Structural Aspects of Energy Failure States in the Brain

1983 ◽  
pp. 1-11 ◽  
Author(s):  
H. Kalimo ◽  
L. Paljärvi ◽  
Y. Olsson ◽  
B. K. Siesjö
2021 ◽  
Vol 16 ◽  
pp. 263310552110115
Author(s):  
Maoxue Tang ◽  
Umrao R Monani

Considering its small size relative to the rest of the body, the mammalian brain has a disproportionately high energy requirement. This energy is supplied to the brain mainly in the form of glucose through the principal cerebral glucose transporter, Glut1. Inactivation of even a single copy of the Glut1 gene, SLC2A1, has dire consequences for the brain, starving cerebral neurons of energy and triggering the debilitating neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). Considering the monogenic nature of Glut1 DS, the disease serves as an excellent paradigm to study the larger family of brain energy failure syndromes. Here we review how studies of Glut1 DS are proving instructive to the brain’s energy needs, focusing first on the requirements, both spatial and temporal of the transporter, second, on proposed mechanisms linking low Glut1 to brain dysfunction and, finally on efforts to treat the disease and thus restore nutritional support to the brain. These studies promise not only to inform mechanisms and treatments for the relatively rare Glut1 DS but also the myriad other conditions involving the Glut1 protein.


Author(s):  
V. F. Allison ◽  
R. S. Sohal

Relatively little is known regarding the structure and function of glial cells in the brain of invertebrate organisms. Fine structural aspects of the interrelationships between glial cells and neurons in the brain of the housefly are described. Three types of glial cells have been identified in the brain of the housefly. Cell bodies of the neurons and two glial cell types are located at the periphery of the brain and surround a centrally located neuropil. Soma of the neurons are completely surrounded by a single or multiple layers of glioplasm which precludes the existence of synaptic sites on the cell body (Fig. 1). Synaptic sites are restricted to the neuropil region. Thin processes of glioplasm also invaginated the perikaryon.


2002 ◽  
Vol 12 (2) ◽  
pp. 195-216 ◽  
Author(s):  
Iain Morley

Neuropsychological and developmental studies suggest human musical ability has a deep evolutionary history; but we do not find evidence of the manufacture and use of instruments, with which musical behaviours have often been assumed to be equated, until 70,000 years after the advent of Homo sapiens. This anomaly is addressed by examining the evidence from the fossil record for the evolution of the physiology and neurology required for musical behaviours, with the aim of identifying the development of the physiological and neurological capacity to produce and process melody and/or rhythm. Aural and vocal sophistication appear to have developed in tandem, beginning with full bipedalism around 1.75 million years ago, until a vocal apparatus similar to the modern was present in Homo heidelbergensis 400,000–300,000 years ago. Prosodic and structural aspects of both speech and music production and processing are lateralized in the brain in similar ways suggesting evolutionarily-shared foundations for these mechanisms.


e-Neuroforum ◽  
2016 ◽  
Vol 22 (3) ◽  
Author(s):  
Leon Stefanovski ◽  
Amna Ghani ◽  
Anthony Randal McIntosh ◽  
Petra Ritter

AbstractTo understand human cognition, it is essential to study the brain on multiple levels, from microscopic to macroscopic scales. Computational connectomics is a new area of neuroscience where scientists seek to combine empirical observations within a computational theory of the brain. The whole-brain network modeling and simulation platform, The Virtual Brain (TVB), is a remarkable innovation in the field of computational connectomics. By combining the connectivity of individual persons with local biologically realistic populationmodels, TVB allows simulation and prediction of the local activity of neuronal populations and the global activity unfolding along the gray matter, both of which can be linked to empiricalmeasures of electrical, hemodynamic, and structural aspects of the brain. TVB is currently used to study the structural, functional, and computational alterations in the diseased brain with reported successes in stroke and epilepsy. Subjectspecific brain models provided by TVB will result in robust and efficient personalized diagnostics, prognostics, and treatment.


2016 ◽  
Vol 3 (4) ◽  
Author(s):  
Mukesh Kumar Garg ◽  
Preeti Sharma ◽  
Mustafa Nadeem Kirmani

The brain is the most important organ of human body. It is dynamic in terms of functional and structural aspects. Each human function is determined by brain. It was thought in the beginning that brain or its tissues do not regenerate once they are damaged. The recent research in neurosciences has shown that brain tissues have the ability to regenerate themselves. This phenomenon is known as neuronal plasticity.  There have been multiple mechanisms which explain this phenomenon. Post injury experiences, neurochemical and neurophysiological aspects are some of the underlying mechanisms. The current paper attempts to explain the neurophysiological aspects of neuroplasticity. It has significant therapeutic implications.


Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1431
Author(s):  
Hyunwook Cho ◽  
Jung-Mi Hah

c-Jun N-terminal kinase (JNK) plays an important role in cell death caused by various stimuli. Because the isoform JNK3 is mainly expressed in the brain, it is believed to play a pivotal role in various neurodegenerative diseases, including Alzheimer’s disease (AD) and Parkinson’s disease (PD), which still lack plausible therapeutics. To develop a novel and selective JNK3 inhibitor, we conducted a decadal review (2011 to 2021) of published articles on JNK inhibitors, particularly those focusing on a structural perspective and docking insights. We observed the structures of three isoforms of JNK, namely holo-proteins and co-crystal structures, with JNK3 inhibitors and summarized the significant structural aspects of selective JNK3 inhibitors as AD therapeutics.


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