BACKGROUND: There is limited information regarding children's risk of Alzheimer disease (AD) if both parents are affected. OBJECTIVE: To determine the risk of AD in families in which both parents have AD. DESIGN: Retrospective study. SETTING: University research center. PARTICIPANTS: A total of 111 families in which both parents had a clinical diagnosis of AD. Main Outcome Measure Frequency of AD in the children of spouses with AD. RESULTS: The 111 couples with AD had 297 children surviving to adulthood; 22.6% of these adult children have developed AD. The risk of AD in these children increases with age, being 31.0% (58 of 187) in those older than 60 years and 41.8% (41 of 98) in those older than 70 years. Many children (79.0%) at risk in these families are still younger than 70 years, meaning that the occurrence of AD will increase in the coming years. A family history of AD beyond the parents did not change the risk of AD in the children but did reduce the median age at onset in affected children. The apolipoprotein E epsilon4 allele played an important part in this phenomenon but did not explain all cases of AD in the children. CONCLUSIONS: When both parents have AD, there is an increased risk of AD in their children beyond that of the general population. The role of family history and the specific genes involved in this phenomenon require a better definition.
BACKGROUND: There is limited information regarding children's risk of Alzheimer disease (AD) if both parents are affected. OBJECTIVE: To determine the risk of AD in families in which both parents have AD. DESIGN: Retrospective study. SETTING: University research center. PARTICIPANTS: A total of 111 families in which both parents had a clinical diagnosis of AD. Main Outcome Measure Frequency of AD in the children of spouses with AD. RESULTS: The 111 couples with AD had 297 children surviving to adulthood; 22.6% of these adult children have developed AD. The risk of AD in these children increases with age, being 31.0% (58 of 187) in those older than 60 years and 41.8% (41 of 98) in those older than 70 years. Many children (79.0%) at risk in these families are still younger than 70 years, meaning that the occurrence of AD will increase in the coming years. A family history of AD beyond the parents did not change the risk of AD in the children but did reduce the median age at onset in affected children. The apolipoprotein E epsilon4 allele played an important part in this phenomenon but did not explain all cases of AD in the children. CONCLUSIONS: When both parents have AD, there is an increased risk of AD in their children beyond that of the general population. The role of family history and the specific genes involved in this phenomenon require a better definition.
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