ArticleTranslational psychiatry2021
Neurotrophic factor-α1, a novel tropin is critical for the prevention of stress-induced hippocampal CA3 cell death and cognitive dysfunction in mice: comparison to BDNF.
Article in Translational psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- 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
- 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
- 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
- Neurotrophic factor alpha 1 gene therapy in Alzheimer's disease: scope and advancements.Frontiers in molecular neuroscience · 2025Review
- Cannabis Dependence is Associated with Reduced Hippocampal Subregion Volumes Independently of Sex: Findings from an ENIGMA Addiction Working Group Multi-Country Study.Cannabis and cannabinoid research · 2024Article
- Article
- Agomirs upregulating carboxypeptidase E expression rescue hippocampal neurogenesis and memory deficits in Alzheimer's disease.Translational neurodegeneration · 2024Article
- Hippocampal delivery of neurotrophic factor-α1/carboxypeptidase E gene prevents neurodegeneration, amyloidosis, memory loss in Alzheimer's Disease male mice.Molecular psychiatry · 2023Article
- Carboxypeptidase E conditional knockout mice exhibit learning and memory deficits and neurodegeneration.Translational psychiatry · 2023Article
- Restoring carboxypeptidase E rescues BDNF maturation and neurogenesis in aged brains.Life medicine · 2023Article
- Prenatal Exposure to Air Pollution and Early-Life Stress Effects on Hippocampal Subregional Volumes and Associations With Visuospatial Reasoning.Biological psychiatry global open science · 2022Article
- Paeoniflorin ameliorates cognitive impairment in Parkinson's disease via JNK/p53 signaling.Metabolic brain disease · 2022Article
- Neurotrophic Factor-α1/Carboxypeptidase E Functions in Neuroprotection and Alleviates Depression.Frontiers in molecular neuroscience · 2022Review
- Alterations in Self-Aggregating Neuropeptides in Cerebrospinal Fluid of Patients with Parkinsonian Disorders.Journal of Parkinson's disease · 2022Article
- Novel interaction between neurotrophic factor-α1/carboxypeptidase E and serotonin receptor, 5-HTR1E, protects human neurons against oxidative/neuroexcitotoxic stress via β-arrestin/ERK signaling.Cellular and molecular life sciences : CMLS · 2021Article
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10 authors at 1 institution in 1 country.
Funding
Abstract
Stress leads to brain pathology including hippocampal degeneration, cognitive dysfunction, and potential mood disorders. Hippocampal CA3, a most stress-vulnerable region, consists of pyramidal neurons that regulate cognitive functions e.g. learning and memory. These CA3 neurons express high levels of the neuroprotective protein, neurotrophic factor-α1 (NF-α1), also known as carboxypeptidase E (CPE), and receive contacts from granule cell projections that release BDNF which has neuroprotective activity. Whether NF-α1-CPE and/or BDNF are critical in protecting these CA3 neurons against severe stress-induced cell death is unknown. Here we show that social combined with the physical stress of maternal separation, ear tagging, and tail snipping at weaning in 3-week-old mice lacking NF-α1-CPE, led to complete hippocampal CA3 degeneration, despite having BDNF and active phosphorylated TrkB receptor levels similar to WT animals. Mice administered TrkB inhibitor, ANA12 which blocked TrkB phosphorylation showed no degeneration of the CA3 neurons after the weaning stress paradigm. Furthermore, transgenic knock-in mice expressing CPE-E342Q, an enzymatically inactive form, replacing NF-α1-CPE, showed no CA3 degeneration and exhibited normal learning and memory after the weaning stress, unlike NF-α1-CPE-KO mice. Mechanistically, we showed that radio-labeled NF-α1-CPE bound HT22 hippocampal cells in a saturable manner and with high affinity (Kd = 4.37 nM). Subsequently, treatment of the HT22
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