V. Bigl/T. Arendt: Die Alzheimersche Krankheit. 
Wissenschaft u. Fortschritt 38 (1988), 178-181.

14763 Xinwei Cao/Thomas Su''dhof: A transcriptively active complex of
APP with Fe65 and histone acetyltransferase Tip60.
Science 6 July 2001, 115-120.

D. Goldgaber a.o.: Characterization and chromosomal localization of a cDNS
encoding brain of Alzheimer's disease. Science 235 (1987), 877-880.

14803 Michael Gros'': Stoppt Alzheimer - spielt Schach! Spektrum 2001/6, 22.

5433 Maika Grummt: Erkenntnisse zum Vergessen - ein neues Modell der 
Alzheimer-Krankheit. Spektrum 1993/6, 21-22. Oft kann selbst der Arzt kaum 
zwischen einem fruehen Stadium der Alzheimer-Krankheit und einer weniger 
gravierenden Gedaechtnisschwaeche unterscheiden. Erst die Sektion des Gehirns 
verschafft Klarheit: Bei Alzheimer-Kranken sind jene Teile, die an Gedaechtnis
und Wahrnehmung [wieso nur diese Teile?] durchsetzt mit auffaelligen 
Knoetchen, die aus faserigen Ablagerungen von beta-Amyloid bestehen. Dieses 
kleine Eiweissprotein geht aus einem viel groesseren Vorlaeuferprotein hervor,
dem beta-APP (beta-amyloid precursor protein). Dieses Vorlaeuferprotein ist 
ein Zellrezeptor, der eine Kaskade von Vorgaengen in Gang setzt, die den 
Kalziumspiegel im Inneren der Zellen erhoehen. Bei Nervenzellen kann das 
moeglicherweise zum Absterben der Zellfortsaetze fuehren.

J. Hardy: Molecular biology and Alzheimer's disease. More questions than
answers? Trends Neurosci. 3 (1980), 269-278.

5351 Susan Katz Miller: Alzheimer's gene "the most important ever found".
New Scientist 21 August 1993, 17.

9136 Jean Marx: Dissecting how presenilins function - and malfunction.
Science 13 December 1996, 1838-1840.

14738 Jean Marx: Elusive protein auditions for several new roles.
Science 6 July 2001, 28-29. APP, the amyloid precursor protein, is hot
among neurobiologists.

M. Podlisny/G. Lee/D. Selkoe: Gene dosage of the amyloid beta-precursor
protein in Alzheimer's disease. Science 238 (1987), 669-671.

5412 Jim Schnabel: Alzheimer's disease: Arthritis of the brain?
New Scientist 19 June 1993, 22-26.
Billions of dollars have been poured into the search for a cure for 
Alzheimer's disease. Can the destructive advance of this neurological 
disorder be stopped by anti-inflammatory compounds related to aspirin? That 
is exactly what medical researchers in the US and Canada are trying to prove. 
This summer, in the journal "Neurology", Joe Rogers (Sun Health Research 
Institute in Sun City, Arizona) and Pat McGeer (University of British Columbia
in Vancouver) will unveil the results of an apparently promising clinical 
trial of an aspirin-like drug called indomethacin on Alzheimer's patients. 
The clinical trial is based on a radical theory as to what causes brain cells 
to die in Alzheimer's disease. The two researchers argue that Alzheimer's 
disease is essentially an inflammatory condition akin to rheumatoid arthritis,
the neurological damage is caused by a local overheating of the immune system,
in which biochemical and cellular defence mechanisms turn against the brain 
cells they are meant to defend. In the last years research efforts were 
directed at unravelling the role of a peptide called beta-amyloid, which is 
released by cells as a fragment of a much larger molecule, the amyloid 
precursor protein (APP). But no one could prove that beta-amyloid actually 
kills brain cells. However, McGeer and Roberts, see no great conflict between 
their ideas and the beta-amyloid hypothesis, being willing to concede that 
beta-amyloid can kill neurons directly, but think that most of the damage is 
caused by the peptide' immunologic effects, specifically, its ability ot 
activate the complement cascade.

D. Selkoe: The molecular pathology of Alzheimer's disease.
Neuron 6 (1991), 487-498.

St. George-Hyslop a.o.: The genetic defect causing familiar Alzheimer's
disease maps on chromosome 21. Science 235 (1987), 885-890.

R. Tanzi a.o.: Amyloid beta-protein gene: cDNA, mRNA distribution, and genetic
linkage near the Alzheimer locus. Science 235 (1987), 880-884.

11416 Gretchen Vogel: Possible new cause of Alzheimer's disease found.
Science 9 January 1998, 174.