Abstract
Down syndrome (trisomy 21), a complex mix of physical, mental, and biochemical issues, includes an increased risk of Alzheimer’s disease and childhood leukemia, a decreased risk of other tumors, and a high frequency of overweight/obesity. Certain features related to the third copy of chromosome 21 (which carries the APP gene and several anti-angiogenesis genes) create an environment favorable for Alzheimer’s disease and unfavorable for cancer. This environment may be enhanced by two bioactive compounds from fat cells, leptin, and adiponectin. This paper outlines these fat-related disease mechanisms and suggests new avenues of research to reduce disease risk in Down syndrome.
Highlights
Unusual and poorly understood relationships exist between Down syndrome (DS), Alzheimer’s disease and cancer
Possible mechanisms include comorbid hypothyroidism, decreased resting metabolic rate, preference for high carbohydrate foods, certain behavioral tendencies that increase with age and high leptin levels; increased leptin levels from leptin resistance correlate with obesity [14]
The DS features important to the present discussion are the high rates of overweight/obesity, the increased risk of childhood leukemia and Alzheimer’s disease and the low risk of solid tumors
Summary
Unusual and poorly understood relationships exist between Down syndrome (DS), Alzheimer’s disease and cancer. In people without DS, there is an inverse relationship between risk of Alzheimer’s disease and cancer [5]. Two metabolically active compounds produced by fat cells, leptin and adiponectin, are involved in this inverse relationship [4], and these compounds could play a role in the Alzheimer’s disease cancer risk pattern in DS as well. This paper reviews epidemiologic associations between DS, Alzheimer’s disease and cancer, the genetic influences of trisomy 21, and how leptin and adiponectin could promote or inhibit these genetic influences.
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