ArticleCell reports2022
The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Retromer-targeted therapy for neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain.Science advances · 2026Article
- RhoGEF12 regulates endosomal SORL1-retromer and its inhibition is therapeutic in human neuronal models of Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity.The Journal of cell biology · 2025Article
- Cell-death pathways and tau-associated neuronal vulnerability in Alzheimer's disease.Cell reports · 2025Article
- γ-secretase facilitates retromer-mediated retrograde transport.Journal of cell science · 2025Article
- Microglia heterogeneity during neuroinflammation and neurodegeneration in the mouse retina.Brain structure & function · 2024Article
- Endosomal traffic disorders: a driving force behind neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Advances in the cell biology of the trafficking and processing of amyloid precursor protein: impact of familial Alzheimer's disease mutations.The Biochemical journal · 2024Review
- In vivo validation of late-onset Alzheimer's disease genetic risk factors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- γ-secretase facilitates retromer-mediated retrograde transport.bioRxiv : the preprint server for biology · 2024Article
- TDP-43-stratified single-cell proteomics of postmortem human spinal motor neurons reveals protein dynamics in amyotrophic lateral sclerosis.Cell reports · 2024Article
- TMEM106B core deposition associates with TDP-43 pathology and is increased in risk SNP carriers for frontotemporal dementia.Science translational medicine · 2024Article
- OXR1 maintains the retromer to delay brain aging under dietary restriction.Nature communications · 2024Article
- Article
- FAM91A1-TBC1D23 complex structure reveals human genetic variations susceptible for PCH.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- α-Synuclein propagation leads to synaptic abnormalities in the cortex through microglial synapse phagocytosis.Molecular brain · 2023Article
- On the causal role of retromer-dependent endosomal recycling in Alzheimer's disease.Nature cell biology · 2023Article
- Multi-omic approach characterises the neuroprotective role of retromer in regulating lysosomal health.Nature communications · 2023Article
- An aging, pathology burden, and glial senescence build-up hypothesis for late onset Alzheimer's disease.Nature communications · 2023Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Disruption of retromer-dependent endosomal trafficking is considered pathogenic in late-onset Alzheimer's disease (AD). Here, to investigate this disruption in the intact brain, we turn to a genetic mouse model where the retromer core protein VPS35 is depleted in hippocampal neurons, and then we replete VPS35 using an optimized viral vector protocol. The VPS35 depletion-repletion studies strengthen the causal link between the neuronal retromer and AD-associated neuronal phenotypes, including the acceleration of amyloid precursor protein cleavage and the loss of synaptic glutamate receptors. Moreover, the studies show that the neuronal retromer can regulate a distinct, dystrophic, microglia morphology, phenotypic of hippocampal microglia in AD. Finally, the neuronal and, in part, the microglia responses to VPS35 depletion were found to occur independent of tau. Showing that the neuronal retromer can regulate AD-associated pathologies in two of AD's principal cell types strengthens the link, and clarifies the mechanism, between endosomal trafficking and late-onset sporadic AD.
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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.