{'fraction_non_alphanumeric': 0.02570093457943925, 'fraction_numerical': 0.014485981308411215, 'mean_word_length': 5.9288025889967635, '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}}
Autopsy of an Elderly Man With Incidentally Diagnosed TDP-43 Proteinopathy.

P examination of patients with subclinical or early clinical neurodegenerative disease improves understanding of the important correlation between specific clinical signs and pathologic features and helps to determine the stage or anatomic hierarchy of common neurodegenerative diseases such as Alzheimer disease (AD) and Parkinson disease. We recently reported the pathologic features of preclinical or early clinical corticobasal degeneration and progressive supranuclear palsy, which were diagnosed by immunohistochemical examination of serial forensic autopsy cases, without case selection.1,2 Proteinopathy of 43-kDa TAR (transactive response) DNA-binding protein (TDP-43) is the major cause of frontotemporal lobar degeneration (FTLD), a neurodegenerative disorder that presents as either behavioral or language impairment and has a prevalence similar to that of AD in men and women younger than 65 years.3 In the clinical diagnosis of frontotemporal dementia (FTD), there are 2 main clinical presentations: behavioral variant FTD (bvFTD) and primary progressive aphasia. There are in turn 3 primary progressive aphasia variants: semantic variant (svPPA), nonfluent or agrammatic variant, and logopenic variant.4 The cytopathology and distribution pattern of TDP-43-immunoreactive deposits generally differ among these clinical phenotypes.5 Conversely, pathology in the early stage of FTLD with TDP-43 proteinopathy (FTLDTDP) remains poorly understood, possibly because of a dearth of autopsy cases with preclinical or early clinical TDP-43 proteinopathy. Nevertheless, several recent studies have revealed TDP-43-immunoreactive accumulation in cognitively normal elderly people.6–8 The autopsied brain that we describe here appeared normal for the patient’s age. However, we diagnosed pathologic TDP-43 proteinopathy incidentally in the absence of an obvious clinical history of FTD. The ethics committee of Toyama University approved this study, which was performed in accordance with the ethical standards established in the 1964 Declaration of Helsinki.