Common mouse models do not correspond to human pathogenesis and therefore the use of animals cannot accurately determine the course of the development of Alzheimer*s disease. Although mouse models with familial Alzheimer’s disease (FAD) mutations have amyloid beta-induced synaptic and remembrance deficits, they only recapitulate other important pathological key events in Alzheimer’s disease incompletely, for instance the distinctive “neurofibrillary tangle pathology”, as the researchers report in their publication.

To construct their new innovative approach, they cultured human nerve precursor cells with FAD mutations from Alzheimer’s patients in a string imbedded in Matrigel.

The cells carried either a mutation of the amyloid beta precursor protein or of the presenilin 1 protein. With their model, the researchers were able to show that the FAD mutations are capable of triggering the amyloid-beta-deposits as well as their plaques. After several weeks of culture the building of the well-known “tangles” structures followed. Thus an old working hypothesis regarding pathogenesis could be confirmed.

The researchers plan to extend their model to include immune cells.

They have published their cell culture model in the journal Nature.

Literature:
Se Hoon Choi, Hye Young Kim, Matthias Hebisch, Christopher Sliwinski, Seungkyu Lee, Carla D'Avanzo, Hechao Chen, Basavaraj Hooli, Caroline Asselin, Julien Muffat, Justin B. Klee, Can Zhang, Brian J. Wainger, Michael Peitz, Dora M. Kovacs, Clifford J. Woolf, Steven L. Wagner, Rudolph E. Tanzi & Doo Yeon Kim (2014): A three-dimensional human neural cell culture model of Alzheimer's disease. doi: 10.1038 / nature13800

Abstract:
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13800.html

Source:
http://www.sueddeutsche.de/wissen/d-alzheimermodell-demenz-in-schaelchen-1.2171504
http://edoc.hu-berlin.de/dissertationen/capell-anja-2005-07-05/HTML/chapter1.html