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RE‐EVALUATION OF ARCHIVAL “DLDH” CASES FOR FRONTOTEMPORAL LOBAR DEGENERATION WITH UBIQUITIN INCLUSIONS: ANTIGEN RETRIEVAL IS ESSENTIAL
Author(s) -
Gearing Marla,
Cooper Deborah,
Glass Jonathan
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.707.14
Subject(s) - frontotemporal lobar degeneration , ubiquitin , pathology , immunohistochemistry , frontotemporal dementia , semantic dementia , antigen , pathological , antibody , antigen retrieval , biology , dementia , chemistry , medicine , immunology , biochemistry , disease , gene
The neuropathologic subtypes of frontotemporal lobar degeneration (FTLD) can frequently be differentiated immunohistochemically. The identification of abnormal deposits of tau, ubiquitin, and, more recently, TAR DNA‐binding protein 43 (TDP‐43) and alpha‐internexin may allow separation of neuropathologic subtypes, whereas the lack of staining for these proteins may lead to a diagnosis of “dementia lacking distinctive histology” (DLDH). Because of the importance of accurate pathological diagnosis for the understanding of these disorders, we investigated whether a wider panel of antibodies and more sensitive immunohistochemical methods could allow for better neuropathologic characterization. We undertook a study of 13 autopsy cases with non‐specific diagnoses such as DLDH. We relabeled these brains with antibodies to tau, ubiquitin, TDP‐43, and alpha‐internexin. In addition, we tested the effect of antigen retrieval on the ability to detect the ubiquitin immunolabel. In 7 of the 13 cases, ubiquitin‐immunoreactive inclusions were identified. These cases also immunolabeled with the antibody to TDP‐43. This pattern of staining supported a reclassification to FTLD with ubiquitin inclusions (FTLD‐U). In all of these cases, the antigen retrieval method markedly enhanced ubiquitin immunolabel and was critical for the identification of FTLD‐U pathology. Supported by 1P50‐AG025688.