Cognitive dysfunctions associated with white matter damage due to cardiovascular burden – determinants and interpretations

2014 ◽  
Vol 45 (3) ◽  
pp. 334-345 ◽  
Author(s):  
Paweł Krukow
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Cardiovascular Diseases ◽  
Cognitive Disorder ◽  
Theoretical Background ◽  
Dynamic Aspect ◽  
Pathological Changes ◽  
White Matter Damage ◽  
Neuropsychological Disorders ◽  
Considerable Research

AbstractAlthough considerable research has been devoted to cognitive functions deteriorating due to diseases of cardiovascular system, rather less attention has been paid to their theoretical background. Progressive vascular disorders as hypertension, atherosclerosis and carotid artery stenosis generate most of all pathological changes in the white matter, that cause specific cognitive disorder: disconnection syndromes, and disturbances in the dynamic aspect of information processing. These features made neuropsychological disorders secondary to cardiovascular diseases different than the effects of cerebral cortex damage, which may be interpreted modularly.

Accumulation of 4-hydroxy-2-nonenal-modified proteins in the white matter damage in chronic cerebral hypo-perfusion rat mode

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S262-S262
Author(s):  
Terubumi Watanabe ◽  
Yoshiko Yanagi ◽  
Takao Urabe ◽  
Yoshikuni Mizuno
Keyword(s):  
White Matter ◽  
White Matter Damage ◽  
Modified Proteins

scholarly journals Linking metabolic dysfunction with cardiovascular diseases: Brn-3b/POU4F2 transcription factor in cardiometabolic tissues in health and disease

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Vishwanie S. Budhram-Mahadeo ◽  
Matthew R. Solomons ◽  
Eeshan A. O. Mahadeo-Heads
Keyword(s):  
Transcription Factor ◽  
Cardiovascular Diseases ◽  
Cell Fate ◽  
Target Genes ◽  
Cardiovascular Responses ◽  
Normal Function ◽  
Valuable Insight ◽  
Metabolic Dysfunction ◽  
Pathological Changes ◽  
Cardiac Responses

AbstractMetabolic and cardiovascular diseases are highly prevalent and chronic conditions that are closely linked by complex molecular and pathological changes. Such adverse effects often arise from changes in the expression of genes that control essential cellular functions, but the factors that drive such effects are not fully understood. Since tissue-specific transcription factors control the expression of multiple genes, which affect cell fate under different conditions, then identifying such regulators can provide valuable insight into the molecular basis of such diseases. This review explores emerging evidence that supports novel and important roles for the POU4F2/Brn-3b transcription factor (TF) in controlling cellular genes that regulate cardiometabolic function. Brn-3b is expressed in insulin-responsive metabolic tissues (e.g. skeletal muscle and adipose tissue) and is important for normal function because constitutive Brn-3b-knockout (KO) mice develop profound metabolic dysfunction (hyperglycaemia; insulin resistance). Brn-3b is highly expressed in the developing hearts, with lower levels in adult hearts. However, Brn-3b is re-expressed in adult cardiomyocytes following haemodynamic stress or injury and is necessary for adaptive cardiac responses, particularly in male hearts, because male Brn-3b KO mice develop adverse remodelling and reduced cardiac function. As a TF, Brn-3b regulates the expression of multiple target genes, including GLUT4, GSK3β, sonic hedgehog (SHH), cyclin D1 and CDK4, which have known functions in controlling metabolic processes but also participate in cardiac responses to stress or injury. Therefore, loss of Brn-3b and the resultant alterations in the expression of such genes could potentially provide the link between metabolic dysfunctions with adverse cardiovascular responses, which is seen in Brn-3b KO mutants. Since the loss of Brn-3b is associated with obesity, type II diabetes (T2DM) and altered cardiac responses to stress, this regulator may provide a new and important link for understanding how pathological changes arise in such endemic diseases.

THE METABOLISM OF NORMAL BRAIN AND HUMAN GLIOMAS IN RELATION TO CELL TYPE AND DENSITY

1955 ◽  
Vol 33 (3) ◽  
pp. 395-403 ◽  
Author(s):  
Irving H. Heller ◽  
K. A. C. Elliott
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Brain Tumors ◽  
Corpus Callosum ◽  
Oxygen Uptake ◽  
Glial Cells ◽  
Cerebellar Cortex ◽  
Unit Weight ◽  
Uptake Rates ◽  
The Brain

Per unit weight, cerebral and cerebellar cortex respire much more actively than corpus callosum. The rate per cell nucleus is highest in cerebral cortex, lower in corpus callosum, and still lower in cerebellar cortex. The oxygen uptake rates of the brain tumors studied, with the exception of an oligodendroglioma, were about the same as that of white matter on the weight basis but lower than that of cerebral cortex or white matter on the cell basis. In agreement with previous work, an oligodendroglioma respired much more actively than the other tumors. The rates of glycolysis of the brain tumors per unit weight were low but, relative to their respiration rate, glycolysis was higher than in normal gray or white matter. Consideration of the figures obtained leads to the following tentative conclusions: Glial cells of corpus callosum respire more actively than the neurons of the cerebellar cortex. Neurons of the cerebral cortex respire on the average much more actively than neurons of the cerebellar cortex or glial cells. Considerably more than 70% of the oxygen uptake by cerebral cortex is due to neurons. The oxygen uptake rates of normal oligodendroglia and astrocytes are probably about the same as the rates found per nucleus in an oligodendroglioma and in astrocytomas; oligodendroglia respire much more actively than astrocytes.

scholarly journals Diffuse White Matter Damage Is Absent in Neuromyelitis Optica

2009 ◽  
Vol 31 (1) ◽  
pp. 76-79 ◽  
Author(s):  
F. Aboul-Enein ◽  
M. Krššák ◽  
R. Höftberger ◽  
D. Prayer ◽  
W. Kristoferitsch
Keyword(s):  
White Matter ◽  
Neuromyelitis Optica ◽  
White Matter Damage ◽  
Diffuse White Matter
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