Alzheimer’s disease is a terrible and devastating condition. Not just for the patients themselves, but also for their loved ones. Witnessing the fading of shared memories from the minds of the afflicted ones, until no glimpse of recognition remains in their eyes when they look at you is a highly unpleasant experience.
Difference between a normal, healthy brain (left) and a brain of a person with Alzheimer's disease (right).
(Source: Wikimedia Commons, user: Garrondo)
As average lifespan increases, it is not unreasonable to assume that the prevalence of Alzheimer’s disease will increase as well. A good motivation to investigate the disease, hopefully leading to a better understanding of it, which, in turn might lead to some form of treatment or prevention.
Luckily, many researchers around the world are working on this. Recently, a few articles have appeared that provide some new pieces of the puzzle that is Alzheimer’s disease.
A first study, published in PLoS ONE, has identified several genes which, when in mutated form, occur in both early- and late-onset Alzheimer’s, suggesting that both are actually the same disease, and that the difference in the age of onset might be explained by other factors (Cruchaga et al., 2012). In the words of the authors:
Rare coding variants in APP, PSEN1 and PSEN2, increase risk for or cause late onset AD. Dividing AD into late onset and early onset is probably not useful from a mechanistic point of view because mutations in APP, PSEN1 and PSEN2 can be found in early onset and late onset AD.
A second study, also in PLoS ONE, studied how the defective tau protein spreads through a brain by engineering mice to express pathological ‘human’ tau proteins in their brains (Liu et al., 2012). The researchers found that the defective protein spread from neuron to neuron through the synapses connecting them. In the words of the authors:
We have demonstrated that tau pathology initiating in the EC [entorhinal cortex] can spread to other synaptically connected brain areas as the mice age, supporting the idea that AD progresses via an anatomical cascade as opposed to individual events occurring in differentially vulnerable regions. Thus, our NT transgenic mouse provides a model in which the spatial and temporal propagation of the disease can be predicted, and correlative functional outcomes can now be tested. Given that the earliest Braak stages are not associated with cognitive decline, identifying an EC based “biomarker” for pathology or dysfunction and developing therapeutic strategies to prevent propagation are likely to be both possible, and beneficial.
For more information about Alzheimer’s disease, be sure to check the site of the Alzheimer’s Association, where loads of information can be found, including a nice Brain Tour which introduces one to how Alzheimer’s disease manifests in the brain. On their site, you can also sign a petition. In the words of the association:
The time is now. Alzheimer's can't wait. We need a federal commitment in order to change the course of Alzheimer's disease. Tell President Obama millions of families are counting on him to fulfill the potential of the National Alzheimer's Project Act when he releases his upcoming Budget Request to Congress in February.
References
Alzheimer’s Association
Cruchaga, C.; Chakraverty, S.; Mayo, K.; Vallania, F.L.M.; Mitra, R.D.; Faber, K.; Williamson, J.; Bird, T.; Diaz-Arrastia, R.; Foroud, T.M.; Boeve, B.F.; Graff-Radford, N.R.; St. Jean, P.; Lawson, M.; Ehm, M.G.; Mayeux, R. and Goate, A.M. (2012). Rare Variants in APP, PSEN1 and PSEN2 Increase Risk for AD in Late-Onset Alzheimer’s Disease Families. PLoS ONE. 7(2):e31039. Doi:10.1371/journal.pone.0031039.
Liu, L.; Drouet, V.; Wu, J.W.; Witter, M.P.; Small, S.A.; Clelland, C. and Duff, K. (2012). Trans-Synaptic Spread of Tau Pathology In Vivo. PLoS ONE. 7(2):e31302. Doi:10.1371/journal.pone.0031302.
