{'fraction_non_alphanumeric': 0.020560747663551402, 'fraction_numerical': 0.019626168224299065, 'mean_word_length': 4.95, '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}}
Early intervention in Alzheimer disease

The heritability of Alzheimer disease (AD) in the general population, usually occurring after age 65, has been a matter of intense interest once it was clear that highly penetrant autosomal dominant genes accounted for only a tiny fraction of the genetic component of AD. Twin studies have established that the heritability of AD is high.1 No one disputes that the type 4 allele for apolipoprotein E ( APOE4 ) multiplies risk, shifting average age at the onset of clinical symptoms downward, especially when 2 copies of APOE4 have been inherited.2 Rare autosomal dominant forms of early onset AD were identified in the early 1990s. In persons with mutations in the APP ,3,4 PSEN1 ,5 or PSEN2 6 genes, AD usually develops before age 65, and there are prodromal cognitive and structural brain changes decades before a diagnostic threshold is reached.

From these starting points, the initial progress to define the mode of AD inheritance, to identify polymorphisms associated with risk among the hundreds of candidate genes,7 and …