The node-based overlap between this network and other networks is calculated as the Szymkiewicz-Simpson coefficient of their respective nodes. Up to the top 10 are shown below.
|Estrogen receptor-α is localized to neurofibrillary tangles in Alzheimer's disease v1.0.0||50%|
|Tau Modifications v1.9.5||46%|
|Tau in physiology and pathology v1.0.0||34%|
|Alzheimer's disease pathological lesions activate the spleen tyrosine kinase. v1.0.0||29%|
|Alzheimer’s disease and the autophagic-lysosomal system v1.0.0||27%|
|Inert and seed-competent tau monomers suggest structural origins of aggregation v1.0.0||25%|
|Abnormal Alzheimer-like phosphorylation of tau-protein by cyclin-dependent kinases cdk2 and cdk5 v1.0.0||25%|
|Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0||24%|
|Protein phosphatase 2A dysfunction in Alzheimer’s disease v1.0.0||24%|
|Neuronal uptake and propagation of a rare phosphorylated high-molecular-weight tau derived from Alzheimer’s disease brain v1.0.1||24%|
The amount of Aβ produced could be altered by delayed axonal transport, as well as the precise species of metabolites of APPproduced— e.g., Aβ40 or 42, monomeric Aβ, or Aβ-oligomers or Aβ-derived diffusible ligands (ADDLs) (Lambert et al., 1998; Walsh et al., 2000).
For the sake of completeness, we also refer to tau- 3R transgenic mice that developed another type of pathology in the hippocampus, e.g., straight fila- ments formed in aged mice older than 18 mo (Ishi- hara, 2001b), which was proposed to be relevant for AD, given the age-dependence.
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.