Abstract
No treatments are currently available for Alzheimer disease (AD) (1). Serum levels of advanced glycation end products (AGEs), a large group of pro-oxidant and pro-inflammatory compounds, and particularly carboxymethyl lysine (CML) and the AGE precursor methylglyoxal (MG), are generated endogenously and by dietary consumption (2). Accumulating evidence in preclinical and small human clinical studies suggests that modifying dietary AGE consumption might affect the accumulation of AD pathology and dementia in older adults, especially those with type 2 diabetes (T2D) (3–5).
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