Myelin sheath in the context of "Secretory cell"

Oligodendrocytes (from Greek 'cells with a few branches'), also known as oligodendroglia, are a type of neuroglia whose main function is to provide the myelin sheath to neuronal axons in the central nervous system (CNS). Myelination gives metabolic support to, and insulates the axons of most vertebrates. A single oligodendrocyte can extend its processes to cover up to 40 axons, that can include multiple adjacent axons. The myelin sheath is segmented along the axon's length at gaps known as the nodes of Ranvier. In the peripheral nervous system the myelination of axons is carried out by Schwann cells.

Oligodendrocytes are found exclusively in the CNS, which comprises the brain and spinal cord. They are the most widespread cell lineage, including oligodendrocyte progenitor cells, pre-myelinating cells, and mature myelinating oligodendrocytes in the CNS white matter. Non-myelinating oligodendrocytes are found in the grey matter surrounding and lying next to neuronal cell bodies. They are known as neuronal satellite cells, and their presence is not understood.

Schwann cells or neurolemmocytes (named after German physiologist Theodor Schwann) are the principal glia of the peripheral nervous system (PNS). Glial cells function to support neurons and in the PNS, also include satellite cells, olfactory ensheathing cells, enteric glia and glia that reside at sensory nerve endings, such as the Pacinian corpuscle. The two types of Schwann cells are myelinating and nonmyelinating. Myelinating Schwann cells wrap around axons of motor and sensory neurons to form the myelin sheath.The Schwann cell promoter is present in the downstream region of the human dystrophin gene that gives shortened transcript that are again synthesized in a tissue-specific manner.

During the development of the PNS, the regulatory mechanisms of myelination are controlled by feedforward interaction of specific genes, influencing transcriptional cascades and shaping the morphology of the myelinated nerve fibers.

The endoneurium (also called endoneurial channel, endoneurial sheath, endoneurial tube, or Henle's sheath) is a layer of delicate connective tissue around the myelin sheath of each myelinated nerve fiber in the peripheral nervous system. Its component cells are called endoneurial cells. The endoneuria with their enclosed nerve fibers are bundled into groups called nerve fascicles, each fascicle within its own protective sheath called a perineurium. If sufficiently large, nerves containing multiple fascicles, each with its blood supply and fatty tissue, may be bundled within yet another sheath, the epineurium.

The endoneurium contains a liquid known as endoneurial fluid, which contains little protein. In the peripheral nervous system the endoneurial fluid is notionally equivalent to cerebrospinal fluid in the central nervous system. Peripheral nerve injuries commonly release increased amounts of endoneurial fluid into surrounding tissues; these can be detected by magnetic resonance neurography, thereby assisting in locating injuries to peripheral nerves.

A demyelinating disease refers to any disease affecting the nervous system where the myelin sheath surrounding neurons is damaged. This damage disrupts the transmission of signals through the affected nerves, resulting in a decrease in their conduction ability. Consequently, this reduction in conduction can lead to deficiencies in sensation, movement, cognition, or other functions depending on the nerves affected.

Various factors can contribute to the development of demyelinating diseases, including genetic predisposition, infectious agents, autoimmune reactions, and other unknown factors. Proposed causes of demyelination include genetic predisposition, environmental factors such as viral infections or exposure to certain chemicals. Additionally, exposure to commercial insecticides like sheep dip, weed killers, and flea treatment preparations for pets, which contain organophosphates, can also lead to nerve demyelination. Chronic exposure to neuroleptic medications may also cause demyelination. Furthermore, deficiencies in vitamin B12 can result in dysmyelination.

HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. It is a syndrome of progressive deterioration of memory, cognition, behavior, and motor function in HIV-infected individuals during the late stages of the disease, when immunodeficiency is severe. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of HIV-associated dementia (HAD) are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss.

HAD typically occurs after years of HIV infection and is associated with low CD4+ T cell levels and high plasma viral loads. It is sometimes seen as the first sign of the onset of AIDS. Prevalence is between 10 and 24% in Western countries and has only been seen in 1–2% of India-based infections. With the advent of highly active antiretroviral therapy (HAART), the incidence of HAD has declined in developed countries, although its prevalence is increasing. HAART may prevent or delay the onset of HAD in people with HIV infection, and may also improve mental function in people who already have HAD.

Sphingomyelin (SPH, /ˌsfɪŋɡoʊˈmaɪəlɪn/) is a type of sphingolipid found in animal cell membranes, especially in the membranous myelin sheath that surrounds some nerve cell axons. It usually consists of phosphocholine and ceramide, or a phosphoethanolamine head group; therefore, sphingomyelins can also be classified as sphingophospholipids. In humans, SPH represents ~85% of all sphingolipids, and typically makes up 10–20 mol % of plasma membrane lipids.

Sphingomyelin was first isolated by German chemist Johann L.W. Thudicum in the 1880s. The structure of sphingomyelin was first reported in 1927 as N-acyl-sphingosine-1-phosphorylcholine. 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.