The Experts below are selected from a list of 264 Experts worldwide ranked by ideXlab platform

Rui Diogo - One of the best experts on this subject based on the ideXlab platform.

  • Introduction to Evolutionary Developmental Pathology, or Evo-Devo-Path: on Neodarwinism, Natural Mutants, Hopeful Monsters, Syndromes, Genomics, Variations, Humans, Apes, Chameleons, and Dinosaurs
    Current Molecular Biology Reports, 2020
    Co-Authors: Rui Diogo
    Abstract:

    During the second half of the twentieth century, few authors attempted to combine the increasing knowledge obtained from the study of model organisms and human medicine with data from comparative anatomy, evolutionary biology, “natural mutants,” and variations in order to investigate the links between development, Pathology, and macroevolution. However, in the last decades, there has been a renewed interest on these subjects, with the rise of Evolutionary Developmental Pathology (Evo-Devo-Path), a field that is attracting more and more attention across the globe, not only from the scientific community but also from the media and broader public. This is because this field is mainly related to a deeper understanding of Developmental anomalies and disease within an evolutionary framework, paying a special attention to “natural mutants,” such as cyclopic sheep, humans with severe congenital malformations, and to so-called “hopeful monsters,” such as chameleons and, to a certain extent, dinosaurs, as will be explained in this issue. These are hot topics within the broader community and for the media, that have been also of main interest to biologists for a long time, for instance to renowned authors such as Étienne Geoffroy Saint-Hilaire, Waddington, Goldschmidt, Gould and Per Alberch. However, these issues became somewhat neglected with the rise of genetics and the increased focus on the “Devo” within Evolutionary Developmental Biology (Evo-Devo), in particular on molecular biology studies and therefore on experimentally produced—and not so much on “natural”—mutations. Another main, and related, reason was the prevalence of Neodarwinism within biology—sometimes defended in a quasi-religious way and using extremist ideas, such as reducing evolution to “selfish genes,” that, we now know, do not correspond to the complex and multifaceted reality of biological evolution within this planet. These subjects will be discussed in this special, and very timely, issue precisely about Evo-Devo-Path, which attests the increasing interest in this field, and thus on natural mutants, “hopeful monsters,” and other ideas of the authors named just above, and shows how new knowledge and tools, for instance about the cardiopharyngeal muscles and syndromes and about genomics and transposable elements, are quickly being integrated in crucial discussions within this field.

  • effects of hyperthyroidism in the development of the appendicular skeleton and muscles of zebrafish with notes on evolutionary Developmental Pathology evo devo path
    Scientific Reports, 2019
    Co-Authors: Fedor Shkil, Natalia Siomava, Elena E Voronezhskaya, Rui Diogo
    Abstract:

    The hypothalamus-pituitary-thyroid (HPT) axis plays a crucial role in the metabolism, homeostasis, somatic growth and development of teleostean fishes. Thyroid hormones regulate essential biological functions such as growth and development, regulation of stress, energy expenditure, tissue compound, and psychological processes. Teleost thyroid follicles produce the same thyroid hormones as in other vertebrates: thyroxin (T4) and triiodothyronine (T3), making the zebrafish a very useful model to study hypo- and hyperthyroidism in other vertebrate taxa, including humans. Here we investigate morphological changes in T3 hyperthyroid cases in the zebrafish to better understand malformations provoked by alterations of T3 levels. In particular, we describe musculoskeletal abnormalities during the development of the zebrafish appendicular skeleton and muscles, compare our observations with those recently done by us on the normal Developmental of the zebrafish, and discuss these comparisons within the context of evolutionary Developmental Pathology (Evo-Devo-Path), including human pathologies.

  • Musculoskeletal study of cebocephalic and cyclopic lamb heads illuminates links between normal and abnormal development, evolution and human pathologies.
    Scientific reports, 2019
    Co-Authors: Rui Diogo, Natalia Siomava, Daria Razmadze, Nora Douglas, Jose S. M. Fuentes, Andre J. Duerinckx
    Abstract:

    This paper is part of the emerging field of Evolutionary Developmental Pathology, dedicated to study the links between normal and abnormal development, evolution and human pathologies. We analyzed the head musculoskeletal system of several ‘natural mutant’ newborn lambs displaying various degrees of abnormality, from mild defects to cebocephaly and to cyclopia, and compared them with humans. Interestingly, muscle defects are less marked than osteological ones, and contrarily to the latter they tend to display left-right assymetries. In individuals with cebocephalic and even cyclopic skulls almost all head muscles are normal. The very few exceptions are some extraocular muscles and facial muscles that normally attach to osteological structures that are missing in the abnormal heads: such muscles are instead attached to the ‘nearest topological neighbor’ of the missing osteological structure, a pattern also found in cyclopic humans. These observations support Alberch’s ill-named “logic of monsters” - as a byproduct of strong Developmental/topological constraints anatomical patterns tend to repeat themselves, even severe malformations displayed by distantly related taxa. They also support the idea that mammalian facial muscles reverted to an ancestral ‘nearest-neighbor’ muscle-bone type of attachment seen in non-vertebrate animals and in vertebrate limbs, but not in other vertebrate head muscles.

  • Radial polydactyly: putting together evolution, development and clinical anatomy.
    The Journal of hand surgery European volume, 2018
    Co-Authors: Bríd Crowley, Susan Stevenson, Rui Diogo
    Abstract:

    Evolutionary Developmental Pathology, a new biological field, connects the study of evolution, development and human pathologies. In radial polydactyly, traditional studies have focused mainly on s...

  • Dinosaurs, chameleons, humans, and evo-devo path: linking Étienne Geoffroy's teratology, Waddington's homeorhesis, Alberch's logic of "monsters," and Goldschmidt hopeful "monsters".
    Journal of Experimental Zoology Part B: Molecular and Developmental Evolution, 2017
    Co-Authors: Rui Diogo, Geoffrey Guinard, Raul E. Diaz Jr
    Abstract:

    Since the rise of evo-devo (evolutionary Developmental biology) in the 1980s, few authors have attempted to combine the increasing knowledge obtained from the study of model organisms and human medicine with data from comparative anatomy and evolutionary biology in order to investigate the links between development, Pathology, and macroevolution. Fortunately, this situation is slowly changing, with a renewed interest in evolutionary Developmental Pathology (evo-devo-path) in the past decades, as evidenced by the idea to publish this special, and very timely, issue on "Developmental Evolution in Biomedical Research." As all of us have recently been involved, independently, in works related in some way or another with evolution and Developmental anomalies, we decided to join our different perspectives and backgrounds in the present contribution for this special issue. Specifically, we provide a brief historical account on the study of the links between evolution, development, and pathologies, followed by a review of the recent work done by each of us, and then by a general discussion on the broader Developmental and macroevolutionary implications of our studies and works recently done by other authors. Our primary aims are to highlight the strength of studying Developmental anomalies within an evolutionary framework to understand morphological diversity and disease by connecting the recent work done by us and others with the research done and broader ideas proposed by authors such as Étienne Geoffroy Saint-Hilaire, Waddington, Goldschmidt, Gould, and Per Alberch, among many others to pave the way for further and much needed work regarding abnormal development and macroevolution.

Peter Riederer - One of the best experts on this subject based on the ideXlab platform.

  • what have we learned from the streptozotocin induced animal model of sporadic alzheimer s disease about the therapeutic strategies in alzheimer s research
    Journal of Neural Transmission, 2013
    Co-Authors: Melita Salkovicpetrisic, Ana Knezovic, Siegfried Hoyer, Peter Riederer
    Abstract:

    Experimental models that faithfully mimic the Developmental Pathology of sporadic Alzheimer's disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs' efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated.

  • What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer’s disease, about the therapeutic strategies in Alzheimer’s research
    Journal of Neural Transmission, 2013
    Co-Authors: Melita Salkovic-petrisic, Ana Knezovic, Siegfried Hoyer, Peter Riederer
    Abstract:

    Experimental models that faithfully mimic the Developmental Pathology of sporadic Alzheimer’s disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs’ efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated.

Anthony A. Grace - One of the best experts on this subject based on the ideXlab platform.

  • Developmental Pathology, dopamine, stress and schizophrenia.
    International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2010
    Co-Authors: Daniel J. Lodge, Anthony A. Grace
    Abstract:

    Psychological stress is a contributing factor for a wide variety of neuropsychiatric diseases including substance use disorders, anxiety, depression and schizophrenia. However, it has not been conclusively determined how stress augments the symptoms of these diseases. Here we review evidence that the ventral hippocampus may be a site of convergence whereby a number of seemingly discrete risk factors, including stress, may interact to precipitate psychosis in schizophrenia. Specifically, aberrant hippocampal activity has been demonstrated to underlie both the elevated dopamine neuron activity and associated behavioral hyperactivity to dopamine agonists in a verified animal model of schizophrenia. In addition, stress, psychostimulant drug use, prenatal infection and select genetic polymorphisms all appear to augment ventral hippocampal function that may therefore exaggerate or precipitate psychotic symptoms. Such information is critical for our understanding into the Pathology of psychiatric disease with the ultimate aim being the development of more effective therapeutics.

  • Developmental Pathology dopamine and stress a model for the age of onset of schizophrenia symptoms
    Schizophrenia Bulletin, 2004
    Co-Authors: Judy L Thompson, Michael F Poguegeile, Anthony A. Grace
    Abstract:

    : It is unknown why the onset of schizophrenia is typically during late adolescence or early adulthood. The fact that numerous brain maturational processes normally occur during this age period has led researchers to postulate how such processes may be related to the onset of symptoms. To help elucidate the question of age of onset, we selectively review schizophrenia-associated abnormalities of dopamine and related systems, including glutamate and hypothalamic-pituitary-adrenal systems; relevant models of pathophysiology; and the systems' Developmental aspects. Based on current findings and conceptualizations, a model is then proposed in which, during adolescence, interactive pathological and normal adolescence-associated processes trigger a positive feedback system that results in a rapid increase in Pathology that is proposed to underlie the development of active psychotic symptoms during late adolescence or early adulthood.

Ana Knezovic - One of the best experts on this subject based on the ideXlab platform.

  • what have we learned from the streptozotocin induced animal model of sporadic alzheimer s disease about the therapeutic strategies in alzheimer s research
    Journal of Neural Transmission, 2013
    Co-Authors: Melita Salkovicpetrisic, Ana Knezovic, Siegfried Hoyer, Peter Riederer
    Abstract:

    Experimental models that faithfully mimic the Developmental Pathology of sporadic Alzheimer's disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs' efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated.

  • What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer’s disease, about the therapeutic strategies in Alzheimer’s research
    Journal of Neural Transmission, 2013
    Co-Authors: Melita Salkovic-petrisic, Ana Knezovic, Siegfried Hoyer, Peter Riederer
    Abstract:

    Experimental models that faithfully mimic the Developmental Pathology of sporadic Alzheimer’s disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs’ efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated.

Siegfried Hoyer - One of the best experts on this subject based on the ideXlab platform.

  • what have we learned from the streptozotocin induced animal model of sporadic alzheimer s disease about the therapeutic strategies in alzheimer s research
    Journal of Neural Transmission, 2013
    Co-Authors: Melita Salkovicpetrisic, Ana Knezovic, Siegfried Hoyer, Peter Riederer
    Abstract:

    Experimental models that faithfully mimic the Developmental Pathology of sporadic Alzheimer's disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs' efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated.

  • What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer’s disease, about the therapeutic strategies in Alzheimer’s research
    Journal of Neural Transmission, 2013
    Co-Authors: Melita Salkovic-petrisic, Ana Knezovic, Siegfried Hoyer, Peter Riederer
    Abstract:

    Experimental models that faithfully mimic the Developmental Pathology of sporadic Alzheimer’s disease (sAD) in humans are important for testing the novel therapeutic approaches in sAD treatment. Widely used transgenic mice AD models have provided valuable insights into the molecular mechanisms underlying the memory decline but, due to the particular β-amyloid-related gene manipulation, they resemble the familial but not the sporadic AD form, and are, therefore, inappropriate for this purpose. In line with the recent findings of sAD being recognised as an insulin resistant brains state (IRBS), a new, non-transgenic, animal model has been proposed as a representative model of sAD, developed by intracerebroventricular application of the betacytotoxic drug streptozotocin (STZ-icv). The STZ-icv-treated animals (mostly rats and mice) develop IRBS associated with memory impairment and progressive cholinergic deficits, glucose hypometabolism, oxidative stress and neurodegeneration that share many features in common with sAD in humans. The therapeutic strategies (acetylcholinesterase inhibitors, antioxidants and many other drugs) that have been tested until now on the STZ-icv animal model have been reviewed and the comparability of the drugs’ efficacy in this non-transgenic sAD model and the results from clinical trials on sAD patients, evaluated.