scholarly journals Role of Class III phosphoinositide 3-kinase in the brain development: possible involvement in specific learning disorders

2016 ◽  
Vol 139 (2) ◽  
pp. 245-255 ◽  
Author(s):  
Yutaka Inaguma ◽  
Ayumi Matsumoto ◽  
Mariko Noda ◽  
Hidenori Tabata ◽  
Akihiko Maeda ◽  
...  
Adeptus ◽  
2018 ◽  
Author(s):  
Ludmiła Janion

„Let’s not be too eager about equality” – brain sex, heteronormativity, and the scientific mystiqueThe article analyses the role of brain sex in Polish public discourse of the last years. The authors of a popular book Brain Sex claim that differences between women and men stem from differences in the brain structure, and because of that they are universal and unchangeable; feminism is based on misrepresentation of science. This thesis was overtaken by right-wing journalists, as it gave scientific justification to conservative gender politics and contemplementarity – the gender ontology of the Catholic church. However, in the rightwing journalism a significant aspect of brain sex theory is silenced, namely, the claim that homo- and transsexuality result from disorders in brain development; they are unchangeable and should be accepted. Despite its conservative roots, brain sex was popularized in liberal media as well. The aura of science that accompanied this popular theory allowed to naturalize its anti-feminism and heteronormativity. This phenomenon is discussed on the basis of media activity of two Polish scientists who are popular both in right-wing and liberal media: Anna Grabowska and Jerzy Vetulani. Both present brain sex theory as objective, universally accepted truth, which is attacked in the name of the leftist ideology by ignorant activists who deny science. „Nie popadajmy w przesadę z tą równością” – płeć mózgu, heteronorma i mistyka naukowościArtykuł analizuje rolę płci mózgu w polskim dyskursie publicznym ostatnich lat. Autorzy niezwykle popularnej w Polsce książki Płeć mózgu twierdzą, że różnice między kobietami i mężczyznami wynikają z różnic w budowie mózgów, a przez to są uniwersalne i niezmienne, feminizm zaś jest oparty na fałszowaniu nauki. Teza ta została podchwycona przez prawicowych publicystów, ponieważ nadawała naukową legitymację konserwatywnej polityce płci oraz komplementaryzmowi – ontologii płci przyjętej przez Kościół katolicki. W prawicowym piśmiennictwie przemilcza się jednak istotny aspekt płci mózgu, mianowicie twierdzenie, że homo- i transseksualność wynikają z wad w rozwoju mózgu, są niezmienne i powinny być akceptowane. Mimo swoich konserwatywnych korzeni płeć mózgu była popularyzowana także w mediach liberalnych. Nimb naukowości, którym otaczany był popularny pogląd, pozwalał naturalizować związane z nim antyfeminizm i heteronormatywność. Zjawisko to omówione jest na podstawie działalności popularyzatorskiej dwojga naukowców, cieszących się popularnością zarówno w prawicowych, jak i liberalnych mediach: Anny Grabowskiej i Jerzego Vetulaniego. Oboje przedstawiali płeć mózgu jako obiektywną, powszechnie uznawaną naukową prawdę, z którą w imię lewicowej ideologii próbują walczyć nieakceptujący ustaleń nauki aktywiści.


Epigenomics ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 371-380 ◽  
Author(s):  
Andrew M Shafik ◽  
Emily G Allen ◽  
Peng Jin

N6-methyladenosine (m6A) is a dynamic RNA modification that regulates various aspects of RNA metabolism and has been implicated in many biological processes and transitions. m6A is highly abundant in the brain; however, only recently has the role of m6A in brain development been a focus. The machinery that controls m6A is critically important for proper neurodevelopment, and the precise mechanisms by which m6A regulates these processes are starting to emerge. However, the role of m6A in neurodegenerative and neuropsychiatric diseases still requires much elucidation. This review discusses and summarizes the current body of knowledge surrounding the function of the m6A modification in regulating normal brain development, neurodegenerative diseases and outlines possible future directions.


Neonatology ◽  
2019 ◽  
Vol 115 (4) ◽  
pp. 423-431 ◽  
Author(s):  
Hendrik J. Niemarkt ◽  
Tim G. De Meij ◽  
Christ-jan van Ganzewinkel ◽  
Nanne K.H. de Boer ◽  
Peter Andriessen ◽  
...  

2019 ◽  
Author(s):  
Budhachandra Khundrakpam ◽  
Suparna Choudhury ◽  
Uku Vainik ◽  
Noor Al-Sharif ◽  
Neha Bhutani ◽  
...  

AbstractStudies have pointed to the role of the brain in mediating the effects of the social environment of the developing child on life outcomes. Since brain development involves nonlinear trajectories, these effects of the child’s social context will likely have age-related differential associations with the brain. However, there is still a dearth of integrative research investigating the interplay between neurodevelopmental trajectories, social milieu and life outcomes. We set out to fill this gap, focusing specifically on the role of socioeconomic status, SES (indexed by parental occupation) on brain and cognitive development by analyzing MRI scans from 757 typically-developing subjects (age = 3-21 years). We observed nonlinear interaction of age and SES on cortical thickness, specifically a significant positive association between SES and thickness around 9-13 years at several cortical regions. Using a moderated mediation model, we observed that cortical thickness mediated the link between SES and language abilities, and this mediation was moderated by ‘age’ in a quadratic pattern, indicating a pronounced SES-effect during early adolescence. Our results, drawn from cross-sectional data, provide a basis for further longitudinal studies to test whether early adolescence may be a sensitive time window for the impact of SES on brain and cognitive development.


2019 ◽  
Vol 41 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Simon Spichak ◽  
Timothy G. Dinan ◽  
John F. Cryan

How does the immune system impact brain development? The exciting and somewhat unexpected relationship between the immune system and the brain has become one of the most fascinating topics in neuroscience. Even though the immune system was initially implicated in resolving viral and bacterial threats, it is now becoming more evident that it also plays a role in processes in the brain, both under healthy and pathological conditions. This novel role of the immune system in brain health has been implicated in various psychopathologies where neurodevelopment, stress and mood are central. In particular, its role in healthy brain development is becoming more evident, and understanding neuroimmune communication is becoming crucial in treating neurodevelopmental and mood disorders in later life. In the brain, glia function as part of the innate immune system and are programmed to respond to pathogens and physical injury. They also play an important role in neuronal development and pruning. These cells communicate with and respond to chemical signals, such as cytokines and chemokines, which can then initiate or downregulate inflammatory responses. Finally, the trillions of microbes residing in the gut can also stimulate cytokine and chemokine responses in the periphery and play an important role in both immunity and brain development.


2019 ◽  
Author(s):  
J. Shashi Kiran Reddy ◽  
Georg Northoff

Antón-Bolaños et al. (2019) report a newly identified neural pathway mechanism, where the patterned spontaneous activity regulates the excitability of a neural network essential for the formation and maintenance of functional sensory maps in the brain. Findings from the study suggest that the patterned spontaneous activity prevalent during the embryonic development of the brain; at the early stages of innervation to the cortex, contributes to the formation of these sensory maps. Synesthesia is a neural phenomenon caused by the unusual links between sensory information, where synesthetic subjects demonstrate atypical functional and neural connectivity caused by the differences in cortical wiring during brain development. So, based on the findings from Antón-Bolaños et al. (2019), one can anticipate the role of spontaneous activity in promoting synesthetic condition. Thus, it will be interesting to study, if the intrinsic spontaneous activity influences the differential cortical wiring and the formation of sensory maps in synesthesia.


2015 ◽  
Vol 49 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yutaka Inaguma ◽  
Hidenori Ito ◽  
Ikuko Iwamoto ◽  
Ayumi Matsumoto ◽  
Takanori Yamagata ◽  
...  

2021 ◽  
Vol 15 ◽  
Author(s):  
Blandine Ponroy Bally ◽  
Keith K. Murai

Down Syndrome (DS) is the most common genetic cause of intellectual disability in which delays and impairments in brain development and function lead to neurological and cognitive phenotypes. Traditionally, a neurocentric approach, focusing on neurons and their connectivity, has been applied to understanding the mechanisms involved in DS brain pathophysiology with an emphasis on how triplication of chromosome 21 leads to alterations in neuronal survival and homeostasis, synaptogenesis, brain circuit development, and neurodegeneration. However, recent studies have drawn attention to the role of non-neuronal cells, especially astrocytes, in DS. Astrocytes comprise a large proportion of cells in the central nervous system (CNS) and are critical for brain development, homeostasis, and function. As triplication of chromosome 21 occurs in all cells in DS (with the exception of mosaic DS), a deeper understanding of the impact of trisomy 21 on astrocytes in DS pathophysiology is warranted and will likely be necessary for determining how specific brain alterations and neurological phenotypes emerge and progress in DS. Here, we review the current understanding of the role of astrocytes in DS, and discuss how specific perturbations in this cell type can impact the brain across the lifespan from early brain development to adult stages. Finally, we highlight how targeting, modifying, and/or correcting specific molecular pathways and properties of astrocytes in DS may provide an effective therapeutic direction given the important role of astrocytes in regulating brain development and function.


2020 ◽  
Vol 245 (13) ◽  
pp. 1130-1141
Author(s):  
Santosh R D’Mello

Histone deacetylases (HDACs) are a family of enzymes that deacetylate histones as well as a large number of other nuclear, cytoplasmic, and mitochondrial proteins. The deacetylation of histones transforms chromatin to a transcriptionally repressed state, whereas deacetylation of other cellular proteins regulates their functional activity through modulation of subcellular location, their interaction with other proteins, and in the case of transcription factors, their DNA-binding ability. A compelling body of evidence derived from the utilization of pharmacological inhibitors indicates that histone deacetylases are important regulators of brain development as well as the pathogenesis of neurodegenerative diseases. However, because most of the pharmacological inhibitors used are non-selective with regard to the different members of the HDAC family, the significance of individual HDAC proteins to brain development and degeneration has been difficult to delineate. This review focuses on HDAC3. Experiments conducted using more recently developed isoform selective inhibitors and molecular genetic approaches demonstrate that HDAC3 regulates different steps of neurodevelopment, including neurogenesis, gliogenesis, glial cell fate determination, and the myelination of oligodendrocytes and Schwann cells. However, specific posttranslational modifications and alterations in its binding partners transform HDAC3 from a protein that is beneficial to the brain to one that is neurotoxic. The role of HDAC3 in the promotion of neurodegeneration and the inhibition of recovery after nerve injury is reviewed. The role of HDAC3 in the regulation of memory in the adult and aging brain is also described. Impact statement Brain development and degeneration are highly complex processes that are regulated by a large number of molecules and signaling pathways the identities of which are being unraveled. Accumulating evidence points to histone deacetylases and epigenetic mechanisms as being important regulators of these processes. In this review, we describe that histone deacetylase-3 (HDAC3) is a particularly crucial regulator of both neurodevelopment and neurodegeneration. In addition, HDAC3 regulates memory formation, synaptic plasticity, and the cognitive impairment associated with normal aging. Understanding how HDAC3 functions contributes to the normal development and functioning of the brain while also promoting neurodegeneration could lead to the development of therapeutic approaches for neurodevelopmental, neuropsychiatric, and neurodegenerative disorders.


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