we find strong significant associations between the rate of protein-coding substitutions and the rate of testis size evolution. Such an association has never, to our knowledge, been tested before for any gene or phenotype.ConclusionsWe describe a new approach to tackle one of the most fundamental questions in biology: how do individual genes give rise to biological diversity? The ability to detect genotype-phenotype associations that have acted across species has the potential to build a picture of how natural selection has sculpted phenotypic change over millions of years.

Craniofacial Evolution: From Australopithecus to Modern Man.

Through the analysis and evaluation of the size and morphology of teeth and jaws, it is possible to differentiate animal species including man, allowing the theory of human evolution to be established. Hominin evolution is characterized by two main features, the transition to bipedality and the increase in brain size. This had an important impact on the structure and function of the hominine skull. The aim of this article is to retrace the evolutionary steps that led to Homo Sapiens, the direct ancestor of modern man. For the following paper, scientific articles from Medline (PubMed) and Google Scholar database were used from 1929 to 2018. Hominid evolution is characterized by 2 main features, the transition to bipedality and the increase in brain size. The fossils found show that both trends have had an important impact on the morphology and function of the skull of modern man. The basicranial flexion and growth have led to the facial modifications typical of modern man. The main changes concern the mandibular evolution with the appearance of the chin, the formation of the Spee curve due to mandibular arch growth, the formation of the temporomandibular joint as a hinge joint with a sliding socket as the condyle and a better function and maximum efficiency than its predecessors thanks to respect for the divine proportions of the face. Knowledge of ontogenesis allows us to know the factors underlying human form and function, analyze and evaluate them in the clinical context.

Molecular evolutionary analysis of human primary microcephaly genes

BackgroundThere has been a rapid increase in the brain size relative to body size during mammalian evolutionary history. In particular, the enlarged and globular brain is the most distinctive anatomical feature of modern humans that set us apart from other extinct and extant primate species. Genetic basis of large brain size in modern humans has largely remained enigmatic. Genes associated with the pathological reduction of brain size (primary microcephaly-MCPH) have the characteristics and functions to be considered ideal candidates to unravel the genetic basis of evolutionary enlargement of human brain size. For instance, the brain size of microcephaly patients is similar to the brain size of Pan troglodyte and the very early hominids like the Sahelanthropus tchadensis and Australopithecus afarensis.ResultsThe present study investigates the molecular evolutionary history of subset of autosomal recessive primary microcephaly (MCPH) genes; CEP135, ZNF335, PHC1, SASS6, CDK6, MFSD2A, CIT, and KIF14 across 48 mammalian species. Codon based substitutions site analysis indicated that ZNF335, SASS6, CIT, and KIF14 have experienced positive selection in eutherian evolutionary history. Estimation of divergent selection pressure revealed that almost all of the MCPH genes analyzed in the present study have maintained their functions throughout the history of placental mammals. Contrary to our expectations, human-specific adoptive evolution was not detected for any of the MCPH genes analyzed in the present study.ConclusionBased on these data it can be inferred that protein-coding sequence of MCPH genes might not be the sole determinant of increase in relative brain size during primate evolutionary history.

Brain Allometry Across Macroevolutionary Scales in Squamates Suggests a Conserved Pattern in Snakes

Despite historical interest in brain size evolution in vertebrates, few studies have assessed variation in brain size in squamate reptiles such as snakes and lizards. Here, we analyzed the pattern of brain allometry at macroevolutionary scale in snakes and lizards, using body mass and snout vent length as measures of body size. We also assessed potential energetic trade-offs associated with relative brain size changes in Crotalinae vipers. Body mass showed a conserved pattern of brain allometry across taxa of snakes, but not in lizards. Body length favored changes of brain allometry in both snakes and lizards, but less variability was observed in snakes. Moreover, we did not find evidence for trade-offs between brain size and the size of other organs in Crotalinae. Thus, despite the contribution of body elongation to changes in relative brain size in squamate reptiles, snakes present low variation in brain allometry across taxa. Although the mechanisms driving this conserved pattern are unknown, we hypothesize that the snake body plan plays an important role in balancing the energetic demands of brain and body size increase at macroevolutionary scales. We encourage future research on the evolution of brain and body size in snakes to test this hypothesis.

Sex differences in the pelvis did not evolve de novo in modern humans.

It is commonly assumed that the strong sexual dimorphism of the human pelvis evolved for delivering the relatively large human foetuses. Here we compare pelvic sex differences across modern humans and chimpanzees using a comprehensive geometric morphometric approach. Even though the magnitude of sex differences in pelvis shape was two times larger in humans than in chimpanzees, we found that the pattern is almost identical in the two species. We conclude that this pattern of pelvic sex differences did not evolve de novo in modern humans and must have been present in the common ancestor of humans and chimpanzees, and thus also in the extinct Homo species. We further suggest that this shared pattern was already present in early mammals and propose a hypothesis of facilitated variation as an explanation: the conserved mammalian endocrine system strongly constrains the evolution of the pattern of pelvic differences but enables rapid evolutionary change of the magnitude of sexual dimorphism, which in turn facilitated the rapid increase in hominin brain size.

Human Diet Evolution: Meat, Fire, and Tapeworms

The human diet today is very different than the diets of other primates, implying major changes following the split of the human and chimpanzee/bonobo lineages about 6 million years ago. For example, at various timepoints our ancestors began consistently eating meat, cooking food with fire, and consuming products from domesticated plants and animals. Such dietary shifts are important to study because they were likely associated with important cultural and biological changes like tool use and increased brain size. However, the timing of some of these dietary shifts is extremely difficult to study with only archeological and fossil data, leading to uncertainty. In this article, we discuss how studies of human tapeworm parasites can help. Tapeworms could only have been acquired once meat was being consistently consumed and then may have later adapted to heat stress from human cooking.

The link between relative brain size and cognitive ageing in female guppies (Poecilia reticulata) artificially selected for variation in brain size.

Cognitive ageing is the general process when certain mental skills gradually deteriorate with age. Across species, there is a pattern of a slower brain structure degradation rate in large-brained species. Hence, having a larger brain might buffer the impact of cognitive ageing and positively affect survival at older age. However, few studies have investigated the link between relative brain size and cognitive ageing at the intraspecific level. In particular, experimental data on how brain size affects brain function also into higher age is largely missing. We used 288 female guppies (Poecilia reticulata), artificially selected for large and small relative brain size, to investigate variation in colour discrimination and behavioural flexibility, at 4-6, 12 and 24months of age. These ages are particularly interesting since they cover the life span from sexual maturation until maximal life length under natural conditions. We found no evidence for a slower cognitive ageing rate in large-brained females in neither initial colour discrimination nor reversal learning. Behavioural flexibility was predicted by large relative brain size in the youngest group, but the effect of brain size disappeared with increasing age. This result suggests that cognitive ageing rate is faster in large-brained female guppies, potentially due to the faster ageing and shorter lifespan in the large-brained selection lines. It also means that cognition levels align across different brain sizes with older age. We conclude that there are cognitive consequences of ageing that vary with relative brain size in advanced learning abilities, whereas fundamental aspects of learning can be maintained throughout the ecologically relevant life span.

A Connectomic Hypothesis for the Hominization of the Brain.

Cognitive abilities of the human brain, including language, have expanded dramatically in the course of our recent evolution from nonhuman primates, despite only minor apparent changes at the gene level. The hypothesis we propose for this paradox relies upon fundamental features of human brain connectivity, which contribute to a characteristic anatomical, functional, and computational neural phenotype, offering a parsimonious framework for connectomic changes taking place upon the human-specific evolution of the genome. Many human connectomic features might be accounted for by substantially increased brain size within the global neural architecture of the primate brain, resulting in a larger number of neurons and areas and the sparsification, increased modularity, and laminar differentiation of cortical connections. The combination of these features with the developmental expansion of upper cortical layers, prolonged postnatal brain development, and multiplied nongenetic interactions with the physical, social, and cultural environment gives rise to categorically human-specific cognitive abilities including the recursivity of language. Thus, a small set of genetic regulatory events affecting quantitative gene expression may plausibly account for the origins of human brain connectivity and cognition.