ArticleThe American journal of pathology2006
Pro-NGF from Alzheimer's disease and normal human brain displays distinctive abilities to induce processing and nuclear translocation of intracellular domain of p75NTR and apoptosis.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 78 citations in OpenAlex.
- The Nerve Growth Factor Receptor (NGFR/p75International journal of molecular sciences · 2023Review
- Age-induced nitrative stress decreases retrograde transport of proNGF via TrkA and increases proNGF retrograde transport and neurodegeneration via p75Frontiers in molecular neuroscience · 2023Article
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- Getting Into the Brain: The Intranasal Approach to Enhance the Delivery of Nerve Growth Factor and Its Painless Derivative in Alzheimer's Disease and Down Syndrome.Frontiers in neuroscience · 2022Article
- proNGF Involvement in the Adult Neurogenesis Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Review
- Peptides Derived from Growth Factors to Treat Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Neurotrophins as Key Regulators of Cell Metabolism: Implications for Cholesterol Homeostasis.International journal of molecular sciences · 2021Review
- The p75FEBS open bio · 2021Article
- Article
- Decoding the Role of CD271 in Melanoma.Cancers · 2020Review
- RIP at the Synapse and the Role of Intracellular Domains in Neurons.Neuromolecular medicine · 2020Review
- Nerve Growth Factor Pathobiology During the Progression of Alzheimer's Disease.Frontiers in neuroscience · 2019Review
- proBDNF is modified by advanced glycation end products in Alzheimer's disease and causes neuronal apoptosis by inducing p75 neurotrophin receptor processing.Molecular brain · 2018Article
- The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease.Aging and disease · 2015Review
- Resilience of precuneus neurotrophic signaling pathways despite amyloid pathology in prodromal Alzheimer's disease.Biological psychiatry · 2015Article
- Role of neurotrophic factor alterations in the neurodegenerative process in HIV associated neurocognitive disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014Review
- A role for the tyrosine kinase ACK1 in neurotrophin signaling and neuronal extension and branching.Cell death & disease · 2013Article
- A DR6/p75(NTR) complex is responsible for β-amyloid-induced cortical neuron death.Cell death & disease · 2013Article
- SILAC-based proteomic analysis to investigate the impact of amyloid precursor protein expression in neuronal-like B103 cells.Electrophoresis · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pro form of neurotrophic growth factor (pro-NGF), purified by chromatography from human Alzheimer's disease (AD)-affected brains (ADhbi-pro-NGF), has been shown to induce apoptotic cell death in neuronal cell cultures through its interaction with the p75 neurotrophin receptor (p75NTR). In the present work, we report that ADhbi-pro-NGF stimulates processing of p75NTR with alpha- and gamma-secretases, yielding a 20-kd intracellular domain (p75(ICD)) that translocates to the nucleus. This process was accompanied by delayed apoptosis. In AD, p75(ICD) was significantly increased in human entorhinal cortex. Although human frontal cortex has been described as showing a higher pro-NGF increase in AD, the increase in the entorhinal cortex paralleled p75NTR processing in its intracellular domain. In addition, pro-NGF isolated from AD-affected brains differed functionally from pro-NGF isolated from comparably aged control brains, with pro-NGF isolated from control brains being unstable and undergoing degradation to NGF when added to cell culture. As p75(ICD) and pro-NGF are both mediators of apoptosis and are both found in increased levels in the cerebral cortex in AD, the present data have implications for understanding neuronal degeneration in AD.
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