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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Excitotoxic mechanisms of neurodegeneration in transmissible spongiform encephalopathies.

Endogenous excitatory amino acids (EAAs) such as glutamic or aspartic acids have been proposed to mediate the brain damage to EAA receptor-rich brain sites that is caused by a variety of external toxic agents (glutamic acid, domoic acid, kainic acid, ibogaine, trimethyltin (TMT), 3-nitropropionic acid (3-NPA)), as well as from such naturally-occurring age-related neurodegenerative diseases as Alzheimer's disease, Huntington's chorea, and Parkinson's disease. Sites often damaged include the hypothalamus (glutamate), the hippocampal and neocortical pyramidal neurons (domoic acid), the cerebellar Purkinje neurons (ibogaine) and the corpus striatum (3-NPA, amphetamine). The excitotoxic damage occurs to neuronal cell bodies and their dendrites, resulting in a characteristics appearance of pyknotic neurons surrounded by their vacuolated, swollen dendrites. Axons passing through the region that lack EAA receptors are completely spared. However, astrocytes with swollen perikarya and nuclei (Alzheimer's type II "reactive" astrocytes) are often observed in the vicinity of the lesions. Animal and human "Prion Diseases" or "Transmissible Spongiform Encephalopathies" (TSEs) result (after a period of months to years) in a neurodegenerative picture characterized by pyknotic neurons surrounded by vacuoles with numerous reactive astrocytes in the vicinity of the damage. In addition, amyloid deposits composed of a protease-resistant protein (PrPSc) characteristic of the particular host species with the disease are found near the degenerating neurons. By using different strains of the scrapies TSE agent to inoculate hamsters and mice, reproducible models of hypothalamic, hippocampal, or cerebellar damage resulting in the appropriate functional deficits may be obtained. Because of the close similarity in the appearance, localization, and functional consequences from TSE neuropathology compared to some of the well-known EAA syndromes, we propose that excitotoxic mechanisms may play a role in the pathogenesis of TSE neurodegenerative diseases. The similarity in pathogenesis of the neurodegenerative processes in excitotoxicity compared to TSE diseases also implies that neuroprotective strategies against excitotoxicity may also be effective against TSEs.[1]


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