Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.neurobiolaging.2015.05.016 http://scihub22266oqcxt.onion/10.1016/j.neurobiolaging.2015.05.016 C4602365!4602365 !26103884     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 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\26103884 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Neurobiol+Aging 2015 ; 36 (9 ): 2468-74 Nephropedia Template TP {{tp|p=26103884 |t=2015. Down syndrome individuals with Alzheimer s disease have a distinct neuroinflammatory phenotype compared to sporadic Alzheimer s disease |pdf=|usr=}}{{26103884 }} gab.com Text Down syndrome individuals with Alzheimer s disease have a distinct neuroinflammatory phenotype compared to sporadic Alzheimer s disease JO: Neurobiol Aging http://www.kidney.de/pget.php?&tw=1&pmid=26103884 #FOAvip Down syndrome (DS) is the most common genetic cause of intellectual disability and is primarily caused by the triplication of chromosome 21. The overexpression of amyloid precursor protein gene may be sufficient to drive Alzheimer's disease (AD) neuropathology that is observed in virtually all individuals with DS by the age of 40 years. There is relatively little information about inflammation in the DS brain and how the genetics of DS may alter inflammatory responses and modify the course of AD pathogenesis in this disorder. Using the macrophage classification system of M1, M2a, M2b, and M2c inflammatory phenotypes, we have shown that the early stages of AD are associated with a bias toward an M1 or M2a phenotype. In later stages of AD, markers of M1, M2a and M2c are elevated. We now report the inflammatory phenotype in a DS autopsy series to compare this with the progression in sporadic AD. Tissue from young DS cases (under 40 years of age, pre-AD) show a bias toward M1 and M2b states with little M2a or M2c observed. Older DS cases (over 40 with AD pathology) show a distinct bias toward an M2b phenotype. Importantly, this is distinct from sporadic AD where the M2b phenotype has been rarely, if ever observed in postmortem studies. Stimulated by immune complex activation of microglial cells and toll-like receptor activation, the M2b phenotype represents a unique neuroinflammatory state in diseased brain and may have significant implications for therapeutic intervention for persons with DS. Twit Text FOAVip Down syndrome individuals with Alzheimer s disease have a distinct neuroinflammatory phenotype compared to sporadic Alzheimer s disease ????Neurobiol Aging http://www.kidney.de/pget.php?&tw=1&pmid=26103884 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26103884 #FOAvip English Wikipedia <ref>{{Cite pmid|26103884 }}</ref> Down syndrome individuals with Alzheimer s disease have a distinct neuroinflammatory phenotype compared to sporadic Alzheimer s disease #MMPMID26103884 Wilcock DM ; Hurban J ; Helman AM ; Sudduth TL ; McCarty KL ; Beckett TL ; Ferrell JC ; Murphy MP ; Abner EL ; Schmitt FA ; Head E Neurobiol Aging 2015[Sep]; 36 (9 ): 2468-74 PMID26103884 show ga Down syndrome (DS) is the most common genetic cause of intellectual disability and is primarily caused by the triplication of chromosome 21. The overexpression of amyloid precursor protein gene may be sufficient to drive Alzheimer's disease (AD) neuropathology that is observed in virtually all individuals with DS by the age of 40 years. There is relatively little information about inflammation in the DS brain and how the genetics of DS may alter inflammatory responses and modify the course of AD pathogenesis in this disorder. Using the macrophage classification system of M1, M2a, M2b, and M2c inflammatory phenotypes, we have shown that the early stages of AD are associated with a bias toward an M1 or M2a phenotype. In later stages of AD, markers of M1, M2a and M2c are elevated. We now report the inflammatory phenotype in a DS autopsy series to compare this with the progression in sporadic AD. Tissue from young DS cases (under 40 years of age, pre-AD) show a bias toward M1 and M2b states with little M2a or M2c observed. Older DS cases (over 40 with AD pathology) show a distinct bias toward an M2b phenotype. Importantly, this is distinct from sporadic AD where the M2b phenotype has been rarely, if ever observed in postmortem studies. Stimulated by immune complex activation of microglial cells and toll-like receptor activation, the M2b phenotype represents a unique neuroinflammatory state in diseased brain and may have significant implications for therapeutic intervention for persons with DS. |Adolescent [MESH] |Adult [MESH] |Age Factors [MESH] |Aged [MESH] |Aged, 80 and over [MESH] |Alzheimer Disease/*complications [MESH] |Amyloid beta-Peptides/metabolism [MESH] |Amyloid beta-Protein Precursor/genetics/metabolism [MESH] |Brain/metabolism/pathology [MESH] |Case-Control Studies [MESH] |Cytokines/*genetics [MESH] |Disease Progression [MESH] |Down Syndrome/*complications [MESH] |Encephalitis/*diagnosis/*etiology [MESH] |Female [MESH] |HLA-DR Antigens/metabolism [MESH] |Humans [MESH] |Macrophages [MESH] |Male [MESH] |Middle Aged [MESH] |Peptide Fragments/metabolism [MESH] |Phenotype [MESH]Down syndrome individuals with Alzheimer s disease have a distinct n(epmc).pdf DeepDyve Pubget Overpricing