ArticleProceedings of the National Academy of Sciences of the United States of America2010
Dissecting the involvement of tropomyosin-related kinase A and p75 neurotrophin receptor signaling in NGF deficit-induced neurodegeneration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- Reduction in hippocampal cholinergic neurostimulating peptide enhances memory impairment in AppAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Modulatory Role of Arbutin on Hepatic Inflammation and Apoptosis After Mild Repetitive Traumatic Brain Injury in Experimental Rats: Involvement of NGF/TrkA and IL-6/JAK2/STAT3 Immune Signaling Crosstalk.Biochemistry research international · 2026Article
- Multimodal beneficial effects of BNN27, a nerve growth factor synthetic mimetic, in the 5xFAD mouse model of Alzheimer's disease.Molecular psychiatry · 2025Article
- Article
- Chronic basal forebrain activation improves spatial memory, boosts neurotrophin receptor expression, and lowers BACE1 and Aβ42 levels in the cerebral cortex in mice.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Review
- Review
- Live-Cell Imaging of Single Neurotrophin Receptor Molecules on Human Neurons in Alzheimer's Disease.International journal of molecular sciences · 2021Article
- In vivo functions of p75Trends in pharmacological sciences · 2021Review
- Risk Factors for Retinal Ganglion Cell Distress in Glaucoma and Neuroprotective Potential Intervention.International journal of molecular sciences · 2021Review
- Small molecule modulation of the p75 neurotrophin receptor suppresses age- and genotype-associated neurodegeneration in HIV gp120 transgenic mice.Experimental neurology · 2021Article
- proNGF Measurement in Cerebrospinal Fluid Samples of a Large Cohort of Living Patients With Alzheimer's Disease by a New Automated Immunoassay.Frontiers in aging neuroscience · 2021Article
- The Biology and Pathobiology of Glutamatergic, Cholinergic, and Dopaminergic Signaling in the Aging Brain.Frontiers in aging neuroscience · 2021Review
- Aging-relevant human basal forebrain cholinergic neurons as a cell model for Alzheimer's disease.Molecular neurodegeneration · 2020Article
- Article
- Exercise as a Positive Modulator of Brain Function.Molecular neurobiology · 2018Review
- The Cyanthin Diterpenoid and Sesterterpene Constituents of Hericium erinaceus Mycelium Ameliorate Alzheimer's Disease-Related Pathologies in APP/PS1 Transgenic Mice.International journal of molecular sciences · 2018Article
- ProNGF Drives Localized and Cell Selective Parvalbumin Interneuron and Perineuronal Net Depletion in the Dentate Gyrus of Transgenic Mice.Frontiers in molecular neuroscience · 2017Article
- NGF and proNGF Reciprocal Interference in Immunoassays: Open Questions, Criticalities, and Ways Forward.Frontiers in molecular neuroscience · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
NGF, the principal neurotrophic factor for basal forebrain cholinergic neurons (BFCNs), has been correlated to Alzheimer's disease (AD) because of the selective vulnerability of BFCNs in AD. These correlative links do not substantiate a comprehensive cause-effect mechanism connecting NGF deficit to overall AD neurodegeneration. A demonstration that neutralizing NGF activity could have consequences beyond a direct interference with the cholinergic system came from studies in the AD11 mouse model, in which the expression of a highly specific anti-NGF antibody determines a neurodegeneration that encompasses several features of human AD. Because the transgenic antibody binds to mature NGF much more strongly than to proNGF and prevents binding of mature NGF to the tropomyosin-related kinase A (TrkA) receptor and to p75 neurotrophin receptor (p75NTR), we postulated that neurodegeneration in AD11 mice is provoked by an imbalance of proNGF/NGF signaling and, consequently, of TrkA/p75NTR signaling. To test this hypothesis, in this study we characterize the phenotype of two lines of transgenic mice, one in which TrkA signaling is inhibited by neutralizing anti-TrkA antibodies and a second one in which anti-NGF mice were crossed to p75NTR(exonIII(-/-)) mice to abrogate p75NTR signaling. TrkA neutralization determines a strong cholinergic deficit and the appearance of beta-amyloid peptide (Abeta) but no tau-related pathology. In contrast, abrogating p75NTR signaling determines a full rescue of the cholinergic and Abeta phenotype of anti-NGF mice, but tau hyperphosphorylation is exacerbated. Thus, we demonstrate that inhibiting TrkA signaling activates Abeta accumulation and that different streams of AD neurodegeneration are related in complex ways to TrkA versus p75NTR signaling.
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