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.

Brain Mass (Energy) Resistant to Hyperglycaemic Oversupply: A Systematic Review

Cerebral energy supply is determined by the energy content of the blood. Accordingly, the brain is undersupplied during hypoglycaemia. Whether or not there is an additional cerebral energy demand that depends upon the energy content of the brain is considered differently in two opposing theoretical approaches. The Selfish-Brain theory postulates that the brain actively demands energy from the body when needed, while long-held theories, the gluco-lipostatic theory and its variants, deny such active brain involvement and view the brain as purely passively supplied. Here we put the competing theories to the test. We conducted a systematic review of a condition in which the rival theories make opposite predictions, i.e., experimental T1DM. The Selfish-Brain theory predicts that induction of experimental type 1 diabetes causes minor mass (energy) changes in the brain as opposed to major glucose changes in the blood. This prediction becomes our hypothesis to be tested here. A total of 608 works were screened by title and abstract, and 64 were analysed in full text. According to strict selection criteria defined in our PROSPERO preannouncement and complying with PRISMA guidelines, 18 studies met all inclusion criteria. Thirteen studies provided sufficient data to test our hypothesis. The 13 evaluable studies (15 experiments) showed that the diabetic groups had blood glucose concentrations that differed from controls by +294 ± 96% (mean ± standard deviation) and brain mass (energy) that differed from controls by −4 ± 13%, such that blood changes were an order of magnitude greater than brain changes (T = 11.5, df = 14, p < 0.001). This finding confirms not only our hypothesis but also the prediction of the Selfish-Brain theory, while the predictions of the gluco-lipostatic theory and its variants were violated. The current paper completes a three-part series of systematic reviews, the two previous papers deal with a distal and a proximal bottleneck in the cerebral brain supply, i.e., caloric restriction and cerebral artery occlusion. All three papers demonstrate that accurate predictions are only possible if one regards the brain as an organ that regulates its energy concentrations independently and occupies a primary position in a hierarchically organised energy metabolism.Systematic Review Registration:https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=156816, PROSPERO, identifier: CRD42020156816.

Decreases in Brain Size and Encephalization in Anatomically Modern Humans

Growth in human brain size and encephalization is well documented throughout much of prehistory and believed to be responsible for increasing cognitive faculties. Over the past 50,000 years, however, both body size and brain mass have decreased but little is known about the scaling relationship between the two. Here, changes to the human brain are examined using matched body remains to determine encephalization levels across an evolutionary timespan. The results find decreases to encephalization levels in modern humans as compared to earlier Holocene <i>H. sapiens</i> and Late Pleistocene anatomically modern <i>Homo</i>. When controlled for lean body mass, encephalization changes are isometric, suggesting that much of the declines in encephalization are driven by recent increases in obesity. A meta-review of genome-wide association studies finds some evidence for selective pressures acting on human cognitive ability, which may be an evolutionary consequence of the more than 5% loss in brain mass over the past 50,000 years.

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.

Neurological susceptibility to environmental exposures: pathophysiological mechanisms in neurodegeneration and multiple chemical sensitivity

The World Health Organization lists air pollution as one of the top five risks for developing chronic non-communicable disease, joining tobacco use, harmful use of alcohol, unhealthy diets and physical inactivity. This review focuses on how host defense mechanisms against adverse airborne exposures relate to the probable interacting and overlapping pathophysiological features of neurodegeneration and multiple chemical sensitivity. Significant long-term airborne exposures can contribute to oxidative stress, systemic inflammation, transient receptor subfamily vanilloid 1 (TRPV1) and subfamily ankyrin 1 (TRPA1) upregulation and sensitization, with impacts on olfactory and trigeminal nerve function, and eventual loss of brain mass. The potential for neurologic dysfunction, including decreased cognition, chronic pain and central sensitization related to airborne contaminants, can be magnified by genetic polymorphisms that result in less effective detoxification. Onset of neurodegenerative disorders is subtle, with early loss of brain mass and loss of sense of smell. Onset of MCS may be gradual following long-term low dose airborne exposures, or acute following a recognizable exposure. Upregulation of chemosensitive TRPV1 and TRPA1 polymodal receptors has been observed in patients with neurodegeneration, and chemically sensitive individuals with asthma, migraine and MCS. In people with chemical sensitivity, these receptors are also sensitized, which is defined as a reduction in the threshold and an increase in the magnitude of a response to noxious stimulation. There is likely damage to the olfactory system in neurodegeneration and trigeminal nerve hypersensitivity in MCS, with different effects on olfactory processing. The associations of low vitamin D levels and protein kinase activity seen in neurodegeneration have not been studied in MCS. Table 2 presents a summary of neurodegeneration and MCS, comparing 16 distinctive genetic, pathophysiological and clinical features associated with air pollution exposures. There is significant overlap, suggesting potential comorbidity. Canadian Health Measures Survey data indicates an overlap between neurodegeneration and MCS (p < 0.05) that suggests comorbidity, but the extent of increased susceptibility to the other condition is not established. Nevertheless, the pathways to the development of these conditions likely involve TRPV1 and TRPA1 receptors, and so it is hypothesized that manifestation of neurodegeneration and/or MCS and possibly why there is divergence may be influenced by polymorphisms of these receptors, among other factors.

Meningovascular syphilis presenting as a brain mass in an immunocompetent male

We present a case of an HIV-negative man with syphilitic meningovascular disease with subjacent involvement of brain parenchyma leading to a mass-forming inflammatory lesion that was pathologically distinct from a typical gumma. Syphilis was diagnosed after tissue obtained from a brain biopsy demonstrated spirochetes consistent with Treponema pallidum and confirmed by 16S rRNA sequencing.

Modified formulas for calculation of encephalization: quotient in dogs

Objective Dogs are a breed of animals that play important roles in security service, companionship, hunting, guard, work and models of research for application in humans. Intelligence is the key factor to success in life, most especially for dogs that are used for security purposes at the airports, seaports, public places, houses, schools and farms. However, it has been reported that there is correlation between intelligence, body weight, height and craniometry in human. In view of this, literatures were searched on body weight, height and body surface areas of ten dogs with intent to determining their comparative level of intelligence using encephalization quotient. Results Findings revealed that dogs have relationship of brain allometry with human as proven by encephalization quotient $$\left( {{\text{EQ}}} \right)\, = \,{\text{Brain Mass}}/0.{14}\, \times \,{\text{Body weight}}^{{0.{528}}} ,{\text{ Brain Mass}}/0.{12}\, \times \,{\text{Body Weight}}^{{0.{66}}}$$ EQ = Brain Mass / 0.14 × Body weight 0.528 , Brain Mass / 0.12 × Body Weight 0.66 and Brain Mass (E) = kpβ, where p is the body weight; k = 0.14 and β = 0.528, respectively. Saganuwa’s formula yielded better results as compared with the other formulas. Dogs with body surface area (BSA), weight and height similar to that of human are the most intelligent. Doberman pinscher is the most intelligent followed by German shepherd, Labrador retriever, Golden retriever, respectively.