Publications by authors named "Yasuo Ihara"

Social interaction is a prime driver for the evolution of animal behaviour. Dyadic interaction, in particular, has been the focus of intensive research on the evolution of mutualistic, altruistic, selfish or spiteful behaviours. Meanwhile, triadic interaction has been the minimal framework for the study of animal coalition as observed in some species of primates, as well as in carnivores and cetaceans, where two or more individuals act jointly against a third party in a competitive context.

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The evolution of a cultural trait may be affected by niche construction, or changes in the selective environment of that trait due to the inheritance of other cultural traits that make up a cultural background. This study investigates the evolution of a cultural trait, such as the acceptance of the idea of contraception, that is both vertically and horizontally transmitted within a homogeneous social network. Individuals may conform to the norm, and adopters of the trait have fewer progeny than others.

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Spatial distribution of human culture reflects both descent from the common ancestor and horizontal transmission among neighbouring populations. To analyse empirically documented geographical variations in cultural repertoire, we will describe a framework for Bayesian statistics in a spatially explicit model. To consider both horizontal transmission and mutation of the cultural trait in question, our method employs a network model in which populations are represented by nodes.

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Geographic patterns of cultural variations are affected by how cultural traits are transmitted within and between populations. It has been argued that cultural traits are transmitted in different manners depending on their characteristics; for example, words for basic concepts are less liable to horizontal transmission between populations (i.e.

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Cultural macroevolution concerns a long-term evolutionary process involving transmission of non-genetic or cultural traits between populations as well as birth and death of populations. To understand the spatial dynamics of cultural macroevolution, we present a one-locus model of cultural diffusion in which a cultural trait is transmitted on a network of populations. Borrowing the method of ancestral backward process from population genetics, our model explores the lineage of a trait variant sampled in the present generation to quantify when and where the variant was invented.

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Presenilin (PS) with a genetic mutation generates abundant β-amyloid protein (Aβ) 43. Senile plaques are formed by Aβ43 in the cerebral parenchyma together with Aβ42 at middle ages. These brains cause the early onset of Alzheimer's disease (AD), which is known as familial Alzheimer's disease (FAD).

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In humans, support from partners and alloparents is crucial for successful child-rearing and optimal child development. However, the complex relationships among childcare support, children's outcomes and parental characteristics have not been fully examined. We investigate how three sources of partner and alloparental support-partner's childcare participation, support from children's grandparents and support from non-kin-can be associated with child social development.

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This study evaluates the hypothesis that some documented cases of long-distance sea crossing by the Late Pleistocene Homo sapiens occurred as a result of accidental drifting, rather than by intentional seafaring. For that purpose, we use an existing computer simulation framework, with some modifications, to investigate the likelihood that a planned or unplanned island colonization by a small group of individuals will persist to establish a viable population. Within the original framework, planned colonization was operationally characterized as being initiated by equal numbers of unrelated young men and women, whereas for unplanned colonization, those who migrate inadvertently were regarded in effect as a random sample of the whole population.

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Some dialect words are shared among geographically distant groups of people without close interaction. Such a pattern may indicate the current or past presence of a cultural centre exerting a strong influence on peripheries. For example, concentric distributions of dialect variants in Japan may be explicable by repeated inventions of new variants at Kyoto, the ancient capital, with subsequent outward diffusion.

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Article Synopsis
  • Aβ1-42 and Aβ1-43 are processed by γ-secretase into shorter Aβ peptides (Aβ1-38 and Aβ1-40), with their production and deposition in human brains correlating to Alzheimer's disease progression.
  • As Alzheimer's disease advances, the levels of deposited Aβ1-43 increase in proportion to Aβ1-42, while Aβ1-38 correlates with Aβ1-40, indicating related mechanisms of deposition.
  • The study reveals that γ-secretase activity varies in Alzheimer’s disease brains, leading to increased production of certain Aβs, highlighting its role in the disease pathology.
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Tau is a microtubule (MT)-associated protein that is localized to the axon. In Alzheimer's disease, the distribution of tau undergoes a remarkable alteration, leading to the formation of tau inclusions in the somatodendritic compartment. To investigate how this mislocalization occurs, we recently developed immunohistochemical tools that can separately detect endogenous mouse and exogenous human tau with high sensitivity, which allows us to visualize not only the pathological but also the pre-aggregated tau in mouse brain tissues of both sexes.

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Social learning not only takes the form of random copying of other individuals, but also involves learners' choice of what to learn or from whom to learn. Best-of-k learning refers to a kind of success-biased social learning strategy in which a learner randomly samples k exemplars from the population and imitates the most "successful" one, or the one gaining the highest payoff. While it is intuitive that best-of-k learning can promote the spread of superior variants and thereby enable cumulative cultural evolution, a previous mathematical analysis has shown that it may sometimes result in maladaptive cultural evolution when the payoffs associated with cultural variants vary stochastically.

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The neuropathology of Alzheimer's disease (AD) is characterized by the accumulation and aggregation of amyloid β (Aβ) peptides into extracellular plaques of the brain. The Aβ peptides, composed of 40 amino acids, are generated from amyloid precursor proteins (APP) by β- and γ-secretases. Aβ is deposited not only in cerebral parenchyma but also in leptomeningeal and cerebral vessel walls, known as cerebral amyloid angiopathy (CAA).

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Tau is a microtubule-associated protein (MAP) that is localized to the axon. In Alzheimer's disease (AD), the distribution of tau undergoes a remarkable alteration, leading to the formation of tau inclusions in the somatodendritic compartment. While the abnormal aggregated tau has been extensively studied in human patient tissues and animal models of AD, how normal tau localizes to the axon, which would be the foundation to understand how the mis-localization occurs, has not been well studied due to the poor detectability of normal unaggregated tau in vivo.

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Despite the generally low level of inter-population genetic differentiation in humans as compared with great apes, it has long been acknowledged that there is a considerable amount of geographic variations in human phenotypes, for example, skin pigmentation, cranial morphology, and soft-tissue facial morphology, to name but a few. Indeed, recent studies have suggested that the extent of inter-population diversity in some human phenotypes is greater than expected from random drift alone. Such an excess of phenotypic diversity is often attributed to adaptation to local environment.

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Tauopathy is a type of dementia defined by the accumulation of filamentous tau inclusions in neural cells. Most types of dementia in the elderly, including Alzheimer's disease, are tauopathies. Although it is believed that tau protein abnormalities and/or the loss of its functions results in neurodegeneration and dementia, the mechanism of tauopathy remains obscure.

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Article Synopsis
  • Aβ deposition is a key characteristic of Alzheimer's disease, resulting from the breakdown of amyloid precursor proteins and varies across individuals with AD and cerebral amyloid angiopathy.
  • Advanced imaging techniques like MALDI-IMS allowed researchers to map the distribution of various Aβ species in human brains, revealing that specific peptides, like Aβ1-42 and Aβ1-43, accumulate in amyloid plaques, while others settle in blood vessels.
  • A solitary amino acid change between Aβ1-41 and Aβ1-42 led to significant differences in their spatial distribution, emphasizing the potential of MALDI-IMS for enhancing our understanding of Aβ biology in Alzheimer's disease.
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γ-secretase inhibitors (GSI) are drugs developed to decrease amyloid-β peptide (Aβ) production by inhibiting intramembranous cleavage of β-amyloid protein precursor (βAPP). However, a large phase 3 trial of semagacestat, a potential non-transition state analog (non-TSA) GSI, in patients with Alzheimer's disease (AD) was terminated due to unexpected aggravation of cognitive deficits and side effects. Here, we show that some semagacestat effects are clearly different from a phenotype caused by a loss of function of presenilins, core proteins in the γ-secretase complex.

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The amyloid β (Aβ) protein is a major component of senile plaques, one of the neuropathological hallmarks of Alzheimer's disease. Amyloidogenic processing of amyloid precursor protein (APP) by β- and γ-secretases leads to production of Aβ. APP contains tandem triple repeats of the GXXXG motif in its extracellular juxtamembrane and transmembrane regions.

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Group-wise cooperation, or cooperation among three or more individuals, is an integral part of human societies. It is likely that group-wise cooperation also played a crucial role in the survival of early hominins, who were confronted with novel environmental challenges, long before the emergence of Homo sapiens. However, previous theoretical and empirical studies, focusing mainly on modern humans, have tended to suggest that evolution of cooperation in sizable groups cannot be explained by simple direct reciprocity and requires some additional mechanisms (reputation, punishment, etc.

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Tau is a key protein in the pathogenesis of various neurodegenerative diseases, which are categorized as tauopathies. Because the extent of tau pathologies is closely linked to that of neuronal loss and the clinical symptoms in Alzheimer's disease, anti-tau therapeutics, if any, could be beneficial to a broad spectrum of tauopathies. To learn more about tauopathy, we developed a novel transgenic nematode (Caenorhabditis elegans) model that expresses either wild-type or R406W tau in all the neurons.

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Neurofibrillary tangles, composed of hyperphosphorylated tau fibrils, are a pathological hallmark of Alzheimer's disease; the neurofibrillary tangle load correlates strongly with clinical progression of the disease. A growing body of evidence indicates that tau oligomer formation precedes the appearance of neurofibrillary tangles and contributes to neuronal loss. Here we show that tau oligomer formation can be inhibited by compounds whose chemical backbone includes 1,2-dihydroxybenzene.

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Introduction: The A673T mutation in the amyloid precursor protein (APP) protects against Alzheimer's disease by reducing β-amyloid protein (Aβ) production. This mutation reduced the release of the soluble APP fragment (sAPPβ), which is processed by β-secretase, suggesting a concomitant decrease in the β-carboxyl fragment of APP (C99), which is a direct substrate of γ-secretase for Aβ production. However, it remains controversial whether the level of C99 is significantly reduced in cells expressing APP that carry A673T as the cause of reduced Aβ production.

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The carboxyl-terminal sequence of tau composes the framework for its intracellular inclusions that appear in diverse neurodegenerative disorders known as tauopathies. However, microtubule-associated protein 2 (MAP2), which contains a homologous carboxyl-terminal sequence of tau, is undetectable in the mature tau inclusions. The mechanisms underlying this phenomenon have remained largely unknown.

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