Review Article : Molecular and Cellular Mechanisms Underlying the Cognitive Deficits Associated With Neurofibromatosis 1

2002 ◽  
Vol 17 (8) ◽  
pp. 622-626 ◽  
Author(s):  
Rui M. Costa ◽  
Alcino J. Silva
Keyword(s):  
Cognitive Deficits ◽  
Review Article ◽  
Neurofibromatosis 1 ◽  
Cellular Mechanisms

Review Article : Cognitive Deficits in Neurofibromatosis 1

2002 ◽  
Vol 17 (8) ◽  
pp. 605-612 ◽  
Author(s):  
Kathryn North ◽  
Shelley Hyman ◽  
Belinda Barton
Keyword(s):  
Cognitive Deficits ◽  
Review Article ◽  
Neurofibromatosis 1

scholarly journals Mitochondrial donation in translational medicine; from imagination to reality

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Hesam Saghaei Bagheri ◽  
Farhad Bani ◽  
Savas Tasoglu ◽  
Amir Zarebkohan ◽  
Reza Rahbarghazi ◽  
...  
Keyword(s):  
Translational Medicine ◽  
Specific Activity ◽  
Current Knowledge ◽  
Review Article ◽  
Target Cells ◽  
Therapeutic Effects ◽  
Cellular Mechanisms ◽  
Pathological Conditions ◽  
Mitochondrial Transfer ◽  
Mitochondrial Donation

Abstract The existence of active crosstalk between cells in a paracrine and juxtacrine manner dictates specific activity under physiological and pathological conditions. Upon juxtacrine interaction between the cells, various types of signaling molecules and organelles are regularly transmitted in response to changes in the microenvironment. To date, it has been well-established that numerous parallel cellular mechanisms participate in the mitochondrial transfer to modulate metabolic needs in the target cells. Since the conception of stem cells activity in the restoration of tissues’ function, it has been elucidated that these cells possess a unique capacity to deliver the mitochondrial package to the juxtaposed cells. The existence of mitochondrial donation potentiates the capacity of modulation in the distinct cells to achieve better therapeutic effects. This review article aims to scrutinize the current knowledge regarding the stem cell’s mitochondrial transfer capacity and their regenerative potential.

Review Article : Neurofibromatosis 1: Clinical Review and Exceptions to the Rules

2002 ◽  
Vol 17 (8) ◽  
pp. 613-621 ◽  
Author(s):  
Helen Young ◽  
Shelley Hyman ◽  
Kathryn North
Keyword(s):  
Clinical Review ◽  
Review Article ◽  
Neurofibromatosis 1

scholarly journals Specific cognitive deficits in children with hyperkinetic disorder

2018 ◽  
pp. 3-9
Author(s):  
R. F. Gasanov
Keyword(s):  
Mental Retardation ◽  
Hierarchical Structure ◽  
Cognitive Deficits ◽  
Child Psychopathology ◽  
Cognitive Deficit ◽  
Review Article ◽  
Uneven Development ◽  
Hyperkinetic Disorder ◽  
Wide Range ◽  
The Hierarchical Structure

In this review article, features of a specific cognitive deficit in children with hyperkinetic disorder are considered. The uneven development of higher mental functions observed in these cases, the hierarchical structure of the detected defects, neuropsychological features is determined, in the author’s opinion, to distinguish hyperkinetic disorder of childhood from atonic forms of mental retardation and other hyperdynamic syndromes in a wide range of child psychopathology, creating a model of a specificcognitive deficit.

scholarly journals Premyelinated Central Axons Express Neurotoxic NMDA Receptors: Relevance to Early Developing White-Matter Injury

2014 ◽  
Vol 35 (4) ◽  
pp. 543-553 ◽  
Author(s):  
Tahani Huria ◽  
Narasimha Murthy Beeraka ◽  
Badrah Al-Ghamdi ◽  
Robert Fern
Keyword(s):  
White Matter ◽  
Cognitive Deficits ◽  
Ischemic Injury ◽  
Cellular Component ◽  
White Matter Injury ◽  
Loss Of Function ◽  
Cellular Mechanisms ◽  
Axon Injury ◽  
Subunit Expression ◽  
Gold Labelling

Ischemic-type injury to developing white matter is associated with the significant clinical condition cerebral palsy and with the cognitive deficits associated with premature birth. Premyelinated axons are the major cellular component of fetal white matter and loss of axon function underlies the disability, but the cellular mechanisms producing ischemic injury to premyelinated axons have not previously been described. Injury was found to require longer periods of modelled ischemia than at latter developmental points. Ischemia produced initial hyperexcitability in axons followed by loss of function after Na+ and Ca2+ influx. N-methyl-D-aspartate- (NMDA) type glutamate receptor (GluR) agonists potentiated axon injury while antagonists were protective. The NMDA GluR obligatory Nr1 subunit colocalized with markers of small premyelinated axons and expression was found at focal regions of axon injury. Ischemic injury of glial cells present in early developing white matter was NMDA GluR independent. Axons in human postconception week 18 to 23 white matter had a uniform prediameter expansion phenotype and postembedded immuno-gold labelling showed Nr1 subunit expression on the membrane of these axons, demonstrating a shared key neuropathologic feature with the rodent model. Premyelinated central axons therefore express high levels of functional NMDA GluRs that confer sensitivity to ischemic injury.

Sign in / Sign up

Export Citation Format

Share Document