| Literature DB >> 26659578 |
Gabor G Kovacs1, Isidro Ferrer2, Lea T Grinberg3,4, Irina Alafuzoff5, Johannes Attems6, Herbert Budka7, Nigel J Cairns8, John F Crary9,10, Charles Duyckaerts11, Bernardino Ghetti12, Glenda M Halliday13, James W Ironside14, Seth Love15, Ian R Mackenzie16, David G Munoz17, Melissa E Murray18, Peter T Nelson19, Hitoshi Takahashi20, John Q Trojanowski21, Olaf Ansorge22, Thomas Arzberger23, Atik Baborie24, Thomas G Beach25, Kevin F Bieniek18, Eileen H Bigio26, Istvan Bodi27, Brittany N Dugger25,28, Mel Feany29, Ellen Gelpi30, Stephen M Gentleman31, Giorgio Giaccone32, Kimmo J Hatanpaa33, Richard Heale6, Patrick R Hof10, Monika Hofer22, Tibor Hortobágyi34, Kurt Jellinger35, Gregory A Jicha36, Paul Ince37, Julia Kofler38, Enikö Kövari39, Jillian J Kril40, David M Mann41, Radoslav Matej42, Ann C McKee43, Catriona McLean44, Ivan Milenkovic45,46, Thomas J Montine47, Shigeo Murayama48, Edward B Lee21, Jasmin Rahimi45, Roberta D Rodriguez49, Annemieke Rozemüller50, Julie A Schneider51,52, Christian Schultz53, William Seeley3, Danielle Seilhean11, Colin Smith14, Fabrizio Tagliavini32, Masaki Takao54, Dietmar Rudolf Thal55,56, Jon B Toledo21, Markus Tolnay57, Juan C Troncoso58, Harry V Vinters59,60, Serge Weis61, Stephen B Wharton37, Charles L White33, Thomas Wisniewski62,63,64, John M Woulfe65, Masahito Yamada66, Dennis W Dickson67.
Abstract
Pathological accumulation of abnormally phosphorylated tau protein in astrocytes is a frequent, but poorly characterized feature of the aging brain. Its etiology is uncertain, but its presence is sufficiently ubiquitous to merit further characterization and classification, which may stimulate clinicopathological studies and research into its pathobiology. This paper aims to harmonize evaluation and nomenclature of aging-related tau astrogliopathy (ARTAG), a term that refers to a morphological spectrum of astroglial pathology detected by tau immunohistochemistry, especially with phosphorylation-dependent and 4R isoform-specific antibodies. ARTAG occurs mainly, but not exclusively, in individuals over 60 years of age. Tau-immunoreactive astrocytes in ARTAG include thorn-shaped astrocytes at the glia limitans and in white matter, as well as solitary or clustered astrocytes with perinuclear cytoplasmic tau immunoreactivity that extends into the astroglial processes as fine fibrillar or granular immunopositivity, typically in gray matter. Various forms of ARTAG may coexist in the same brain and might reflect different pathogenic processes. Based on morphology and anatomical distribution, ARTAG can be distinguished from primary tauopathies, but may be concurrent with primary tauopathies or other disorders. We recommend four steps for evaluation of ARTAG: (1) identification of five types based on the location of either morphologies of tau astrogliopathy: subpial, subependymal, perivascular, white matter, gray matter; (2) documentation of the regional involvement: medial temporal lobe, lobar (frontal, parietal, occipital, lateral temporal), subcortical, brainstem; (3) documentation of the severity of tau astrogliopathy; and (4) description of subregional involvement. Some types of ARTAG may underlie neurological symptoms; however, the clinical significance of ARTAG is currently uncertain and awaits further studies. The goal of this proposal is to raise awareness of astroglial tau pathology in the aged brain, facilitating communication among neuropathologists and researchers, and informing interpretation of clinical biomarkers and imaging studies that focus on tau-related indicators.Entities:
Keywords: ARTAG; Aging; Tau; Tau astrogliopathy
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Year: 2015 PMID： 26659578 PMCID： PMC4879001 DOI： 10.1007/s00401-015-1509-x
Source DB: PubMed Journal: Acta Neuropathol ISSN： 0001-6322 Impact factor: 17.088