Family History of Alzheimer's Disease and Subjective Memory Performance.

People with a first-degree family history of Alzheimer's disease are at an increased risk of developing dementia. Subjective memory impairment among individuals with no measurable cognitive deficits may also indicate elevated dementia risk. It remains unclear whether nondemented people with a positive family history of Alzheimer's disease are more likely to experience cognitive deficits and whether such an association reflects underlying neuropathology. We therefore investigated subjective memory impairment and hippocampal cortical thickness in 40 healthy older adults and 35 patients with amnestic mild cognitive impairment. We found greater subjective memory impairment and left hemispheric hippocampal cortical thinning associated with a first-degree family history of Alzheimer's disease in healthy older adults. This suggests that subjective memory impairment could reflect preclinical stage neurodegeneration among individuals with the family history risk factor.

Precuneus Structure Changes in Amnestic Mild Cognitive Impairment.

Patients with amnestic mild cognitive impairment (aMCI) are at risk for developing Alzheimer's disease. Due to their prominent memory impairment, structural magnetic resonance imaging (MRI) often focuses on the hippocampal region. However, recent positron-emission tomography data suggest that within a network of frontal and temporal changes, patients with aMCI show metabolic alterations in the precuneus, a key region for higher cognitive functions. Using high-resolution MRI and whole-brain cortical thickness analyses in 28 patients with aMCI and 25 healthy individuals, we wanted to investigate whether structural changes in the precuneus would be associated with cortical thickness reductions in frontal and temporal brain regions in patients with aMCI. In contrast to healthy people, patients with aMCI showed an association of cortical thinning in the precuneus with predominantly left-hemispheric thickness reductions in medial temporal and frontal cortices. Our data highlight structural neuronal network characteristics among patients with aMCI.

Family History of Alzheimer's Disease and Cortical Thickness in Patients With Dementia.

A first-degree family history of Alzheimer's disease reflects genetic risks for the neurodegenerative disorder. Recent imaging data suggest localized effects of genetic risks on brain structure in healthy people. It is unknown whether this association can also be found in patients who already have dementia. Our aim was to investigate whether family history risk modulates regional medial temporal lobe cortical thickness in patients with Alzheimer's disease. We performed high-resolution magnetic resonance imaging and cortical unfolding data analysis on 54 patients and 53 nondemented individuals. A first-degree family history of Alzheimer's disease was associated with left hemispheric cortical thinning in the subiculum among patients and controls. The contribution of Alzheimer's disease family history to regional brain anatomy changes independent of cognitive impairment may reflect genetic risks that modulate onset and clinical course of the disease.

Education and Genetic Risk Modulate Hippocampal Structure in Alzheimer's Disease.

Genetic and environmental protective factors and risks modulate brain structure and function in neurodegenerative diseases and their preclinical stages. We wanted to investigate whether the years of formal education, a proxy measure for cognitive reserve, would influence hippocampal structure in Alzheimer's disease patients, and whether apolipoprotein Eε4 (APOE4) carrier status and a first-degree family history of the disease would change a possible association. Fifty-eight Alzheimer's disease patients underwent 3T magnetic resonance imaging. We applied a cortical unfolding approach to investigate individual subregions of the medial temporal lobe. Among patients homozygous for the APOE4 genotype or carrying both APOE4 and family history risks, lower education was associated with a thinner cortex in multiple medial temporal regions, including the hippocampus. Our data suggest that the years of formal education and genetic risks interact in their influence on hippocampal structure in Alzheimer's disease patients.