In early 2005, a team of researchers at Washington University School of Medicine in St. Louis announced that in a mouse brain model of an Alzheimer’s-like disease, cells quickly recuperated after brain plaques were cleared. Prior to the group’s study, in which they injected mice with an antibody for the amyloid beta peptide (a key component of brain plaques), it was widely thought that damage to nerve cells caused by plaques was irreversible. Thus, the scientists were surprised to find that many nerve cells regained normal structure over the course of just a few days once plaques were successfully removed. The results appear promising for humans with Alzheimer’s disease, some of which may soon be able to undergo experimental treatment with amyloid beta

The neuron-specific intermediate filaments known as neurofilaments were targeted in the mouse brain coronal thin section shown above with chicken anti NF-H antibodies followed by goat anti-chicken secondary antibodies conjugated to Alexa Fluor 488. In addition, glial fibrillary acidic protein, an intermediate filament protein that is a key structural element of astroglia, was immunofluorescently labeled with primary anti-GFAP rabbit monoclonal antibodies followed by goat anti-rabbit Fab fragments conjugated to Alexa Fluor 568. Hoechst 33342 was employed as a nuclear counterstain. Images were recorded in grayscale with a 12-bit digital camera coupled to a Nikon Eclipse 80i microscope equipped with bandpass emission fluorescence filter optical blocks. During the processing stage, individual image channels were pseudocolored with RGB values corresponding to each of the fluorophore emission spectral profiles.