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Neuropathological comorbidity associated with argyrophilic grain disease
Author(s) -
Yokota Osamu,
Miki Tomoko,
Ikeda Chikako,
Nagao Shigeto,
Takenoshita Shintaro,
Ishizu Hideki,
Haraguchi Takashi,
Kuroda Shigetoshi,
Terada Seishi,
Yamada Norihito
Publication year - 2018
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/neup.12429
Subject(s) - putamen , caudate nucleus , progressive supranuclear palsy , pathology , neuropathology , corticobasal degeneration , psychology , tauopathy , neuroscience , medicine , disease , neurodegeneration
Argyrophilic grain disease ( AGD ) is a common four‐repeat tauopathy in elderly people. While dementia is a major clinical picture of AGD , recent studies support the possibility that AGD may be a pathological base in some patients with mild cognitive impairment, late‐onset psychosis, bipolar disorder and depression. AGD often coexists with various other degenerative changes. The frequency of AGD in progressive supranuclear palsy ( PSP ) cases was reported to range from 18.8% to 80%. The frequency of AGD in corticobasal degeneration ( CBD ) cases tends to be higher than that in PSP cases, ranging from 41.2% to 100%. Conversely, in our previous study of the frequencies of mild PSP and CBD pathologies in AGD cases, five of 20 AGD cases (25%) had a few G allyas‐positive tufted astrocytes, six cases (30%) had a few granular/fuzzy astrocytes, and one case (5.0%) had a few G allyas‐positive astrocytic plaques in the putamen, caudate nucleus and/or superior frontal gyrus. Both G allyas‐positive tufted astrocytes and G allyas‐negative tau‐positive granular/fuzzy astrocytes preferentially developed in the putamen, caudate nucleus and superior frontal cortex in AGD cases, being consistent with the predilection sites of G allyas‐positive tufted astrocytes in PSP cases. Further, in AGD cases, the quantities of G allyas‐positive tufted astrocytes, overall tau‐positive astrocytes, and tau‐positive neurons in the subcortical nuclei and superior frontal cortex were significantly correlated with S aito AGD stage, respectively. The frequency of AGD in AD cases was reported to reach up to 25% when using four‐repeat tau immunohistochemistry. Pretangles are essential pathologies in AGD ; however, the B raak stage of three‐repeat tau‐positive NFTs, which may indicate mild AD pathology or primary age‐related tauopathy, was not correlated with S aito AGD stage. Clinicians should be aware of the possibility that coexisting AGD may impact clinical and radiological features in cases of other degenerative diseases.