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Modulation of β-amyloid production and fibrillisation

Research output: Contribution to journalLiterature review

  • David Allsop
  • Lance Twyman
  • Yvonne Davies
  • Susan Moore
  • Amber York
  • Linda Swanson
  • Ian Soutar
<mark>Journal publication date</mark>2000
<mark>Journal</mark>Biochemical Society Symposia
Number of pages14
Pages (from-to)1-14
Publication statusPublished
Original languageEnglish


Alzheimer’s disease (AD) is the most common cause of dementia in old age and presently affects an estimated 4 million people in the U.S.A. and 0.75 million people in the U.K. It is a relentless, degenerative brain disease, characterized by progressive cognitive impairment. In the final stages of the disease, patients are often bedridden, doubly incontinent and unable to speak or to recognize close relatives. Pathological changes of Alzheimer’s disease include extensive neuronal loss and the presence of numerous neurofibrillary tangles and senile plaques in the brain. The senile plaques contain amyloid fibrils derived from a 39-43-amino-acid peptide referred to as b-amyloid or Ab. The basic theory of the so-called ‘amyloid hypothesis’ is that the deposition of aggregated forms of Ab in the brain parenchyma triggers a pathological cascade of events that leads to neurofibrillary tangle formation, neuronal loss and the associated dementia [1]. Here we discuss progress towards the identification of inhibitors of Ab production and fibrillization.