Our research addressing the molecular basis of dementia in AD has involved the creation of Aβ and tau transgenic mice. Our work and that of other investigators has shown that plaques and tangles do not cause cognitive deficits in mice. These exciting findings have redirected research away from the structural consequences of the Aβ and tau peptides and turned attention toward studies of their functional consequences. We refer to the specific species of Aβ and tau that underlie memory deficits as Aβ star (Aβ*) and tau star (tau*) (see Figure 1). Aβ* and tau* are potential early causative agents in AD. Investigations of Aβ* and tau* have been made possible by the creation and study of memory and cognitive function in transgenic mice and in non-transgenic rat models of Alzheimer's disease. Identifying Aβ* and tau* is the most logical first step to developing therapies to modulate Aβ-and tau-related brain dysfunction. Successful approaches to the prevention and treatment of AD will depend upon isolating Aβ* and tau* and understanding the cellular mechanisms by which they disrupt brain function.
|Original language||English (US)|
|Title of host publication||Alzheimer's Disease|
|Subtitle of host publication||Advances in Genetics, Molecular and Cellular Biology|
|Number of pages||15|
|ISBN (Print)||0387351345, 9780387351346|
|State||Published - Dec 1 2007|