{'fraction_non_alphanumeric': 0.024390243902439025, 'fraction_numerical': 0.004434589800443459, 'mean_word_length': 5.7388059701492535, '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}}
Lessons from genome‐wide association studies findings in Alzheimer's disease

Alzheimer's disease (AD) is the most common neurodegenerative disorder with a complex genetic background. Recent genome‐wide association studies (GWAS) have placed important new contributors into the genetic framework of early‐ and late‐onset forms of this dementia. Besides confirming the major role of classic allelic variants (e.g. apolipoprotein E) in the development of AD, GWAS have thus far implicated over 20 single nucleotide polymorphisms in AD. In this review, we summarize the findings of 16 AD‐based GWAS performed to date whose public registries are available at the National Human Genome Research Institute, with an emphasis on understanding whether the polymorphic markers under consideration support functional implications to the pathophysiological role of the major genetic risk factors unraveled by GWAS.