The multiple contexts of brain scaling: Phenotypic integration in brain and behavioral evolution

Understanding the adaptive functions of increasing brain size have occupied scientists for decades. Here, taking the general perspective of the Extended Evolutionary Synthesis, the question of how brains change in size will be considered in two developmental frameworks. The first framework will consider the particular developmental mechanisms that control and generate brain mass, concentrating on neurogenesis in a comparative vertebrate context. The consequences of limited adult neurogenesis in mammals, and the dominating role of duration of neurogenesis for mammalian evolution will be discussed for the particular case of the teleost versus mammalian retina, and for paths of brain evolution more generally. The second framework examines brain mass in terms of life history, particularly the features of life history that correlate highly, if imperfectly, with brain mass, including duration of development to adolescence, duration of parental care, body and range size, and longevity. This covariation will be examined in light of current work on genetic causes and consequences of covariation in craniofacial bone groupings. The eventual development of a multivariate structure for understanding brain evolution which specifically integrates formerly separate layers of analysis is the ultimate goal.

Multifaceted Microcephaly-Related Gene MCPH1

MCPH1, or BRIT1, is often mutated in human primary microcephaly type 1, a neurodevelopmental disorder characterized by a smaller brain size at birth, due to its dysfunction in regulating the proliferation and self-renewal of neuroprogenitor cells. In the last 20 years or so, genetic and cellular studies have identified MCPH1 as a multifaceted protein in various cellular functions, including DNA damage signaling and repair, the regulation of chromosome condensation, cell-cycle progression, centrosome activity and the metabolism. Yet, genetic and animal model studies have revealed an unpredicted essential function of MPCH1 in gonad development and tumorigenesis, although the underlying mechanism remains elusive. These studies have begun to shed light on the role of MPCH1 in controlling various pathobiological processes of the disorder. Here, we summarize the biological functions of MCPH1, and lessons learnt from cellular and mouse models of MCPH1.

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.

Genetic Mechanisms Underlying the Evolution of Connectivity in the Human Cortex

One of the most salient features defining modern humans is our remarkable cognitive capacity, which is unrivaled by any other species. Although we still lack a complete understanding of how the human brain gives rise to these unique abilities, the past several decades have witnessed significant progress in uncovering some of the genetic, cellular, and molecular mechanisms shaping the development and function of the human brain. These features include an expansion of brain size and in particular cortical expansion, distinct physiological properties of human neurons, and modified synaptic development. Together they specify the human brain as a large primate brain with a unique underlying neuronal circuit architecture. Here, we review some of the known human-specific features of neuronal connectivity, and we outline how novel insights into the human genome led to the identification of human-specific genetic modifiers that played a role in the evolution of human brain development and function. Novel experimental paradigms are starting to provide a framework for understanding how the emergence of these human-specific genomic innovations shaped the structure and function of neuronal circuits in the human brain.

Comparative analysis of brain in relation to the body length and weight of common carp (Cyprinus carpio) in captive (hatchery) and wild (river system) populations

Cyprinus carpio is the member of family cyprinidae commonly called common carp. This study was aimed to find out the comparison of brain of wild (river system) and captive (hatchery reared) population of common carp. A total of thirty samples (15 from hatchery and 15 from river Swat) were collected. All the specimens were examined in Laboratory of Parasitoloy, Zoology Department, University of Malakand. Findings indicated that wild population were greater in brain size and weight as compared to hatchery reared population. The fish samples collected from captive environment (hatchery) were showing more weight and length as compared to wild population of common carps. The mean value of total weight of hatchery fishes 345±48.68 and the mean value of brain weight of hatchery reared fishes 0.28±0.047. The mean value of wild fish’s total body weight 195.16±52.58 and the mean value of brain weight of wild fishes are 0.45±0.14. Present research calls for the fact that fish in dependent environmental conditions possess brain larger in size as compared to its captive population, it is due to use and disuse of brain in their environmental requirements.

Comparative brain analysis of wild and hatchery reared Mahseer (Tor putitora) relative to their body weight and length

The present study was aimed at comparing the brain size of mahseer (Tor putitora) in relation to their body weight and standard length, to investigate the potential impact of rearing environment on brain development in fish. The weight of the brain and three of its subdivisions cerebellum (CB), optic tectum (OT), and telencephalon (TC) were measured for both wild and hatchery-reared fish. The data was analysed using multiple analysis of covariance (MANCOVA), analysis of covariance (ANCOVA), and discriminate function analysis (DFA). We found the fish reared under hatchery conditions exhibit smaller brain size related to body weight, when compared to the wild ones. A significant (p<0.5) difference was observed in the length of CB and OT concerning the standard body length while no significant difference was found in TC of the fish from both the origins. The results of the current study highlight a logical assumption that neural deficiency affects the behaviour of fish, that’s why the captive-reared fish show maladaptive response and face fitness decline when released to the natural environment for wild stock enhancement. The current study concluded that hatchery-reared fish exhibit variations in gross brain morphology as compared to their wild counterpart.

The evolution and biological correlates of hand preferences in anthropoid primates

The evolution of human right-handedness has been intensively debated for decades. Manual lateralization patterns in non-human primates have the potential to elucidate evolutionary determinants of human handedness. However, restricted species samples and inconsistent methodologies are limiting comparative phylogenetic studies. By combining original data with published literature reports, we assembled data on hand preferences for standardized object manipulation in 1,806 individuals from 38 species of anthropoid primates, including monkeys, apes, and humans. Based on that, we employ quantitative phylogenetic methods to test prevalent hypotheses on the roles of ecology, brain size and tool use in primate handedness evolution. We confirm that human right-handedness represents an unparalleled extreme among anthropoids and found taxa displaying significant population-level handedness to be notably rare. Species-level direction of manual lateralization was largely uniform among non-human primates and neither correlated with phylogeny nor with any of the selected biological predictors. In contrast, we recovered highly variable patterns of hand preference strength, which show signatures of both ecology and phylogeny. In particular, terrestrial primates tend to display weaker hand preferences than arboreal species. These results challenge popular ideas on primate handedness evolution, especially the postural origins hypothesis. Furthermore, they point to a potential adaptive benefit of disparate lateralization strength in primates, a measure of hand preference that has often been overlooked in the past. Finally, our data show that human lateralization patterns do not align with trends found among other anthropoids, suggesting that unique selective pressures gave rise to the unusual hand preferences displayed by our species.

Clinical Aspects of Microcephaly Patients Regarding Endocrine Profile

Introduction: Microcephaly is characterized as an occipitofrontal head circumference (OFC) underneath the third centile or more than 2 standard deviations (SD) below the mean for sex, age, and ethnicity. The term ‘severe’ microcephaly is connected to an OFC more than 3SD below the mean. Microcephaly is associated with a reduction in brain volume and frequently intellectual and/or motor inabilities. The pathogenesis of microcephaly is heterogeneous, extending from hereditary causes to environmental components that can have an effect on developmental process that impact brain size. Objective: The main objective of this study was to compare the BMI and endocrine profile of patients having microcephaly with age matched to normal siblings in their families. Materials and Methods: Study design: Quantitative cross sectional Settings: Services Hospital Lahore Duration: 01 year i.e. 1st January 2020 to 30th December 2020 Methodology: This is a quantitative cross sectional study arrangement based on 12 persons. On the basis of microcephaly, the subjects were separated into the two groups: Group I: Subjects with microcephaly (n=10), Group II: Normal kin as controls (n=2). Five families including add up to of 12 individuals was selected. Ten people with microcephaly (cases) and two normal kin (without microcephaly) were taken as controls. Cooperation of the subjects in this study was selected voluntarily and written informed consent was taken to take part in the study from each individual and from their guardians. The individuals and their guardians were educated about the potential benefits and risks of this study. Results: There was little difference within the mean age of microcephaly individuals as compared to healthy siblings. Conclusion: In light of this study it can be recommended that there's a significant affiliation of BMI and microcephaly but the affiliation of Leptin, Cortisol, GH and TSH with microcephaly seem not be found as proposed by non-significant results. This may moreover emphasize on heredity perspective of this condition. Keywords: Microcephaly, Leptin, Growth Hormone, BMI, TSH

Experts in action: why we need an embodied social brain hypothesis

The anthropoid primates are known for their intense sociality and large brain size. The idea that these might be causally related has given rise to a large body of work testing the ‘social brain hypothesis'. Here, the emphasis has been placed on the political demands of social life, and the cognitive skills that would enable animals to track the machinations of other minds in metarepresentational ways. It seems to us that this position risks losing touch with the fact that brains primarily evolved to enable the control of action, which in turn leads us to downplay or neglect the importance of the physical body in a material world full of bodies and other objects. As an alternative, we offer a view of primate brain and social evolution that is grounded in the body and action, rather than minds and metarepresentation. This article is part of the theme issue ‘Systems neuroscience through the lens of evolutionary theory’.