ABSTRACT
Primary age-related tauopathy (PART) is characterized by the presence of tau neurofibrillary tangles (NFTs) which are typically observed in Alzheimer's disease (AD) brains, with few or without β-amyloid (Aβ) plaques. The diagnosis of PART can be categorized into "definite" or "possible" depending on the amount of Aβ plaques. Definite PART is diagnosed when NFTs are observed and the Braak stage is ≤IV, with Thal Aβ Phase 0 (Crary et al., 2014). According to the neuropathological diagnostic criteria, we reported that PART was frequently observed in the Chinese population according to our findings from specimens in our brain bank, with 47% of brain bank subjects meeting the criteria for PART. There is no consensus on the nature of PART. It remains to be elucidated whether PART is an early form of AD or a novel tauopathy (Duyckaerts et al., 2015; Jellinger et al., 2015).
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Aging/pathology , Alzheimer Disease/pathology , Brain/pathology , Cohort Studies , Neurofibrillary Tangles/pathology , Tauopathies/pathologyABSTRACT
<p><b>OBJECTIVE</b>To explore whether BzATP could promote the growth of primary cultured astrocytes (AS) of rat and its possible mechanism, and whether TGF-β1 was involved in the event.</p><p><b>METHODS</b>The primary cultured ASs were derived from new born Sprague-Dawley rats. Glial fibrillary acidic protein (GFAP) immunofluorescent staining was used to check the purity of cultured AS. Morphometry was used to detect the changes of AS. The proliferation index of AS was detected by BrdU incorporation assay. Western blot was used to detect the changes of GFAP under different conditions. Changes of TGF-β1 gene transcription were detected by RT-PCR. ELISA was utilized to detect the variation of TGF-β1 protein in the supernate.</p><p><b>RESULTS</b>The purity of primary cultured AS reached 99%. BzATP promoted the hypertrophy of AS including the elongation of AS processes and the enlargement of cell bodies, BzATP also promoted the expression of GFAP in existence of Ca²⁺, but had no effect on cell proliferation. BzATP increased the transcription of TGF-β1 mRNA and the release of TGF-β1 protein in existence of Ca²⁺. TGF-β1 neutralizing antibody partially inhibited the expression of GFAP induced by BzATP, but had no effect on AS proliferation and cell morphology.</p><p><b>CONCLUSION</b>BzATP enhanced the hypertrophy of primary cultured AS, increased the expression of GFAP partially through TGF-β1. Mechanisms of the enhancement of AS growth induced by BzATP other than TGF-β1 pathway remain to be elucidated.</p>