ArticleTranslational psychiatry2013
1-42 β-amyloid peptide requires PDK1/nPKC/Rac 1 pathway to induce neuronal death.
Article in Translational psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Resilience mechanisms underlying Alzheimer's disease.Metabolic brain disease · 2025Review
- Amyloid βCells · 2023Article
- Roles of Rac1-Dependent Intrinsic Forgetting in Memory-Related Brain Disorders: Demon or Angel.International journal of molecular sciences · 2023Review
- Secreted endogenous macrosomes reduce Aβ burden and ameliorate Alzheimer's disease.Science advances · 2023Article
- Crosstalk between the Rho and Rab family of small GTPases in neurodegenerative disorders.Frontiers in cellular neuroscience · 2023Review
- Accelerated long-term forgetting: A sensitive paradigm for detecting subtle cognitive impairment and evaluating BACE1 inhibitor efficacy in preclinical Alzheimer's disease.Frontiers in dementia · 2023Review
- SIRT7 Deficiency Protects against AβInternational journal of molecular sciences · 2022Article
- Reducing PDK1/Akt Activity: An Effective Therapeutic Target in the Treatment of Alzheimer's Disease.Cells · 2022Review
- Amyloid β / PKC-dependent alterations in NMDA receptor composition are detected in early stages of Alzheimer´s disease.Cell death & disease · 2022Article
- A brain proteomic signature of incipient Alzheimer's disease in youngScience advances · 2021Article
- Artificial intelligence-based computational framework for drug-target prioritization and inference of novel repositionable drugs for Alzheimer's disease.Alzheimer's research & therapy · 2021Article
- Pharmacological Modulators of Small GTPases of Rho Family in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2021Article
- Small GTPases of the Ras and Rho Families Switch on/off Signaling Pathways in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Cell adhesion to collagen promotes leukemia resistance to doxorubicin by reducing DNA damage through the inhibition of Rac1 activation.Scientific reports · 2019Article
- Inhibition of Rac1-dependent forgetting alleviates memory deficits in animal models of Alzheimer's disease.Protein & cell · 2019Article
- Production of seedable Amyloid-β peptides in model of prion diseases upon PrPNature communications · 2019Article
- Acupuncture Administration Improves Cognitive Functions and Alleviates Inflammation and Nuclear Damage by Regulating Phosphatidylinositol 3 Kinase (PI3K)/Phosphoinositol-Dependent Kinase 1 (PDK1)/Novel Protein Kinase C (nPKC)/Rac 1 Signaling Pathway in Senescence-Accelerated Prone 8 (SAM-P8) Mice.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Association between thiopurine medication exposure and Alzheimer's disease among a cohort of patients with inflammatory bowel disease.Alzheimer's & dementia (New York, N. Y.) · 2019Article
- Rac1 activation links tau hyperphosphorylation and Aβ dysmetabolism in Alzheimer's disease.Acta neuropathologica communications · 2018Article
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1-42 β-Amyloid (Aβ(1-42)) peptide is a key molecule involved in the development of Alzheimer's disease. Some of its effects are manifested at the neuronal morphological level. These morphological changes involve loss of neurites due to cytoskeleton alterations. However, the mechanism of Aβ(1-42) peptide activation of the neurodegenerative program is still poorly understood. Here, Aβ(1-42) peptide-induced transduction of cellular death signals through the phosphatidylinositol 3-kinase (PI3K)/phosphoinositol-dependent kinase (PDK)/novel protein kinase C (nPKC)/Rac 1 axis is described. Furthermore, pharmacological inhibition of PDK1 and nPKC activities blocks Rac 1 activation and neuronal cell death. Our results provide insights into an unsuspected connection between PDK1, nPKCs and Rac 1 in the same signal-transduction pathway and points out nPKCs and Rac 1 as potential therapeutic targets to block the toxic effects of Aβ(1-42) peptide in neurons.
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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.