The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Glycogen synthase kinase 3 alpha and 3 beta do not colocalize with neurofibrillary tangles.

Glycogen synthase kinase (GSK) 3 alpha and 3 beta are two proline-directed serine/ threonine kinases that have been shown in vitro to hyperphosphorylate tau, and therefore, may contribute to neurofibillary tangle (NFT) formation in Alzheimer's disease (AD). We report here that, in the human hippocampal formation of both control and AD individuals, GSK 3 alpha and 3 beta are immunohistochemically localized to neurons within the presubiculum > CA1, CA3, and CA4 subfields of the hippocampus, layers III > II > IV, V, VI of entorhinal cortex, and occasional neurons in layers III, V, and VI of temporal neocortex. By contrast, NFTs occur primarily in CA1. subiculum, layers II and IV of entorhinal cortex, and layers II, III, and V of temporal neocortex. The presubiculum and other subfields are frequently spared. Thus, localization of GSK 3 alpha and GSK 3 beta does not correspond to the expected pattern of neuronal vulnerability to NFT formation in AD. Interpreted within the limitations of immunohistochemical detection, these results argue against a major role of GSK 3 alpha or GSK 3 beta in NFT formation in AD.[1]


  1. Glycogen synthase kinase 3 alpha and 3 beta do not colocalize with neurofibrillary tangles. Harr, S.D., Hollister, R.D., Hyman, B.T. Neurobiol. Aging (1996) [Pubmed]
WikiGenes - Universities