Binding information in short-term memory and in long-term memory are functions sensitive to Alzheimer's disease.They have been found to be affected in patients who meet criteria for familial Alzheimer's disease due to the mutation E280A of the PSEN1 gene.However, only short-term memory binding has been found to be affected in asymptomatic carriers of this mutation.The neural correlates of this dissociation are poorly understood.The present study used diffusion tensor MRI to investigate whether the integrity of white matter structures could offer an account.A sample of 19 familial Alzheimer's disease patients, 18 asymptomatic carriers and 21 non-carrier controls underwent diffusion tensor MRI, neuropsychological and memory binding assessment.The short-term memory binding task required participants to detect changes across two consecutive screens displaying arrays of shapes, colours, or shape-colour bindings.The long-term memory binding task was a Paired Associates Learning Test.Performance on these tasks were entered into regression models.Relative to controls, familial Alzheimer's disease patients performed poorly on both memory binding tasks.Asymptomatic carriers differed from controls only in the short-term memory binding task.White matter integrity explained poor memory binding performance only in familial Alzheimer's disease patients.White matter water diffusion metrics from the frontal lobe accounted for poor performance on both memory binding tasks.Dissociations were found in the genu of corpus callosum which accounted for short-term memory binding impairments and in the hippocampal part of cingulum bundle which accounted for long-term memory binding deficits.The results indicate that white matter structures in the frontal and temporal lobes are vulnerable to the early stages of familial Alzheimer's disease and their damage is associated with impairments in two memory binding functions known to be markers for Alzheimer's disease.