Transmissible degenerative

The most resistant of all infectious agents to chemical inactivation are the prions, which cause transmissible degenerative encephalopathies. 

Taylor D.M. (1998) Inactivation of unconventional agents of the transmissible degenerative... 

The biological starting material contains other proteins, DNA and RNA, either from the medium or secreted by the host cell, and endotoxins. Endogenous and exogenous viruses, mycoplasma, bacteria, and proteins responsible for transmissible degenerative encephalopathies (TDE) must also to be considered as serious contaminants present in biological starting material. 

Taylor, D. M. (1999) Inactivation of unconventional agents of the transmissible degenerative encephalopathies. In Principles and Practice of Disinfection, Preservation and Sterilization (eds A.D. Russell, W.B. Hugo Sc G.A.J. Ayliffe), 3rd edn. Blackwell Science, Oxford. 

Taylor DM (2000) Inactivation of transmissible degenerative encephalopathy agents a review. Vet J 159 10-17... 

The prion diseases are a closely related group of neuro-degenerative conditions which affect both humans and animals. They have previously been described as the subacute spongiform encephalopathies, slow virus diseases and transmissible dementias, and include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and the human prion diseases, Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker disease (GSS), fatal familial insomnia (FFI) and kuru. Prion diseases are... 

There are a myriad of known and suspected mechanisms by which diseases can modify chemical neurotransmission. These can vary from no transmission, as in the case of a degenerated or absent neuron, to too much neurotransmission from a malfunction of the synapse. One of the key consequences of loss of neurons in neuro-degenerative disorders such as Parkinson s disease, Huntington s disease, amyotrophic lateral sclerosis (Lou Gehrig s disease), and Alzheimer s disease, is the fact that no neurotransmission occurs subsequent to neuronal loss (Fig. 4—24). This is a conceptually simple mechanism of disease action with profound consequences. It is also at least in part the mechanism of other disorders, such as stroke, multiple sclerosis, and virtually any disorder in which neurons are irreversibly damaged. 

Parkinsonism is associated with a number of degenerative changes in both the structure and the chemistry of the basal ganglia. The relationship between the symptoms of the disease and these changes is dependent upon what is the normal function in the extrapyramidal motor system of such substances as dopamine, noradrenaline, serotonin, and the melanins, as well as others such as acetylcholine whose levels appear to be normal in Parkinsonism. Nevertheless, normal levels do not exclude disordered function since dynamic systems can involve different rates of turnover with no apparent change in concentrations. Synaptic transmission in the central nervous system has been extensively reviewed [59-61] and only those factors relevant to Parkinsonism will be discussed here. 

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