{'fraction_non_alphanumeric': 0.041294642857142856, 'fraction_numerical': 0.004464285714285714, 'mean_word_length': 5.1438356164383565, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 1, '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}}
Heritability analyses show partial genetic overlap between (non‐Mendelian) early and late onset Alzheimer disease due to an intriguing APOE effect

Alzheimer disease (AD) is a degenerative brain disease, being the most common cause of progressive dementia and listed as the sixth leading cause of mortality in the USA. It is often described as either early onset (EOAD, age at onset, [AAO] <= 65) or late onset (LOAD, [AAO]>65). Non‐Mendelian EOAD (not monogenic; nmEOAD) has irregular inheritance patterns and fluctuating AAO, characteristics also present in LOAD cases. There is still a lack of evidence in the literature depicting the similarities (if any) between nmEOAD and LOAD forms, being unclear how much genetic etiology is shared by the two forms of AD. To shed light to this question, a genome‐wide association study (GWAS) and heritability analyses of nmEOAD and LOAD were performed.