Association of GSK3B with Alzheimer disease and frontotemporal dementia.
|Title||Association of GSK3B with Alzheimer disease and frontotemporal dementia.|
|Publication Type||Journal Article|
|Year of Publication||2008|
|Authors||Schaffer, BAJ, Bertram L, Miller BL, Mullin K, Weintraub S, Johnson N, Bigio EH, Mesulam M, Wiedau-Pazos M, Jackson GR, Cummings JL, Cantor RM, Levey AI, Tanzi RE, Geschwind DH|
|Journal||Archives of neurology|
|Date Published||2008 Oct|
|Keywords||Aged, Aged, 80 and over, Alzheimer Disease, Brain, Case-Control Studies, Dementia, DNA Mutational Analysis, Exons, Female, Genetic Markers, Genetic Predisposition to Disease, Genetic Testing, Genotype, Glycogen Synthase Kinase 3, Humans, Introns, Male, Middle Aged, Mutation, Phosphorylation, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, tau Proteins|
Deposits of abnormally hyperphosphorylated tau are a hallmark of several dementias, including Alzheimer disease (AD), and about 10% of familial frontotemporal dementia (FTD) cases are caused by mutations in the tau gene. As a known tau kinase, GSK3B is a promising candidate gene in the remaining cases of FTD and in AD, for which tau mutations have not been found.
|Alternate Journal||Arch. Neurol.|