ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
p110δ PI3-Kinase Inhibition Perturbs APP and TNFα Trafficking, Reduces Plaque Burden, Dampens Neuroinflammation, and Prevents Cognitive Decline in an Alzheimer's Disease Mouse Model.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Microglia-Mediated Neuroinflammation Through Phosphatidylinositol 3-Kinase Signaling Causes Cognitive Dysfunction.International journal of molecular sciences · 2025Review
- Exploring the Interplay Between Kidney Dysfunction and Cardiovascular Disease.Medical sciences (Basel, Switzerland) · 2025Review
- Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer's Disease.Cells · 2025Review
- Neuroprotection against beta-amyloid toxicity by the novel estrogen receptor modulator STX requires convergent signaling pathways.Frontiers in molecular neuroscience · 2025Article
- The Importance of Phosphoinositide 3-Kinase in Neuroinflammation.International journal of molecular sciences · 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
- Lipids and Secretory Vesicle Exocytosis.Advances in neurobiology · 2023Article
- Efficacy and safety of the integration of traditional Chinese medicine and western medicine in the treatment of diabetes-associated cognitive decline: a systematic review and meta-analysis.Frontiers in pharmacology · 2023Review
- Females exhibit higher GluA2 levels and outperform males in active place avoidance despite increased amyloid plaques in TgF344-Alzheimer's rats.Scientific reports · 2022Article
- Promoting axon regeneration in the central nervous system by increasing PI3-kinase signaling.Neural regeneration research · 2022Review
- Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation.Journal of neuroinflammation · 2021Review
- PI3K inhibitors are finally coming of age.Nature reviews. Drug discovery · 2021Review
- PAM (PIK3/AKT/mTOR) signaling in glia: potential contributions to brain tumors in aging.Aging · 2021Review
- Broader Insights into Understanding Tumor Necrosis Factor and Neurodegenerative Disease Pathogenesis Infer New Therapeutic Approaches.Journal of Alzheimer's disease : JAD · 2021Review
- PI 3-kinase delta enhances axonal PIPEMBO molecular medicine · 2020Article
- Neuroprotective effect of tormentic acid against memory impairment and neuro‑inflammation in an Alzheimer's disease mouse model.Molecular medicine reports · 2020Article
- Presynaptic APP levels and synaptic homeostasis are regulated by Akt phosphorylation of huntingtin.eLife · 2020Article
- Toll-like receptor 4 deficiency ameliorates β2-microglobulin induced age-related cognition decline due to neuroinflammation in mice.Molecular brain · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is associated with the cleavage of the amyloid precursor protein (APP) to produce the toxic amyloid-β (Aβ) peptide. Accumulation of Aβ, together with the concomitant inflammatory response, ultimately leads to neuronal death and cognitive decline. Despite AD progression being underpinned by both neuronal and immunological components, therapeutic strategies based on dual targeting of these systems remains unexplored. Here, we report that inactivation of the p110δ isoform of phosphoinositide 3-kinase (PI3K) reduces anterograde axonal trafficking of APP in hippocampal neurons and dampens secretion of the inflammatory cytokine tumor necrosis factor-alpha by microglial cells in the familial AD APP
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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.