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Currently, identification of clinical isolates of mycobacteria to the species level …. M. asiaticum; 8, M. chelonae; 9, M. moriokaese; 10, M. phlei; 11, M. pulveris; 12, ….. of microRNA-181b in regulating the schizophrenia susceptibility gene EGR3.
MUSIC THERAPY IN ACTION
Music has shown positive effects in a variety of patient populations for improving symptoms related to different diseases and disorders. Here’s a sampling of some of the more common uses of music therapy.
| PATIENT POPULATION | NONMUSIC BEHAVIORS |
| Autism spectrum disorder | Movement, communication, speech and language, social skills, attention, cognition, activities of daily living |
| Alzhteimer’s disease and dementia | Memory, mood, social interaction |
| Traumatic brain injury | Movement, communication, speech and language, social skills, attention, memory, cognition |
| Mental health and mood disorders | Self-esteem, awareness of self and environment, expression, reality testing, social skills, attention, cognition |
| Pain management | Anxiety and stress, mood, feelings of control |
| Cancer | Anxiety and stress, mood, feelings of control, coping skills |
| Movement disorders and stroke | Movement, speech and language, swallowing , respiratory control, memory, cognition |
| Hospice | Anxiety and stress, mood, feelings of control, coping skills |
Elizabeth Stegemöller is a board-certified music therapist and neuroscientist at Iowa State University, where she studies the effects of music on movement and associated neurophysiology in persons with Parkinson’s disease.
Sphingomyelin can accumulate in a rare hereditary disease called Niemann–Pick disease, types A and B. It is a genetically-inherited disease caused by a deficiency in the lysosomal enzyme acid sphingomyelinase, which causes the accumulation of sphingomyelin in spleen, liver, lungs, bone marrow, and brain, causing irreversible neurological damage. Of the two types involving sphingomyelinase, type A occurs in infants. It is characterized by jaundice, an enlarged liver, and profound braindamage. Children with this type rarely live beyond 18 months. Type B involves an enlarged liver and spleen, which usually occurs in the pre-teen years. The brain is not affected. Most patients present with <1% normal levels of the enzyme in comparison to normal levels.
As a result of the autoimmune disease multiple sclerosis (MS), the myelin sheath of neuronal cells in the brain and spinal cord is degraded, resulting in loss of signal transduction capability. MS patients exhibit upregulation of certain cytokines in the cerebrospinal fluid, particularly tumor necrosis factor alpha. This activates sphingomyelinase, an enzyme that catalyzes the hydrolysis of sphingomyelin to ceramide; sphingomyelinase activity has been observed in conjunction with cellular apoptosis.[17]
An excess of sphingomyelin in the red blood cell membrane (as in abetalipoproteinemia) causes excess lipid accumulation in the outer leaflet of the red blood cellplasma membrane. This results in abnormally shaped red cells called acanthocytes.
Sphingomyelin (SPH, ˌsfɪŋɡoˈmaɪəlɪn) is a type of sphingolipidfound in animal cell membranes, especially in the membranous myelin sheath that surrounds some nerve cellaxons. It usually consists of phosphocholine and ceramide, or a phosphoethanolamine head group; therefore, sphingomyelins can also be classified as sphingophospholipids.[1] In humans, SPH represents ~85% of all sphingolipids, and typically make up 10–20 mol % of plasma membrane lipids.
Sphingomyelins contain phosphocholine or phosphoethanolamine as their polar head group and are therefore classified along with glycerophospholipids as phospholipids. Indeed, sphingomyelins resemble phosphatidylcholines in their general properties and three-dimensional structure, and in having no net charge on their head groups . Sphingomyelins are present in the plasma membranes of animal cells and are especially prominent in myelin, a membranous sheath that surrounds and insulates the axons of some neurons—thus the name “sphingomyelins”.[1]
Sphingomyelin was first isolated by GermanchemistJohann L.W. Thudicum in the 1880s.[2] The structure of sphingomyelin was first reported in 1927 as N-acyl-sphingosine-1-phosphorylcholine.[2] Sphingomyelin content in mammals ranges from 2 to 15% in most tissues, with higher concentrations found in nerve tissues, red blood cells, and the ocular lenses. Sphingomyelin has significant structural and functional roles in the cell. It is a plasma membrane component and participates in many signaling pathways. The metabolism of sphingomyelin creates many products that play significant roles in the cell.[2]
Sphingomyelin consists of a phosphocholine head group, a sphingosine, and a fatty acid. It is one of the few membrane phospholipids not synthesized from glycerol. The sphingosine and fatty acid can collectively be categorized as a ceramide. This composition allows sphingomyelin to play significant roles in signaling pathways: the degradation and synthesis of sphingomyelin produce important second messengers for signal transduction.
Sphingomyelin obtained from natural sources, such as eggs or bovine brain, contains fatty acids of various chain length. Sphingomyelin with set chain length, such as palmitoylsphingomyelin with a saturated 16 acyl chain, is available commercially.[3]
Ideally, sphingomyelin molecules are shaped like a cylinder, however many molecules of sphingomyelin have a significant chain mismatch (the lengths of the two hydrophobic chains are significantly different).[4] The hydrophobic chains of sphingomyelin tend to be much more saturated than other phospholipids. The main transition phase temperature of sphingomyelins is also higher compared to the phase transition temperature of similar phospholipids, near 37 C. This can introduce lateral heterogeneity in the membrane, generating domains in the membrane bilayer.[4]
Sphingomyelin undergoes significant interactions with cholesterol. Cholesterol has the ability to eliminate the liquid to solid phase transition in phospholipids. Due to sphingomyelin transition temperature being within physiological temperature ranges, cholesterol can play a significant role in the phase of sphingomyelin. Sphingomyelin are also more prone to intermolecular hydrogen bonding than other phospholipids.[5]
Sphingomyelin is synthesized at the endoplasmic reticulum (ER), where it can be found in low amounts, and at the trans Golgi. It is enriched at the plasma membrane with a greater concentration on the outer than the inner leaflet.[6] The Golgi complex represents an intermediate between the ER and plasma membrane, with slightly higher concentrations towards the trans side.[7]
The synthesis of sphingomyelin involves the enzymatic transfer of a phosphocholine from phosphatidylcholine to a ceramide. The first committed step of sphingomyelin synthesis involves the condensation of L-serine and palmitoyl-CoA. This reaction is catalyzed by serine palmitoyltransferase. The product of this reaction is reduced, yielding dihydrosphingosine. The dihydrosphingosine undergoes N-acylation followed by desaturation to yield a ceramide. Each one of these reactions occurs at the cytosolic surface of the endoplasmic reticulum. The ceramide is transported to the Golgi apparatus where it can be converted to sphingomyelin. Sphingomyelin synthase is responsible for the production of sphingomyelin from ceramide. Diacylglycerol is produced as a byproduct when the phosphocholine is transferred.[8]
Sphingomyelin breakdown is responsible for initiating many universal signaling pathways. It is hydrolyzed by sphingomyelinases (sphingomyelin specific type-C phospholipases).[6] The phosphocholine head group is released into the aqueous environment while the ceramide diffuses through the membrane.
The membranous myelin sheath that surrounds and electrically insulates many nerve cell axons is particularly rich in sphingomyelin, suggesting its role as an insulator of nerve fibers.[1] The plasma membrane of other cells is also abundant in sphingomyelin, though it is largely to be found in the exoplasmic leaflet of the cell membrane. There is, however, some evidence that there may also be a sphingomyelin pool in the inner leaflet of the membrane.[9][10] Moreover, neutral sphingomyelinase-2 – an enzyme that breaks down sphingomyelin into ceramide – has been found to localise exclusively to the inner leaflet, further suggesting that there may be sphingomyelin present there.[11]
The function of sphingomyelin remained unclear until it was found to have a role in signal transduction.[12] It has been discovered that sphingomyelin plays a significant role in cell signaling pathways. The synthesis of sphingomyelin at the plasma membrane by sphingomyelin synthase 2 produces diacylglycerol, which is a lipid-soluble second messenger that can pass along a signal cascade. In addition, the degradation of sphingomyelin can produce ceramide which is involved in the apoptotic signaling pathway.
Sphingomyelin has been found to have a role in cell apoptosis by hydrolyzing into ceramide. Studies in the late 1990s had found that ceramide was produced in a variety of conditions leading to apoptosis.[13] It was then hypothesized that sphingomyelin hydrolysis and ceramide signaling were essential in the decision of whether a cell dies. In the early 2000s new studies emerged that defined a new role for sphingomyelin hydrolysis in apoptosis, determining not only when a cell dies but how.[13]After more experimentation it has been shown that if sphingomyelin hydrolysis happens at a sufficiently early point in the pathway the production of ceramide may influence either the rate and form of cell death or work to release blocks on downstream events.[13]
Sphingomyelin, as well as other sphingolipids, are associated with lipid microdomains in the plasma membrane known as lipid rafts. Lipid rafts are characterized by the lipid molecules being in the lipid ordered phase, offering more structure and rigidity compared to the rest of the plasma membrane. In the rafts, the acyl chains have low chain motion but the molecules have high lateral mobility. This order is in part due to the higher transition temperature of sphingolipids as well as the interactions of these lipids with cholesterol. Cholesterol is a relatively small, nonpolar molecule that can fill the space between the sphingolipids that is a result of the large acyl chains. Lipid rafts are thought to be involved in many cell processes, such as membrane sorting and trafficking, signal transduction, and cell polarization.[14] Excessive sphingomyelin in lipid rafts may lead to insulin resistance.[15]
Due to the specific types of lipids in these microdomains, lipid rafts can accumulate certain types of proteins associated with them, thereby increasing the special functions they possess. Lipid rafts have been speculated to be involved in the cascade of cell apoptosis.[16]
Connie’s comments: Toxic substances (metals, chemicals,etc) for the liver can destroy the myelin sheath that covers our neurons.
Summary: Widowers and life-long single people are at higher risk of developing dementia, a new study reports.
Source: BMJ.
Marriage may lower the risk of developing dementia, concludes a synthesis of the available evidence published online in the Journal of Neurology Neurosurgery & Psychiatry.
Lifelong singletons and widowers are at heightened risk of developing the disease, the findings indicate, although single status may no longer be quite the health hazard it once seemed to be, the researchers acknowledge.
They base their findings on data from 15 relevant studies published up to the end of 2016. These looked at the potential role of marital status on dementia risk, and involved more than 800,000 participants from Europe, North and South America, and Asia.
Married people accounted for between 28 and 80 per cent of people in the included studies; the widowed made up between around 8 and 48 per cent; the divorced between 0 and 16 per cent; and lifelong singletons between 0 and 32.5 per cent.
Pooled analysis of the data showed that compared with those who were married, lifelong singletons were 42 per cent more likely to develop dementia, after taking account of age and sex.
Part of this risk might be explained by poorer physical health among lifelong single people, suggest the researchers.
However, the most recent studies, which included people born after 1927, indicated a risk of 24 per cent, which suggests that this may have lessened over time, although it is not clear why, say the researchers.
The widowed were 20 per cent more likely to develop dementia than married people, although the strength of this association was somewhat weakened when educational attainment was factored in.
But bereavement is likely to boost stress levels, which have been associated with impaired nerve signalling and cognitive abilities, the researchers note.
No such associations were found for those who had divorced their partners, although this may partly be down to the smaller numbers of people of this status included in the studies, the researchers point out.
But the lower risk among married people persisted even after further more detailed analysis, which, the researchers suggest, reflects “the robustness of the findings.”
These findings are based on observational studies so no firm conclusions about cause and effect can be drawn, and the researchers point to several caveats, including the design of some of the included studies, and the lack of information on the duration of widowhood or divorce.
Nevertheless, they proffer several explanations for the associations they found. Marriage may help both partners to have healthier lifestyles, including exercising more, eating a healthy diet, and smoking and drinking less, all of which have been associated with lower risk of dementia.
Couples may also have more opportunities for social engagement than single people–a factor that has been linked to better health and lower dementia risk, they suggest.
In a linked editorial, Christopher Chen and Vincent Mok, of, respectively, the National University of Singapore and the Chinese University of Hong Kong, suggest that should marital status be added to the list of modifiable risk factors for dementia, “the challenge remains as to how these observations can be translated into effective means of dementia prevention.”
The discovery of potentially modifiable risk factors doesn’t mean that dementia can easily be prevented, they emphasise.
“Therefore, ways of destigmatising dementia and producing dementia-friendly communities more accepting and embracing of the kinds of disruptions that dementia can produce should progress alongside biomedical and public health programmes,” they conclude.
Source: Caroline White – BMJ
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Marriage and risk of dementia: systematic review and meta-analysis of observational studies” by Andrew Sommerlad, Joshua Ruegger, Archana Singh-Manoux, Glyn Lewis, and Gill Livingston in Journal of Neurology Neurosurgery & Psychiatry. Published online November 27 2017 doi:10/30/jnnp-2017-316274
Abstract
Marriage and risk of dementia: systematic review and meta-analysis of observational studies
Background Being married is associated with healthier lifestyle behaviours and lower mortality and may reduce risk for dementia due to life-course factors. We conducted a systematic review and meta-analysis of studies of the association between marital status and the risk of developing dementia.
Methods We searched medical databases and contacted experts in the field for relevant studies reporting the relationship, adjusted for age and sex, between marital status and dementia. We rated methodological quality and conducted random-effects meta-analyses to summarise relative risks of being widowed, divorced or lifelong single, compared with being married. Secondary stratified analyses with meta-regression examined the impact of clinical and social context and study methodology on findings.
Results We included 15 studies with 812 047 participants. Compared with those who are married, lifelong single (relative risk=1.42 (95% CI 1.07 to 1.90)) and widowed (1.20 (1.02 to 1.41)) people have elevated risk of dementia. We did not find an association in divorced people.
Further analyses showed that less education partially confounds the risk in widowhood and worse physical health the elevated risk in lifelong single people. Compared with studies that used clinical registers for ascertaining dementia diagnoses, those which clinically examined all participants found higher risk for being unmarried.
Conclusions Being married is associated with reduced risk of dementia than widowed and lifelong single people, who are also underdiagnosed in routine clinical practice. Dementia prevention in unmarried people should focus on education and physical health and should consider the possible effect of social engagement as a modifiable risk factor.
“Marriage and risk of dementia: systematic review and meta-analysis of observational studies” by Andrew Sommerlad, Joshua Ruegger, Archana Singh-Manoux, Glyn Lewis, and Gill Livingston in Journal of Neurology Neurosurgery & Psychiatry. Published online November 27 2017 doi:10/30/jnnp-2017-316274
