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
Alzheimer's disease (AD) is associated with the accumulation of β-amyloids (Aβs) and the formation of Aβ plaques in the brain. Various structural forms and isoforms of Aβs that have variable propensities for oligomerization and toxicity and may differentially affect the development of AD have been identified. In addition, there is evidence that β-amyloids are engaged in complex interactions with the innate and adaptive immune systems, both of which may also play a role in the regulation of AD onset and progression. In this review, we discuss what is currently known about the intricate interplay between β-amyloids and the immune response to Aβs with a more in-depth focus on the possible roles of B cells in the pathogenesis of AD.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475064 | PMC |
http://dx.doi.org/10.3390/cells13191624 | DOI Listing |
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