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10.1007/s00401-016-1560-2 http://scihub22266oqcxt.onion/10.1007/s00401-016-1560-2 C4835519!4835519 !26988843     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26988843 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Acta+Neuropathol 2016 ; 131 (5 ): 737-52 Nephropedia Template TP {{tp|p=26988843 |t=2016. Tau pathology-dependent remodelling of cerebral arteries precedes Alzheimer s disease-related microvascular cerebral amyloid angiopathy |pdf=|usr=}}{{26988843 }} gab.com Text Tau pathology-dependent remodelling of cerebral arteries precedes Alzheimer s disease-related microvascular cerebral amyloid angiopathy JO: Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=26988843 #FOAvip Alzheimer's disease (AD) is characterised by pathologic cerebrovascular remodelling. Whether this occurs already before disease onset, as may be indicated by early Braak tau-related cerebral hypoperfusion and blood-brain barrier (BBB) impairment found in previous studies, remains unknown. Therefore, we systematically quantified Braak tau stage- and cerebral amyloid angiopathy (CAA)-dependent alterations in the alpha-smooth muscle actin (?-SMA), collagen, and elastin content of leptomeningeal arterioles, small arteries, and medium-sized arteries surrounding the gyrus frontalis medialis (GFM) and hippocampus (HIPP), including the sulci, of 17 clinically and pathologically diagnosed AD subjects (Braak stage IV-VI) and 28 non-demented control subjects (Braak stage I-IV). GFM and HIPP paraffin sections were stained for general collagen and elastin with the Verhoeff-van Gieson stain; ?-SMA and CAA/amyloid ? (A?) were detected using immunohistochemistry. Significant arterial elastin degradation was observed from Braak stage III onward and correlated with Braak tau pathology (? = 0.909, 95% CI 0.370 to 0.990, p < 0.05). This was accompanied by an increase in neutrophil elastase expression by ?-SMA-positive cells in the vessel wall. Small and medium-sized arteries exhibited significant CAA-independent ?-SMA loss starting between Braak stage I and II-III, along with accumulation of phosphorylated paired helical filament (PHF) tau in the perivascular space of intraparenchymal vessels. ?-SMA remained at the decreased level throughout the later Braak stages. In contrast, arterioles exhibited significant ?-SMA loss only at Braak stage V and VI/in AD subjects, which was CAA-dependent/correlated with CAA burden (? = -0.422, 95% CI -0.557 to -0.265, p < 0.0001). Collagen content was only significantly changed in small arteries. Our data indicate that vessel wall remodelling of leptomeningeal arteries is an early-onset, Braak tau pathology-dependent process unrelated to CAA and AD, which potentially may contribute to downstream CAA-dependent microvascular pathology in AD. Twit Text FOAVip Tau pathology-dependent remodelling of cerebral arteries precedes Alzheimer s disease-related microvascular cerebral amyloid angiopathy ????Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=26988843 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26988843 #FOAvip English Wikipedia <ref>{{Cite pmid|26988843 }}</ref> Tau pathology-dependent remodelling of cerebral arteries precedes Alzheimer s disease-related microvascular cerebral amyloid angiopathy #MMPMID26988843 Merlini M ; Wanner D ; Nitsch RM Acta Neuropathol 2016[May]; 131 (5 ): 737-52 PMID26988843 show ga Alzheimer's disease (AD) is characterised by pathologic cerebrovascular remodelling. Whether this occurs already before disease onset, as may be indicated by early Braak tau-related cerebral hypoperfusion and blood-brain barrier (BBB) impairment found in previous studies, remains unknown. Therefore, we systematically quantified Braak tau stage- and cerebral amyloid angiopathy (CAA)-dependent alterations in the alpha-smooth muscle actin (?-SMA), collagen, and elastin content of leptomeningeal arterioles, small arteries, and medium-sized arteries surrounding the gyrus frontalis medialis (GFM) and hippocampus (HIPP), including the sulci, of 17 clinically and pathologically diagnosed AD subjects (Braak stage IV-VI) and 28 non-demented control subjects (Braak stage I-IV). GFM and HIPP paraffin sections were stained for general collagen and elastin with the Verhoeff-van Gieson stain; ?-SMA and CAA/amyloid ? (A?) were detected using immunohistochemistry. Significant arterial elastin degradation was observed from Braak stage III onward and correlated with Braak tau pathology (? = 0.909, 95% CI 0.370 to 0.990, p < 0.05). This was accompanied by an increase in neutrophil elastase expression by ?-SMA-positive cells in the vessel wall. Small and medium-sized arteries exhibited significant CAA-independent ?-SMA loss starting between Braak stage I and II-III, along with accumulation of phosphorylated paired helical filament (PHF) tau in the perivascular space of intraparenchymal vessels. ?-SMA remained at the decreased level throughout the later Braak stages. In contrast, arterioles exhibited significant ?-SMA loss only at Braak stage V and VI/in AD subjects, which was CAA-dependent/correlated with CAA burden (? = -0.422, 95% CI -0.557 to -0.265, p < 0.0001). Collagen content was only significantly changed in small arteries. Our data indicate that vessel wall remodelling of leptomeningeal arteries is an early-onset, Braak tau pathology-dependent process unrelated to CAA and AD, which potentially may contribute to downstream CAA-dependent microvascular pathology in AD. |Actins/metabolism [MESH] |Aged [MESH] |Aged, 80 and over [MESH] |Alzheimer Disease/diagnostic imaging/*pathology [MESH] |Analysis of Variance [MESH] |Blood-Brain Barrier/pathology [MESH] |Brain/*metabolism/*pathology [MESH] |Cerebral Amyloid Angiopathy/diagnostic imaging/*pathology [MESH] |Collagen/metabolism [MESH] |Disease Progression [MESH] |Elastin/metabolism [MESH] |Female [MESH] |Humans [MESH] |Male [MESH] |Microvessels/diagnostic imaging/metabolism/*pathology [MESH] |Netherlands [MESH] |Neuroimaging [MESH] |Psychiatric Status Rating Scales [MESH] |Retrospective Studies [MESH]Tau pathology-dependent remodelling of cerebral arteries precedes Alzh(epmc).pdf DeepDyve Pubget Overpricing