ArticleMolecular psychiatry2021
Presenilin 1 phosphorylation regulates amyloid-β degradation by microglia.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- Microglia TFEB activation attenuates Alzheimer's disease pathology by enhancing autophagy-lysosomal function.Journal of neuroinflammation · 2026Article
- Functional border-associated macrophages limit Alzheimer's Disease progression.bioRxiv : the preprint server for biology · 2026Article
- In Silico Phosphoproteomic Analysis Reveals Divergent Regulation of Presenilin 1 and Presenilin 2.Neuromolecular medicine · 2026Article
- Modeling Alzheimer's disease with brain organoids: mechanisms, applications, and future directions.Frontiers in cell and developmental biology · 2026Review
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Allosteric activation of a cell-type-specific GPR120 inhibits amyloid pathology of Alzheimer's disease.Nature aging · 2026Article
- The cGAS-STING Pathway in Dementia: An Emerging Mechanism of Neuroinflammation.Brain sciences · 2025Review
- Expansion of lysosomal capacity in early adult neurons driven by TFEB/HLH-30 protects dendrite maintenance during aging in Caenorhabditis elegans.PLoS biology · 2025Article
- Dural ectopic lymphatic structures accumulate during aging and exhibit dysregulation in neurodegenerative diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Induced Microglial-like Cells Derived from Familial and Sporadic Alzheimer's Disease Peripheral Blood Monocytes Show Abnormal Phagocytosis and Inflammatory Response to PSEN1 E280A Cholinergic-like Neurons.International journal of molecular sciences · 2025Article
- Review
- Regulatory Mechanisms and Therapeutic Implications of Lysosomal Dysfunction in Alzheimer's Disease.International journal of biological sciences · 2025Review
- Upregulation of Na/H Exchanger in Astrogliosis and Early Alzheimer's Disease Pathogenesis.Aging and disease · 2024Article
- DUSP6 regulates Notch1 signalling in colorectal cancer.Nature communications · 2024Article
- An Overview of Apple Varieties and the Importance of Apple Consumption in the Prevention of Non-Communicable Diseases-A Narrative Review.Nutrients · 2024Review
- Interconnections between the Gut Microbiome and Alzheimer's Disease: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2024Review
- Temporal Characterization of the Amyloidogenic APPswe/PS1dE9;hAPOE4 Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Autosomal Dominant Alzheimer's Disease Mutations in Human Microglia Are Not Sufficient to Trigger Amyloid Pathology in WT Mice but Might Affect Pathology in 5XFAD Mice.International journal of molecular sciences · 2024Article
- An exhausted-like microglial population accumulates in aged and APOE4 genotype Alzheimer's brains.Immunity · 2024Article
- Secretase promotes AD progression: simultaneously cleave Notch and APP.Frontiers in aging neuroscience · 2024Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Amyloid-β peptide (Aβ) accumulation in the brain is a hallmark of Alzheimer's Disease. An important mechanism of Aβ clearance in the brain is uptake and degradation by microglia. Presenilin 1 (PS1) is the catalytic subunit of γ-secretase, an enzyme complex responsible for the maturation of multiple substrates, such as Aβ. Although PS1 has been extensively studied in neurons, the role of PS1 in microglia is incompletely understood. Here we report that microglia containing phospho-deficient mutant PS1 display a slower kinetic response to micro injury in the brain in vivo and the inability to degrade Aβ oligomers due to a phagolysosome dysfunction. An Alzheimer's mouse model containing phospho-deficient PS1 show severe Aβ accumulation in microglia as well as the postsynaptic protein PSD95. Our results demonstrate a novel mechanism by which PS1 modulates microglial function and contributes to Alzheimer's -associated phenotypes.
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Registered trials
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.