Regulation and Expression of the Alzheimer's β/A4 Amyloid Protein Precursor in Health, Disease, and Down's Syndrome a

  title={Regulation and Expression of the Alzheimer's $\beta$/A4 Amyloid Protein Precursor in Health, Disease, and Down's Syndrome a},
  author={Konrad T. Beyreuther and Peter Pollwein and Gerd Multhaup and Ursula M{\"o}nning and Gerhard K{\"o}nig and Thomas Dyrks and Walter Schubert and Colin L. Masters},
  journal={Annals of the New York Academy of Sciences},
A four‐ to fivefold overexpression of the gene for the Alzheimer β/A4 amyloid precursor protein (APP) in individuals with Down's Syndrome (DS) appears to be responsible for the fifty year earlier onset of Alzheimer's disease (AD) pathology in DS compared to the normal population. It is therefore likely that a deregulated overexpression of the APP gene is a risk factor for the β/A4 amyloid formation. To test this hypothesis and to get a better understanding of how APP expression is regulated, we… 
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Overlapping binding sites of two different transcription factors in the promoter of the human gene for the Alzheimer amyloid precursor protein.
  • P. Pollwein
  • Biology
    Biochemical and biophysical research communications
  • 1993
Evidence is presented that the transcription factor Sp1 can bind to element A and that another specific complex, called C2A, can be observed, which covers a region overlapping with the Sp1 binding site on the APP promoter.
The promoter of Alzheimer's disease amyloid A4 precursor gene.
Findings suggest that four mechanisms may participate in the regulation of the PAD gene and could be of relevance for the progression of amyloid deposition in Alzheimer's disease.
Amyloid A4 protein and its precursor in Down's syndrome and Alzheimer's disease.
Immunocytochemical studies of brain tissue from 26 patients with Down's syndrome showed that the deposition of A4 protein amyloid began in these patients approximately 50 years earlier than it began in 127 normal aging subjects studied previously, although the rate of deposition was the same.
Amyloid plaque core protein in Alzheimer disease and Down syndrome.
The shared 4-kDa subunit indicates a common origin for the amyloids of the plaque core and of the congophilic angiopathy of Alzheimer disease and Down syndrome.
Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptors.
Stimulation of m1 and m3 receptor subtypes with carbachol increased the basal release of APP derivatives within minutes of treatment, indicating that preexisting APP is released in response to receptor activation and protein kinases mediate neurotransmitter receptor-controlled APP processing.
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Evidence indicates a familial Alzheimer's disease locus on chromosome 14, which is found in early-onset non-Volga German kindreds, and results for the Volga German families were either negative or nonsignificant for markers in this region.