Transcriptional and conformational changes of the tau molecule in Alzheimer's disease.
Mutations in the tau gene cause frontotemporal dementia with parkinsonism, presumably by affecting the balance between tau isoforms (with either three or four microtubule-binding repeats) or by impairing tau-tubulin binding. Although to date no mutations have been found for Alzheimer's disease, it is plausible that tangle pathology in this disorder is also driven by similar molecular modifications. Investigations of Alzheimer brain tissue with new technologies such as laser capture microscopy, quantitative PCR and fluorescence lifetime imaging will shed light on whether transcriptional or conformational alterations play a role in Alzheimer pathogenesis.
Hyman
Bradley T
BT
Department of Neurology, Massachusetts General Hospital, 114 16th Street, Charlestown, MA 02129, USA. bhyman@partners.org
Augustinack
Jean C
JC
Ingelsson
Martin
M
D017398:Alternative Splicing; D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism*; D015870:Gene Expression; D006801:Humans; D008870:Microtubules / Q000378:metabolism; D009154:Mutation; D016874:Neurofibrillary Tangles / Q000502:physiology; D011487:Protein Conformation; D014158:Transcription, Genetic; D016875:tau Proteins / Q000737:chemistry* / Q000235:genetics
D016875:tau Proteins