Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila models

29 Mar 2018

Abstract excerpt

BACKGROUND: Cerebral amyloidosis, neuroinflammation, and tauopathy are key features of Alzheimer's disease (AD), but interactions among these features remain poorly understood. Our previous multiscale molecular network models of AD revealed TYROBP as a key driver of an immune- and microglia-specific network that was robustly associated with AD pathophysiology. Recent genetic studies of AD further identified...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer's disease research and treatments
Share to Inflammation biomarkers and pathways
Share to Neuroinflammation and Neurodegeneration Mechanisms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 29598827
DOI: 10.1186/s13073-018-0530-9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Integrated biology approach reveals molecular and pathological interactions among Alzheimer’s Aβ42, Tau, TREM2, and TYROBP in Drosophila modelsPMID 29598827Read ↗

Integrative approach to sporadic Alzheimer's disease: deficiency of TYROBP in cerebral Aβ amyloidosis mouse normalizes clinical phenotype and complement subnetwork molecular pathology without reducing Aβ burden.Semantic proximity Read ↗

Integrative approach to sporadic Alzheimer's disease: deficiency of TYROBP in a tauopathy mouse model reduces C1q and normalizes clinical phenotype while increasing spread and state of phosphorylation of tau.Semantic proximity Read ↗

Reactive or transgenic increase in microglial TYROBP reveals a TREM2-independent TYROBP-APOE link in wild-type and Alzheimer’s-related miceSemantic proximity Read ↗

Deficiency of TYROBP, an adapter protein for TREM2 and CR3 receptors, is neuroprotective in a mouse model of early Alzheimer's pathology.Semantic proximity Read ↗

Integrated analysis of the aging brain transcriptome and proteome in tauopathySemantic proximity Read ↗

Computational and functional prioritization identifies genes that rescue behavior and reduce tau protein in fly and human cell models of Alzheimer disease.Semantic proximity Read ↗

Revealing the nervous system requirements of Alzheimer’s disease risk genes in <i>Drosophila</i>Semantic proximity Read ↗

Multiscale proteomic modeling reveals protein networks driving Alzheimer's disease pathogenesis.Semantic proximity Read ↗

Revealing the nervous system requirements of Alzheimer disease risk genes in Drosophila.Semantic proximity Read ↗

Systems genetic dissection of Alzheimer’s disease brain gene expression networksSemantic proximity Read ↗

Dynamic changes in the brain protein interaction network correlates with progression of Aβ42 pathology in <i>Drosophila</i>Semantic proximity Read ↗

Effects of TYROBP Deficiency on Neuroinflammation of a Alzheimer's Disease Mouse Model Carrying a PSEN1 p.G378E Mutation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.