ArticleInternational journal of Alzheimer's disease2011
Alzheimer's Disease: APP, Gamma Secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and Their Relationships with Herpes Simplex, C. Pneumoniae, Other Suspect Pathogens, and the Immune System.
Article in International journal of Alzheimer's disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 66 citations in OpenAlex.
- Association between Toxoplasma gondii seropositivity and Alzheimer's disease: a case-control study.Parasitology research · 2026Article
- CD2AP shapes a stromal reduced tumor microenvironment and contributes to immunotherapy in gastric cancer.BMC cancer · 2025Article
- Comprehensive investigation of multiple targets in the development of newer drugs for the Alzheimer's disease.Acta pharmaceutica Sinica. B · 2025Review
- Evaluation of Selected Plant Phenolics via Beta-Secretase-1 Inhibition, Molecular Docking, and Gene Expression Related to Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Mechanistic insights into the role of herpes simplex virus 1 in Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Clinical and Preclinical Studies of Fermented Foods and Their Effects on Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2022Review
- The Potential Role of Gut Microbiota in Alzheimer's Disease: From Diagnosis to Treatment.Nutrients · 2022Review
- Antiherpetic drugs: a potential way to prevent Alzheimer's disease?Alzheimer's research & therapy · 2022Article
- Prediction of functional microexons by transfer learning.BMC genomics · 2021Article
- Herpes simplex virus, early neuroimaging markers and incidence of Alzheimer's disease.Translational psychiatry · 2021Article
- Interaction between genetic factors,Journal of oral microbiology · 2020Review
- A transcriptomic analysis of serial-cultured, tonsil-derived mesenchymal stem cells reveals decreased integrin α3 protein as a potential biomarker of senescent cells.Stem cell research & therapy · 2020Article
- Blood-brain barrier transcytosis genes, risk of dementia and stroke: a prospective cohort study of 74,754 individuals.European journal of epidemiology · 2019Article
- Review
- Brain-Gut-Microbiota Axis in Alzheimer's Disease.Journal of neurogastroenterology and motility · 2019Review
- A genetic signature including apolipoprotein Eε4 potentiates the risk of herpes simplex-associated Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2019Article
- Re-thinking Alzheimer's disease therapeutic targets using gene-based tests.EBioMedicine · 2018Article
- Prediction of Alzheimer's Disease-Associated Genes by Integration of GWAS Summary Data and Expression Data.Frontiers in genetics · 2018Article
- Amyloid-Beta 1-42 Cross-Reactive Antibody Prevalent in Human Sera May Contribute to Intraneuronal Deposition of A-Beta-P-42.International journal of Alzheimer's disease · 2018Article
- Genetic, Transcriptome, Proteomic, and Epidemiological Evidence for Blood-Brain Barrier Disruption and Polymicrobial Brain Invasion as Determinant Factors in Alzheimer's Disease.Journal of Alzheimer's disease reports · 2017Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease susceptibility genes, APP and gamma-secretase, are involved in the herpes simplex life cycle, and that of other suspect pathogens (C. pneumoniae, H. pylori, C. neoformans, B. burgdorferri, P. gingivalis) or immune defence. Such pathogens promote beta-amyloid deposition and tau phosphorylation and may thus be causative agents, whose effects are conditioned by genes. The antimicrobial effects of beta-amyloid, the localisation of APP/gamma-secretase 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-amyloid autoantibodies in the elderly. These autoantibodies, as well as those to nerve growth factor and tau, also observed in Alzheimer's disease, may well be antibodies to pathogens, due to homology between human autoantigens and pathogen proteins. NGF or tau antibodies promote beta-amyloid deposition, neurofibrillary tangles, or cholinergic neuronal loss, and, with other autoantibodies, such as anti-ATPase, 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.
Identifiers
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Registered trials
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