ArticleScientific reports2022
The effects of microglia on tauopathy progression can be quantified using Nexopathy in silico (Nexis) models.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 26 citations in OpenAlex.
- Selective vulnerability of monoaminergic neurons and network spread of alpha-synuclein jointly explain pathology progression in Parkinson's disease models.Neurobiology of disease · 2026Article
- Brain network dynamics determine tau presence while regional vulnerability governs tau load in Alzheimer's disease.Research square · 2026Article
- Extracellular Vesicles in Tauopathies: Mechanisms and Applications.International journal of molecular sciences · 2026Review
- Modeling Alzheimer's disease with brain organoids: mechanisms, applications, and future directions.Frontiers in cell and developmental biology · 2026Review
- WhenAPL bioengineering · 2025Review
- Roles of TREM2 in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Patient-specific functional brain architecture explains cortical patterns of tau PET in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Selective vulnerability and resilience to Alzheimer's disease tauopathy as a function of genes and the connectome.Brain : a journal of neurology · 2025Article
- Key Connectomes and Synaptic-Compartment-Specific Risk Genes Drive Pathological α-Synuclein Spreading.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Back to the Future: Predicting Individual Tau Progression in Alzheimer's Disease.Research square · 2025Article
- Directionality bias underpins divergent spatiotemporal progression of Alzheimer-related tauopathy in mouse models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- A network-level transport model of tau progression in the Alzheimer's brain.Mathematical medicine and biology : a journal of the IMA · 2025Article
- Searching for the cellular underpinnings of the selective vulnerability to tauopathic insults in Alzheimer's disease.Communications biology · 2025Article
- Connectome-based biophysical models of pathological protein spreading in neurodegenerative diseases.PLoS computational biology · 2025Review
- The dual role of microglia in Alzheimer's disease: from immune regulation to pathological progression.Frontiers in aging neuroscience · 2025Review
- Beyond the usual suspects: multi-factorial computational models in the search for neurodegenerative disease mechanisms.Translational psychiatry · 2024Review
- Cellular underpinnings of the selective vulnerability to tauopathic insults in Alzheimer's disease.bioRxiv : the preprint server for biology · 2023Article
- Connectome-based modelling of neurodegenerative diseases: towards precision medicine and mechanistic insight.Nature reviews. Neuroscience · 2023Review
- Network models to enhance the translational impact of cross-species studies.Nature reviews. Neuroscience · 2023Review
- The anti-Alzheimer potential of novel spiroindolin-1,2-diazepine derivatives as targeted cholinesterase inhibitors with modified substituents.Scientific reports · 2023Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The prion-like transsynaptic propagation of misfolded tau along the brain's connectome has previously been modeled using connectome-based network diffusion models. In addition to the connectome, interactions between the general neurological "milieu" in the neurodegenerative brain and proteinopathic species can also contribute to pathology propagation. Such a molecular nexopathy framework posits that the distinct characteristics of neurodegenerative disorders stem from interactions between the network and surrounding molecular players. However, the effects of these modulators remain unquantified. Here, we present Nexopathy in silico ("Nexis"), a quantitative model of tau progression augmenting earlier models by including parameters of pathology propagation defined by the molecular modulators of connectome-based spread. Our Nexis:microglia model provides the first quantitative characterization of this effect on the whole brain by expanding previous models of neuropathology progression by incorporating microglial influence. We show that Trem2, but not microglial homeostasis genes, significantly improved the model's predictive power. Trem2 appears to reduce tau accumulation rate while increasing its interregional spread from the hippocampal seed area, causing higher tau burden in the striatum, pallidum, and contralateral hippocampus. Nexis provides an improved understanding and quantification of microglial contribution to tau propagation and can be flexibly modified to include other modulators of progressive neurodegeneration.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.