Gray Matter Vs White Matter
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The brain is an immensely complex structure, but there are ways we can divide up its anatomical structure into more discrete parts the left and right hemisphere, parietal, temporal, occipital and frontal lobes. Another common divider is to separate the brains gray and white matter. But what are these two structures? How different are they from each other? How significant, and physiologically relevant, is this divide? Read on to find out!
Blood Supply To The Brain
Two sets of blood vessels supply blood and oxygen to the brain: the vertebral arteries and the carotid arteries.
The external carotid arteries extend up the sides of your neck, and are where you can feel your pulse when you touch the area with your fingertips. The internal carotid arteries branch into the skull and circulate blood to the front part of the brain.
The vertebral arteries follow the spinal column into the skull, where they join together at the brainstem and form the basilar artery, which supplies blood to the rear portions of the brain.
The circle of Willis, a loop of blood vessels near the bottom of the brain that connects major arteries, circulates blood from the front of the brain to the back and helps the arterial systems communicate with one another.
Scientists Discover Roadblocks That Stop Brain White Matter Healing
NIH-funded study identifies molecule that may prevent repair.
A new study identifies a molecule that may be critical to the repair of white matter, the fatty tissue wrapped around parts of brain cells that helps speed up communication. Damage to white matter is associated with several conditions, including multiple sclerosis and cerebral palsy, and can occur in the brains of preterm babies. New findings suggest that the molecule triggers a pathway that is normally used by the immune system to prevent excessive damage but may contribute to chronic white matter injury by completely blocking repair operations. The study, published in the May issue of Journal of Clinical Investigation, was funded by the National Institute of Neurological Disorders and Stroke , part of the National Institutes of Health.
This study uncovers a new player in white matter disease and identifies a potential drug target, said Jim Koenig, Ph.D., program director at NINDS. It also describes a unique situation in which the brain tries to take over immune system functions, with devastating results.
A team led by Stephen Back, M.D., Ph.D., professor of pediatrics and neurology at the Oregon Health & Science University in Portland, took a detailed look at the HA fragments to see how they block myelin repair. Using state-of-the-art techniques, Dr. Back and his colleagues were able to create HA fragments of different sizes.
NIHTurning Discovery Into Health®
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White Matter Of The Brain
White matter is found in the deeper tissues of the brain . It contains nerve fibers , which are extensions of nerve cells . Many of these nerve fibers are surrounded by a type of sheath or covering called myelin. Myelin gives the white matter its color. It also protects the nerve fibers from injury. Also, it improves the speed and transmission of electrical nerve signals along extensions of the nerve cells called axons.
The major areas of the brain have one or more specific functions.
The tissue called gray matter in the brain and spinal cord is also known as substantia grisea, and is made up of cell bodies. White matter, or substantia alba, is composed of nerve fibers.
What Increases White Matter In The Brain
Eat well to increase white matter. Omega-3 fatty acids both protect the brain and promote improved cognition and memory, reports Dr. Julius Goepp of Life Extension Foundation . Adults who take in more omega-3 fatty acids have more brain matter and more functional brains, according to a 2007 study published in Neuroscience..
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Scaling Estimate Of The Cortical Thickness
As fasciculated fibers are usually not observed in neocortical gray matter , we identify cortical thickness with gray matter module size, R. Our prediction for the optimal module size R0 can be rewritten by using Equations 4 and 5
Using n ~ 104 , d ~ 1 m , and D ~ 1 m , we predict cortical thickness R0 ~ 1 mm. This estimate agrees well with the existing anatomical data , despite being derived using scaling. By substituting these values into Equation 26, we find that is smaller than one, justifying our perturbation theory approach.
Next, we apply our results to the allometric scaling relationship between cortical thickness, R0, and brain volume, V. We assume that n and D both increase with brain size according to the following power laws: n ~ V1/3 and D ~ V1/6 . Then, by using Equation 27 and the constancy of the optimal local wire diameter d across different species , we predict that R0 ~ V4/27. This prediction agrees well with the empirically obtained power law relationship between cortical thickness and brain volume . Thus, our theory explains why the cortical thickness changes little while brain volume varies by several orders of magnitude between different species.
Optimality Condition For Segregated Designs
In the previous section, we showed that in the regime ND2 2, there is at least one segregated design with local conduction delay shorter than that in HD. However, we did not specify which design is the optimal one. In this section, we give a necessary condition for a segregated design to be optimal in the regime ND2 2 and ND2 G/.
As the advantage of segregation becomes apparent when the total cross-section of global axons ND2 ~ 2, it is natural to expect that a similar condition defines the optimal gray matter module size R0, which minimizes local conduction delays. In other words, the number of neurons in the gray matter module is such that the total cross-sectional area of their global axons is given by 2. As the number of neurons in the sphere of radius R0 is 2/D2 and the number of neurons in the sphere of radius is n, we have
Thus, we can formulate the following theorem:
In the regime ND2 2 and ND2 G/, the minimum local conduction delay is achieved by the segregated design with the gray matter module containing 2/D2 neurons.
To prove this theorem, we consider designs with gray matter module size smaller and greater than R0, and show that they have a local conduction delay greater than that in the design with module size R0.
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Microglia In The Aged Mouse Brain Are Characterized By Increased Phagocytosis And Altered Lipid Homeostasis
To examine age-associated changes in gene expression, microglia were isolated from aged mouse brain, and RNA expression was determined. Microarray analysis of pure microglia showed > 1.5-fold increased expression of 54 transcripts in aged mouse microglia compared to young microglia. To relate the changes in gene expression to a biological function, we applied DAVID software and identified that differentially expressed genes were involved in biological categories such as antigen processing and -presentation, interferon signaling, regulation of macrophage cytokine production, chemotaxis, cell adhesion, phagocytosis of apoptotic cells, and lipid homeostasis.
Increased expression of genes in aged microglia, indicative of a pro-inflammatory status, belonged to categories of antigen presentation, interferon signaling, and cytokine signaling. These groups were represented as a heatmap , and included several histocompatibility two genes and phagocytic receptor genes . Phagocytosis-associated genes were strongly upregulated in aged microglia as validated by quantitative PCR of Axl, CD36, Ctse, Clec7a, and Lamp2 . In addition, aged microglia showed changes in genes involved in cellular lipid homeostasis . The altered genes are depicted in a heat map .
What Are White Matter Lesions
What matter lesions are small groups of dead cells that clump together in the white matter of the brain. The human brain is made of both gray and white matter information is typically stored and archived in the gray area, but the white parts play an important role when it comes to shuttling signals back and forth and retrieving information from one place and bringing it to the next. Lesions can slow or stop this process. Some experts believe that they form as a normal part of aging in most adults, but they can also be a sign of a more serious degenerative condition, particularly when they are large, when there are many, and when they seem to be growing. Alzheimers disease, Multiple Sclerosis, and dementia are three of the most common ailments connected with lesions, but the list is usually quite long.
White Matter Basics
The brains white matter occurs most often in the fibrous pathways and canals responsible for transmitting signals between the larger areas of the brain that process information, known as gray matter. It is very common for theses two distinct parts to work simultaneously to perform basic functions. When white matter dies, vital communication between two collaborating areas of gray matter slows and can even stop.
Why Lesions Occur
Prevention and Treatment
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Implications Of The Review
The findings of this review have several implications. For the clinician, they emphasise the clinical importance of white matter hyperintensities, even when these are found as incidental findings on brain imaging. In such cases doctors might consider detailed screening for risk factors for stroke and dementia, even though the benefit of doing so is not formally proved. Although data showing that treatment of risk factors reduces the progression of white matter hyperintensities are limited, more aggressive antihypertensive treatment was associated with reduced progression in patients after stroke, as well as with a reduction in stroke itself.82
In terms of research, white matter hyperintensities could constitute a potentially useful intermediate marker for the identification of new risk factors for stroke and dementia. Indeed, besides being strongly associated with the risk of stroke and dementia, white matter hyperintensities can be quantified reliably and non-invasively on large samples and can be measured as a continuous trait, thus providing increased statistical power to detect an association. White matter hyperintensities could prove particularly interesting for the identification of novel genetic risk factors, as their heritability was shown to be as high as 55-73%.8384
Immunohistochemistry For Human Brain Tissues
Paraffin-embedded tissue of human brains from AD and control groups were immunostained with IBA1 , CD68 and HLA-DR . Paraffin-embedded tissues from different age groups were immunostained with CD68 and HLA-DR . Sections were deparaffinized with xylene and rehydrated gradually from 100% ethanol to demi water. For antigen retrieval, the sections were placed in 10 mM sodium citrate buffer in a microwave for 12 min.
After rinsing in PBS, sections were pre-incubated in 3% H2O2 for 30 min and then blocked with 10% normal horse serum in PBS with 0.3% Triton-X100 for 30 min. Sections were incubated overnight at 4°C with abovementioned primary antibodies in PBS with 0.3% Triton-X100 and 1% normal horse serum. Sections were incubated with horse anti-mouse biotinylated antibody for 1 h at room temperature, incubated in avidin-biotin-peroxidase complex for 30 min, and then visualized with DAB. Sections were counterstained with Cresyl Violet and mounted with DePeX.
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What Is Its Function
For a long time it was believed that the white matter had secondary functions to the gray matter, but recent studies have demonstrated that it is not like that at all. The main job of the white matter is to convey information, under the form of electrical impulses, from one part of the brain to the other. It therefore connects different parts of the brain and cerebellum and it is at the foundation of the relevant notion of connectivity. This occurs both in close areas that carry out the same function, and in areas far apart that must constantly communicate in order to carry out more complex tasks, such as, for example, recognizing the scent of a rose and calling it by the proper name. Right hemisphere and left hemisphere, basal ganglia and cerebellum, cerebral cortex and spinal marrow are all interconnected thanks to the white matter.
Immunohistochemical images of the white matter at 30 and 40 weeks of gestational age. The asterisk indicates the lateral ventricle. Modified by Back et al. J Neuroscience 2001.
Conduction Delays Limit The Size Of A Highly Connected Network
We begin by considering the time delay in the local circuits of neocortex, because their mode of operationthought to involve recurrent computations seems most sensitive to the detrimental impact of time delay. We derive a scaling relationship between local conduction delay and the number of neurons that can have all-to-all potential connectivity. By assuming that the tolerable delay is on the order of a millisecond, we show that the maximum size of such network is close to that of the cortical column.
Local cortical circuits may be viewed as a network of n neurons with all-to-all potential synaptic connectivity, meaning that the axons and dendrites of most neurons come close enough to form a synapse . In the following we do not distinguish between axons and dendrites in local circuits, and we refer to them as local wires. Mathematical symbols used in this paper are shown in Table 1. The mean conduction delay t in local circuits is given by the average path length between two connected neurons , , divided by the conduction velocity, s:
Experimental measurements and theoretical arguments suggest that conduction velocity, s, scales sublinearly with the diameter, d, of local wires :
where is a constant coefficient and is a positive power smaller than one . By combining Equations 1 and 2, we arrive at the expression for the conduction delay:
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Branching Pipe Designan Example Of Perforated Design
In the previous section, we have shown that in the optimal segregated designs, the size of the module, in which global and local connections are finely intermixed, is given by R0. However, Theorem 2 does not specify other dimensions of the segregated design, such as the total surface area of the white matter tracts. In this section, by considering a specific example, which we name the branching pipe design, we show that the condition A G/R0 can be satisfied in the regime in which our perturbation approach is valid. In other words, we prove that PD exists in the regime ND2 G/.
We specify the branching pipe design as follows . Global axons belong to several cylindrical white matter pipes perforating the gray matter. Higher-order branches split off lower-order pipes at regular intervals. Different order branches have different lengths and different pipe diameter. The length of the zeroth-order branches is given by the linear size of the brain. The length of k + 1st-order branches is given by the interpipe distance among the kth order branches, forming a space-filling structure. The interpipe distance among the finest branches is given by R0 in Equation 20 .
Schematic illustration of branching pipe design with three orders of branches. The distance between kth order branches determines the length of the k + 1st-order branches. The distance between highest-order branches is given by R0.
White Matter Plays A Complex Role In Brain Health
While gray matter is a common focus in topics of brain structure, white matter also plays a critical role in helping the body process information. It connects regions that send and receive signals, affecting the ability to focus and learn, solve problems, and stay balanced when walking. Its a significant area of interest for public health experts, since conditions that impact white matter can lead to significant cognitive impairment and increase the risk of long-term neurological problems.
New research from UNC-Chapel Hill suggests that some diseases affecting white matter may be associated with structural and genetic abnormalities in the brain, which sheds further light on the complex genetic relationship between white matter, brain disease and mental health.
Dr. Bingxin Zhao
Dr. Tengfei Li
The research team identified genetic elements that impact white matter differences and located numerous genes associated with white matter. In a perspective piece accompanying the study, the authors suggest that it presents compelling evidence for the importance of white matter by demonstrating genetic influences on structural connectivity that invoke a host of provocative clinical implications.
For more results on imaging genetics and information on future research, please visit the teams Brain Imaging Genetics Knowledge Portal.
Contact the UNC Gillings School of Global Public Health communications team at .
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Radiographic Assessment Of Wmh Severity
There are two main radiographic approaches to assessment of WMH severity. First, the visual grade rating scales that are used to measure white matter lesion on CT or MRI are based on the site and the severity of white matter disease. MRI-based scales, such as the Fazekas scale, grades WML in both periventricular and deep white matter locations . The Scheltens scale added the location, size, and number of WML in PVH , WMH , basal ganglia hyperintensities and infratentorial foci of hyperintensities . The Rotterdam Scan Study scale rates WML in the periventricular region and subcortical WML. The Age-Related White Matter Changes scales for rating WMH on CT and MRI included the site, size, and number of WML and basal ganglia lesions in 5 different regions of bilateral hemispheres. Second, a volumetric approach to WMH analysis has been based on the various semiautomated protocols using analytical software such as Sparc 5 or MRIcro , which quantify WMH volume on axial FLAIR of the entire brain, or just supratentorially. [