Please check out this site for info on tay sachs: http://en.wikipedia.org/wiki/Tay-Sachs_disease There is lots of info there and links to other sites with info. Please look here for MS info: http://en.wikipedia.org/wiki/Multiple_sclerosis This site explains neuroglia: http://en.wikipedia.org/wiki/Glial_cell
The main kinds of glia are Schwann cells in the PNS; astrocytes and oligodendrocytes in the CNS; and ependymal cells, forming the lining of the ventricles of the brain. In common with neurons, all these glia are produced by cell division in the embryonic neuroectoderm (indeed, early in development some of the dividing stem cells produce both neurons and glia among their ‘daughter’ cells). Unlike neurons, glia can undergo cell division in the adult and are capable of self-renewal and regeneration.
Oligodendrocytes and Schwann cells have, as their main role, the production of the fatty myelin sheaths that insulate many of the fibres or axons of nerve cells, throughout the nervous system. Myelination increases substantially the speed of conduction of nerve impulses (action potentials). Destruction of the myelinating glial cells leads to demyelination, which causes slowing and eventual block of impulse conduction and hence loss of function (both sensation and the control of movement). The results can be devastating, as in the human demyelinating diseases Multiple Sclerosis (MS) and infectious polyneuritis, which respectively affect the CNS and the PNS.
Finally, there is a class of small glial cells, called microglia, uniformly distributed throughout the CNS, which are not ‘born’ in the nervous system but are formed by transformation of certain white blood cells called macrophages or their precursors, monocytes. Microglia are now thought to be part of the immune system, defending the brain against infection and injury. Like the macrophages from which they develop, they act as scavenging cells or phagocytes — removing debris in the developing or injured CNS. Again like macrophages, they can ‘digest’ foreign proteins (parts of viruses or bacteria, for example) and display fragments of them on the outer surface of their membranes (called antigen presentation). These antigen fragments then stimulate certain white blood cells to produce antibodies to the foreign protein. Microglia also, on activation, secrete various enzymes and other molecules that can attack foreign material (proteases, cytokines, reactive oxygen species, and nitric oxide) in the brain. The presumed function of this reaction is to protect the CNS from immunological insult, but it can be damaging. It might, for example, be a factor in killing oligodendrocytes, and hence triggering demyelination in Multiple Sclerosis, an autoimmune disorder.
— Arthur M. Butt (http://www.answers.com/topic/glia)
Tay-Sachs disease is a fatal genetic lipid storage disorder in which harmful quantities of a fatty substance called ganglioside GM2 build up in tissues and nerve cells in the brain. The condition is caused by insufficient activity of an enzyme called beta-hexosaminidase A that catalyzes the biodegradation of acidic fatty materials known as gangliosides. Gangliosides are made and biodegraded rapidly in early life as the brain develops.
Infants with Tay-Sachs disease appear to develop normally for the first few months of life. Then, as nerve cells become distended with fatty material, a relentless deterioration of mental and physical abilities occurs. The child becomes blind, deaf, and unable to swallow. Muscles begin to atrophy and paralysis sets in. Other neurological symptoms include dementia, seizures, and an increased startle reflex to noise. A much rarer form of the disorder occurs in patients in their twenties and early thirties and is characterized by an unsteady gait and progressive neurological deterioration. Persons with Tay-Sachs also have "cherry-red" spots in their eyes. The incidence of Tay-Sachs is particularly high among people of Eastern European and Askhenazi Jewish descent. Patients and carriers of Tay-Sachs disease can be identified by a simple blood test that measures beta-hexosaminidase A activity. Both parents must carry the mutated gene in order to have an affected child. In these instances, there is a 25 percent chance with each pregnancy that the child will be affected with Tay-Sachs disease. Prenatal diagnosis is available if desired.
Source(s):
http://www.ninds.nih.gov/disorders/taysa…