{'fraction_non_alphanumeric': 0.023346303501945526, 'fraction_numerical': 0.005836575875486381, 'mean_word_length': 5.402489626556017, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Advanced glycation end products, diabetes, and the brain

Type 2 diabetes is associated with declines in cognition, including learning and memory, mental flexibility, and mental speed. The degree of decrement tends to be modest and evolves slowly as a person ages. However, some patients diagnosed with type 2 diabetes experience a different course, with increased risk of more severe cognitive deficits including Alzheimer disease (AD) or vascular dementia, suggesting different processes and possibly different risk factors and underlying mechanisms or intermediaries.1

Among the possible intermediaries of brain injury in persons with diabetes are advanced glycation end products (AGEs), i.e., products resulting from chemical reactions occurring in long-lived tissue proteins after chronic exposure to hyperglycemia. AGEs damage organs, including the brain, by increasing oxidative stress and inflammation. Some suggest that AGEs contribute to the aging phenotype by accelerating multisystem decline.2 AGEs may be linked to the current epidemic of diabetes and its comorbidities.3,4 AGEs may be an underlying mechanism for pathologic synergism of diabetes and both AD5 and vascular dementia.6

AGEs are a heterogeneous group of macromolecules formed when sugars react with proteins, lipids, and nucleic acids.2 In vivo, these molecules form through a process known as glycation, the level of which depends on the duration of hyperglycemia and the half-life of the protein of interest. Most clinicians appreciate this process as the one …