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Scrapie and Alzheimer's disease

Alzheimer's disease (AD) is the most common form of dementing illness in both the presenile and senile age-groups (Marsden & Harrison, 1972; Tomlinson et al. 1970). Predominantly a disease of old age, it manifests itself as a slowly progressive mental deterioration over a period of several years, leading eventually to profound dementia. As the proportion of the population in the older age-group increases, it becomes more important to understand the underlying causes of this distressing disease (Roth, 1982). This priority has recently led to an expansion of research on AD and related topics but one of the limitations in these studies has been the lack of satisfactory experimental models. There are no direct analogues of AD in laboratory animals, although senile plaques, a characteristic neuropathological change in AD, are seen in small numbers in very old animals of a few mammalian species (Wisniewski & Terry, 1973). In recent years a number of parallels have been recognized between AD and scrapie, an infectious neurological disease of sheep and goats (Dickinson et al. 1979; Bruce & Dickinson, 1982). Like AD, scrapie follows a slowly progressive and unremitting course. Pathological changes in each disease are confined to the central nervous system and are degenerative, with little or no evidence of inflammatory reaction (for reviews of the pathology of AD and scrapie, see Corsellis (1976) and Fraser (1976) respectively). Most important, using certain scrapie models it is possible to reproduce some of the characteristic pathological features of AD, particularly the occurrence of amyloidcontaining plaques and a selective loss of neurons in the hippocampus. Scrapie is the best understood representative of a group of diseases which also includes Creutzfeldt-Jakob disease and kuru in man and transmissible mink encephalopathy (Marsh, 1976). These diseases are caused by similar replicating agents of an, as yet, unknown molecular nature. Although their unusual physico-chemical properties set them apart from conventional viruses (Millson et al. 1976), they can be regarded as small virus-like organisms in that they replicate and carry information. Scrapie has been transmitted to a range of laboratory animals by injection of infected tissue (usually brain) and has been studied most extensively in mice and hamsters. Serial passage in mice of isolates from diverse natural sheep sources has so far led to the identification of 15 different strains of scrapie, distinguished from each other primarily on the basis of the highly repeatable incubation periods produced in particular mouse genotypes (Dickinson & Fraser, 1977); incubation periods in the various mouse models range from 140 days up to the animal's lifespan. A range of changes is seen in the brains of scrapie mice, the relative extent and distribution of which depend mainly on the scrapie strain, mouse strain and route of infection; in other words, there are many murine scrapie models, each with its own characteristic pattern of pathological change (Fraser, 1976). The most typical lesion is a spongy vacuolar degeneration which is targeted to different areas of brain in different models. With certain combinations of scrapie strain and mouse strain a prominent feature is the occurrence of many small amyloid foci or plaques (Bruce & Fraser, 1975). These are analogous in structure to senile or neuritic plaques, a major diagnostic feature of AD (Terry & Wisniewski, 1970), consisting of a core of extracellular fibrils of amyloid protein surrounded by degenerating neuronal processes and microglial cells. Infection with scrapie is the only known experimental method for producing this type of lesion, although small numbers of senile plaques are associated with 'normal' ageing in a number of species, including humans (Tomlinson, 1979) but not mice (Dayan, 1971; Bruce & Fraser, 1982).On the other hand,neurofibrillary degeneration, the other characteristic feature of AD