ArticleMolecular psychiatry2023
Hippocampal delivery of neurotrophic factor-α1/carboxypeptidase E gene prevents neurodegeneration, amyloidosis, memory loss in Alzheimer's Disease male mice.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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The trial behind it
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Carboxypeptidase E Alleviates Depressive-Like Behaviors in Mice by Regulating BDNF/Nrf2 Axis-Mediated Ferroptosis.Neurochemical research · 2026Article
- Aberrant histone acetylation and dysregulated synaptic plasticity in cognitive impairment induced by a high-methionine diet.Neural regeneration research · 2026Article
- Microplastic-Induced Disruption of Intestinal Barrier Integrity and Triggering Neuroinflammatory Responses Through Gut-Brain Axis Dysregulation Mediated by NF-κB/PPAR-γ/BDNF Signalling Pathways.Molecular neurobiology · 2026Article
- Multi-regional transcriptomic analysis reveals early nociceptive and neuroinflammatory alterations in APP/PS1 mice.Frontiers in immunology · 2026Article
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Neurotrophic factor-α1/carboxypeptidase E regulates critical protein networks to rescue neurodegeneration, defective synaptogenesis and impaired autophagy in Alzheimer's disease mice.Translational neurodegeneration · 2025Article
- Therapeutic efficacy of rehmannioside A on 5×FAD mice in Alzheimer's disease.Scientific reports · 2025Article
- Predicted molecules followed by experimental validation for protecting human neurons from oxidative stress-induced cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Plin4 modulates lipid droplet accumulation and ferroptosis in neurons exposed to benzo[a]pyrene.Cell death discovery · 2025Article
- Boosting Neurogenesis as a Strategy in Treating Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Multi-omics analysis highlights the link of aging-related cognitive decline with systemic inflammation and alterations of tissue-maintenance.bioRxiv : the preprint server for biology · 2025Article
- Changes in the Proteomic Profile After Audiogenic Kindling in the Inferior Colliculus of the GASH/Sal Model of Epilepsy.International journal of molecular sciences · 2025Article
- P2Y1 receptor in Alzheimer's disease.Neural regeneration research · 2025Article
- Neurotrophic factor alpha 1 gene therapy in Alzheimer's disease: scope and advancements.Frontiers in molecular neuroscience · 2025Review
- Neurotrophic factor-α1/carboxypeptidase E controls progression and reversal of Alzheimer's disease pathogenesis in mice.Theranostics · 2025Article
- NRN1 may Modulate Tau Phosphorylation and Neuronal Apoptosis in ADCurrent Alzheimer research · 2025Article
- Lithium Chloride Improves Electrophysiological and Memory Deficits in Rats with Streptozotocin-Induced Alzheimer's Disease.Current Alzheimer research · 2025Article
- Non-Drug and Non-Invasive Therapeutic Options in Alzheimer's Disease.Biomedicines · 2025Review
- From Fundamentals to Innovation in Alzheimer's Disease: Molecular Findings and Revolutionary Therapies.International journal of molecular sciences · 2024Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's Disease (AD) is a prevalent neurodegenerative disease characterized by tau hyperphosphorylation, Aβ1-42 aggregation and cognitive dysfunction. Therapeutic agents directed at mitigating tau aggregation and clearing Aβ1-42, and delivery of growth factor genes (BDNF, FGF2), have ameliorated cognitive deficits, but these approaches did not prevent or stop AD progression. Here we report that viral-(AAV) delivery of Neurotrophic Factor-α1/Carboxypeptidase E (NF-α1/CPE) gene in hippocampus at an early age prevented later development of cognitive deficits as assessed by Morris water maze and novel object recognition assays, neurodegeneration, and tau hyperphosphorylation in male 3xTg-AD mice. Additionally, amyloid precursor protein (APP) expression was reduced to near non-AD levels, and insoluble Aβ1-42 was reduced significantly. Pro-survival proteins: mitochondrial Bcl2 and Serpina3g were increased; and mitophagy inhibitor Plin4 and pro-inflammatory protein Card14 were decreased in AAV-NF-α1/CPE treated versus untreated AD mice. Thus NF-α1/CPE gene therapy targets many regulatory components to prevent cognitive deficits in 3xTg-AD mice and has implications as a new therapy to prevent AD progression by promoting cell survival, inhibiting APP overexpression and tau hyperphosphorylation.
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