The ‘Autocannibalism’ of Choline-containing Membrane Phopholipids in the Pathogenesis of Alzheimer’s Disease
Brains of patients with Alzheimer’s disease exhibit an abundance of possible clues as to the aetiology of the disease and the pathophysiologic processes causing its signs and symptoms (Wurtman, 1985). These include: characteristic aggregations of abnormal proteins in neurons (neurofibrillary tangles) and extracellular spaces (plaques; amyloid); concentrations of a potentially neurotoxic environmental contaminant, aluminium, within affected neurons; and an abnormal aggregate, amyloid, which may itself constitute an infectious particle (‘prion’). Additional clues as to the aetiology and pathogenesis of Alzheimer’s disease may also be provided by the patient’s family history — which sometimes reveals a strong genetic component to the disease — or by data, obtained using scanning devices, which show major reductions in brain blood flow and in oxygen and energy consumption.
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- Ansell, G. B. (1973). Phospholipids and the nervous system. In Ansell, G. B., Hawthorne, J. N. and Dawson, R. M. C. (eds.), Form and Function of Phospholipids. Elsevier, Amsterdam, 377–422.Google Scholar
- Maire, J.-C., Tacconi, M. T., and Wurtman, R. J. (1983). Source of choline for the release of choline and acetylcholine from brain slices. Soc. Neurosci., 9, 283.8 (abstract).Google Scholar
- Pearson, R. C. A., Sofroniew, M. V., Cuello, A. C., Powell, T. P. S., Eckenstein, S., Esiri, M. M., and Wilcock, G. K. (1983). Persistence of cholinergic neurons in the basal nucleus in a brain with senile dementia of the Alzheimer’s type demonstrated by immunohistochemical staining for choline acetyltransferase. Brain Research, 289, 375–9.CrossRefPubMedGoogle Scholar
- Perry, R. H., Candy, J. M., Perry, E. K., Irving, D., Blessed, G., Fairbairn, A. F., and Tomlinson, B. E. (1985). Extensive loss of choline acetyltransferase activity is not reflected by neuronal loss in the nucleus of Meynert in Alzheimer’s disease. Neurosci. Lett., 33, 311–15.CrossRefGoogle Scholar