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Selective vulnerability of neurones in organic dementia

Naturevolume 266pages558559 (1977) | Download Citation



THERE are many causes of the clinical state dementia. Excluding those patients with tumours, infection or vascular disease, there remains a large group1 whose brains are atrophied and contain an excess of senile morphological change (senile plaques, neurofibrillary degeneration and granulovacuolar change) in the cortex. When this condition occurs before the age of 65 years it is known as presenile dementia or Alzheimer's disease; after this age it has been called senile dementia. Since there is no good reason on pathological grounds2 to maintain this distinction, we use the term Alzheimer's disease irrespective of the patient's age. Together with Parkinson's disease and Huntington's chorea, Alzheimer's disease is one of a group of disorders that Gowers (see ref. 2) called abiotrophies, in which nerve cell loss appears to occur in characteristic patterns (that is, substantia nigra, basal ganglia and cortex, respectively). The cause of this cellular death remains unknown. Morphological assessment of possible nerve cell loss2 or glial cell increase3 has been difficult, particularly in Alzheimer's disease. We have sought therefore to complement histological findings by measuring appropriate biochemical constituents of brain as indices of total neural cell numbers. Whole temporal lobes have been homogenised and analysed and the results expressed per lobe. The results4 suggest that whilst the total number of glial cells is relatively unchanged, there is a loss of approximately half the total nerve cell population. This estimate is based on comparison with age-matched controls, and so the selective neuronal loss is probably a disease-related phenomenon. These findings conform with conclusions drawn from morphological data5.

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  1. Miriam Marks Department of Neurochemistry, Institute of Neurology, The National Hospital, Queen Square, London, WC1, UK

    • J. A. SPILLANE
    • , R. H. A. FLACK
    • , D. M. BOWEN
    •  & A. N. DAVISON


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