Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
There is increasing evidence from genetic, immunohistochemical, proteomic and epidemiological studies as well as in model systems that complement activation has an important role in the pathogenesis of Alzheimer's disease (AD). The complement cascade is an essential element of the innate immune response. In the brain complement proteins are integral components of amyloid plaques and complement activation occurs at the earliest stage of the disease. The complement cascade has been implicated as a protective mechanism in the clearance of amyloid, and in a causal role through chronic activation of the inflammatory response. In this review we discuss the potential for complement activation to act as a biomarker for AD at several stages in the disease process. An accurate biomarker that has sufficient predictive, diagnostic and prognostic value would provide a significant opportunity to develop and test for effective novel therapies in the treatment of AD.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1016/j.imbio.2011.07.023 | DOI Listing |
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