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Such pathogens promote beta\u2010amyloid deposition and\n                    <jats:italic>tau<\/jats:italic>\n                    phosphorylation and may thus be causative agents, whose effects are conditioned by genes. The antimicrobial effects of beta\u2010amyloid, the localisation of APP\/gamma\u2010secretase in immunocompetent dendritic cells, and gamma secretase cleavage of numerous pathogen receptors suggest that this network is concerned with pathogen disposal, effects which may be abrogated by the presence of beta\u2010amyloid autoantibodies in the elderly. These autoantibodies, as well as those to nerve growth factor and\n                    <jats:italic>tau<\/jats:italic>\n                    , also observed in Alzheimer\u2032s disease, may well be antibodies to pathogens, due to homology between human autoantigens and pathogen proteins. NGF or\n                    <jats:italic>tau<\/jats:italic>\n                    antibodies promote beta\u2010amyloid deposition, neurofibrillary tangles, or cholinergic neuronal loss, and, with other autoantibodies, such as anti\u2010ATPase, are potential agents of destruction, whose formation is dictated by sequence homology between pathogen and human proteins, and thus by pathogen strain and human genes. Pathogen elimination in the ageing population and removal of culpable autoantibodies might reduce the incidence and offer hope for a cure in this affliction.\n                  <\/jats:p>","DOI":"10.4061\/2011\/501862","type":"journal-article","created":{"date-parts":[[2011,12,29]],"date-time":"2011-12-29T16:01:43Z","timestamp":1325174503000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":54,"title":["Alzheimer\u2032s Disease: APP, Gamma Secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and Their Relationships with Herpes Simplex,\n                    <i>C. Pneumoniae<\/i>\n                    , Other Suspect Pathogens, and the Immune System"],"prefix":"10.1155","volume":"2011","author":[{"given":"Chris","family":"Carter","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2011,12,29]]},"reference":[{"key":"e_1_2_4_1_2","doi-asserted-by":"publisher","DOI":"10.5402\/2011\/394678"},{"key":"e_1_2_4_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuint.2007.11.003"},{"key":"e_1_2_4_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuint.2006.07.007"},{"key":"e_1_2_4_4_2","doi-asserted-by":"crossref","first-page":"940","DOI":"10.4088\/JCP.v66n0720","article-title":"A cluster of cholesterol-related genes confers susceptibility for Alzheimer\u2032s disease","volume":"66","author":"Papassotiropoulos A.","year":"2005","journal-title":"Journal of Clinical Psychiatry"},{"key":"e_1_2_4_5_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0018660"},{"key":"e_1_2_4_6_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pgen.1001130"},{"key":"e_1_2_4_7_2","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp.73.3.261"},{"key":"e_1_2_4_8_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0437937100"},{"key":"e_1_2_4_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ygeno.2010.04.004"},{"key":"e_1_2_4_10_2","doi-asserted-by":"publisher","DOI":"10.3233\/JAD\u20102010\u2010100018"},{"key":"e_1_2_4_11_2","doi-asserted-by":"publisher","DOI":"10.1097\/WNR.0b013e3283329c05"},{"key":"e_1_2_4_12_2","doi-asserted-by":"crossref","first-page":"393","DOI":"10.3233\/JAD-2008-13405","article-title":"Herpes simplex virus type 1 in Alzheimer\u2032s disease: the enemy within","volume":"13","author":"Itzhaki R. 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