Titlebook: Alzheimer‘s Disease; Methods and Protocol Nigel M. Hooper Book 2000 Humana Press 2000

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,Introduction to Alzheimer’s Disease,europathological findings. It was Divry (.) who first demonstrated the presence of amyloid at the center of the senile plaque, by means of Congo red staining. All amyloid deposits were originally thought to be starch-like in nature (hence the name), but it is now apparent that they are formed from a

deriver

,The Genetics of Alzheimer’s Disease,nile dementia” compared with dizygotic twins and siblings. This monozygotic excess has been confirmed in studies applying more rigorous diagnostic criteria although there may be widely disparate ages of onset between twins (.). The most convincing evidence for a genetic contribution to AD has come f

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,Electrophoretic Separation and Immunoblotting of Aβ1–40 and Aβ1–42,β42 isoform (.-.). These observations have led to the hypothesis that Aβ42 may play a critical role in amyloid plaque formation and the development of Alzheimer’s disease. Obviously methods discriminating between the two major Aβ species are important in order to study this notion.

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Posttranslational Modifications of Amyloid Precursor Protein,y on translocation into the ER, the signal peptide of APP is removed from the N-terminus by signal peptidase. APP is then modified cotranslationally by N-glycosylation on NH.-groups of asparagine residues. After passage into the Golgi compartment, the ectodomain of APP is subjected to O-glycosylatio

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,Using β-Secretase Inhibitors to Distiguish the Generation of the Aβ Peptides Terminating at Val-40 PP with a mutation at codon 717 known to increase the formation of Aβ42 led to the appearance of Aβ deposits at the age of 18 mo. These data suggest that the Aβ load in the brain as well as the amyloidogenic properties of the Aβ isoforms directly regulate deposition and senile plaque formation.

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Determining the Transmembrane Topology of the Presenilins,. The second approach is based on selective permeabilization of the plasma membrane using a bacterial pore-forming toxin, streptolysin-O (SLO), and subsequent immunocytochemical probing for cytosolic epitopes using specific antibodies. Both of these methods can be easily adapted to determine the top