Alzheimer's disease selective vulnerability and modelling in transgenic mice

Jürgen Götz*, Nicole Schonrock, Bryce Vissel, Lars M. Ittner

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Neurodegenerative diseases are characterized by 'hot spots' of degeneration. The regions of primary vulnerability vary between different neurodegenerative diseases. Within these regions, some neurons are lost whereas others that are morphologically indiscriminable survive. The enigma of this selective vulnerability is tightly linked to two fundamental problems in the neurosciences. Firstly, it is not understood how many neuronal cell types make up the mammalian brain; estimates are in the order of more than thousand. Secondly, the mechanisms by which some nerve cells undergo functional impairment followed by degeneration while others do not, remain elusive. Understanding the basis for this selective vulnerability has significant implications for understanding the pathogenesis of disease and for developing treatments. Here, we review what is known about selective vulnerability in Alzheimer's disease, frontotemporal dementia and Parkinson's disease. We suggest, since transgenic animal models of disease reproduce aspects of selective vulnerability, that these models offer a valuable system for future investigations into the physiological basis of selective vulnerability.

Original languageEnglish
Title of host publicationHandbook of animal models in Alzheimer's disease
EditorsGemma Casadesus
Place of PublicationAmsterdam
PublisherIOS Press
Number of pages10
ISBN (Electronic)9781607507338
ISBN (Print)9781607507321
Publication statusPublished - 1 Dec 2011
Externally publishedYes

Publication series

NameAdvances in Alzheimer's Disease
ISSN (Print)2210-5727
ISSN (Electronic)2210-5735


  • Aβ amyloid
  • Alzheimer's disease
  • amygdala
  • frontotemporal dementia
  • hippocampus
  • neurofibrillary tangles
  • Parkinson's disease
  • tau


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