Timeline of the landmark discovery of Alzheimer plaques and tangles made by Alois Alzheimer in 1906, followed by the identification of Aβ and tau as principal plaque and tangle components, respectively, over 70 years later.
Another decade later, the first pathogenic mutations were identified in the APP and PSEN genes in Alzheimer’s disease (AD) (1989), and nine years later in the MAPT gene in a subset of cases with frontotemporal dementia (FTD) (1998).
APP encodes the amyloid precursor protein from which Aβ is derived by proteolytic cleavage, and PSEN encodes presenilin, one of four component of the secretase complex that generates Aβ. Tau is a microtubule-associated protein encoded by the MAPT gene.
The microscope used by Alzheimer is shown as well as representative images of plaques and tangles. None of the currently available drugs prevent or delay the neuronal degeneration that characterises AD and FTD as they do not target the underlying biology.
Functional genomics approaches in experimental cellular and animal systems are expected not only to contribute to a better understanding of how Aβ and tau cause neuronal demise, but also to assist in developing more effective therapies.
To read the academic article in its entirety, please go here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3429089/?tool=pubmed
Front Physiol. 2012; 3: 320.
Published online 2012 August 8.
Alzheimer’s disease models and functional genomics—How many needles are there in the haystack?
Jürgen Götz,1,* Miriam Matamales,1 Naeman N. Götz,1 Lars M. Ittner,2 and Anne Eckert3
Articles from Frontiers in Physiology are provided here courtesy of Frontiers Media SA