Amyloidosis pp 243-253 | Cite as

Biochemistry of Cerebral Amyloid in Alzheimer’s Disease, The Unconventional Slow Virus Diseases and Icelandic Cerebrovascular Amyloidosis

  • David Allsop
Chapter

Abstract

It is estimated that 4–5% of the population over the age of 65 are severely demented (1); of these individuals approximately half suffer from Alzheimer’s disease (AD) (2), a progressive degenerative disease of the brain, the aetiology of which is obscure, and for which there is no form of effective treatment. The demonstration of abundant senile plaques and neurofibrillary tangles (NFT) in a brain biopsy specimen is the only means of obtaining an unequivocal diagnosis of this disease during a patient’s lifetime. These hallmark lesions are found mainly in the neocortex (particularly the frontal and temporal lobes) and the hippocampus; their clinical significance has been highlighted by showing correlations between their numbers and (a) the extent of cognitive impairment (3,4) and (b) the characteristic decline in cholinergic function (5,6) which is the best described, but not the only neurotransmitter-related abnormality (for recent reviews of neurotransmitter systems in AD see refs. 7,8). Smaller numbers of plaques and NFT do occur in normal aged individuals (3,4), and even in nondemented individuals at presenile age (9).

Keywords

Plaque Amyloid Amyloid Fibril Complete Amino Acid Sequence Pair Helical Filament Plaque Core 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Copyright information

© Martinus Nijhoff Publishers, Dordrecht 1986

Authors and Affiliations

  • David Allsop
    • 1
  1. 1.Department of BiochemistryUniversity of Nottingham, Medical School, Queen’s Medical CentreNottinghamEngland

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