ArticleJournal of neuropathology and experimental neurology2012
Hippocampal proNGF signaling pathways and β-amyloid levels in mild cognitive impairment and Alzheimer disease.
Article in Journal of neuropathology and experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.
- Finding memo: versatile interactions of the VPS10p-Domain receptors in Alzheimer's disease.Molecular neurodegeneration · 2022Pooled it
- Postmortem Brain, Cerebrospinal Fluid, and Blood Neurotrophic Factor Levels in Alzheimer's Disease: A Systematic Review and Meta-Analysis.Journal of molecular neuroscience : MN · 2018Pooled it
- The Intricate Relationship of Trk Receptors in Brain Diseases and Disorders.Molecular neurobiology · 2025Review
- Spliceosome protein alterations differentiate hubs of the default mode connectome during the progression of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2025Article
- Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia.iScience · 2025Article
- U1-70K and U1A and tau pathogenesis in demented and non-demented individuals with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Oligomeric, phosphorylated, and truncated tau and spliceosome pathology within the entorhinal-hippocampal connectome across stages of Alzheimer's disease.The Journal of comparative neurology · 2023Article
- Therapeutic Candidates for Alzheimer's Disease: Saponins.International journal of molecular sciences · 2023Review
- Hericerin derivatives activates a pan-neurotrophic pathway in central hippocampal neurons converging to ERK1/2 signaling enhancing spatial memory.Journal of neurochemistry · 2023Article
- Vesicular Glutamate Transporter Changes in the Cortical Default Mode Network During the Clinical and Pathological Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- Differential Effects of Toll-Like Receptor Activation and Differential Mediation by MAP Kinases of Immune Responses in Microglial Cells.Cellular and molecular neurobiology · 2022Article
- The emerging role of furin in neurodegenerative and neuropsychiatric diseases.Translational neurodegeneration · 2022Review
- Selective neurodegeneration of the hippocampus caused by chronic cerebral hypoperfusion: F-18 FDG PET study in rats.PloS one · 2022Article
- The Nerve Growth Factor Metabolic Pathway Dysregulation as Cause of Alzheimer's Cholinergic Atrophy.Cells · 2021Review
- Comparative neuropathology in aging primates: A perspective.American journal of primatology · 2021Review
- Peptides Derived from Growth Factors to Treat Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Nerve Growth Factor Compromise in Down Syndrome.Frontiers in aging neuroscience · 2021Review
- Small molecule modulation of the p75 neurotrophin receptor inhibits multiple amyloid beta-induced tau pathologies.Scientific reports · 2020Article
- Relationships between Mitochondrial Dysfunction and Neurotransmission Failure in Alzheimer's Disease.Aging and disease · 2020Review
- Frontal cortex chitinase and pentraxin neuroinflammatory alterations during the progression of Alzheimer's disease.Journal of neuroinflammation · 2020Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
Abstract
Hippocampal precursor of nerve growth factor (proNGF)/NGF signaling occurs in conjunction with β-amyloid (Aβ) accumulations in Alzheimer disease (AD). To assess the involvement of this pathway in AD progression, we quantified these proteins and their downstream pathway activators in postmortem tissues from the brains of subjects with no cognitive impairment (NCI), mild cognitive impairment (MCI), and AD using immunoblotting and ELISA. Hippocampal proNGF was significantly greater in AD cases compared with those in NCI and MCI cases. TrkA was significantly reduced in MCI compared with those in NCI and AD, whereas p75 neurotrophin receptor, sortilin, and neurotrophin receptor homolog 2 remained stable. Akt decreased from NCI to MCI to AD, whereas phospho-Akt and phospho-Akt-to-Akt ratio were elevated in AD compared with those in MCI and NCI. No differences were found in phospho-Erk, Erk, or their ratio across groups. Although c-jun kinase (JNK) remained stable across groups, phospho-JNK and the phospho-JNK-to-JNK ratio increased significantly in AD compared with those in NCI and MCI. Expression levels of Aβ(1-40), Aβ(1-42), and Aβ(40/42) ratio were stable. Statistical analysis revealed a strong positive correlation between proNGF and phospho-JNK, although only proNGF was negatively correlated with cognitive function and only TrkA was negatively associated with pathologic criteria. These findings suggest that alterations in the hippocampal NGF signaling pathway in MCI and AD favor proNGF-mediated proapoptotic pathways, and that this is independent of Aβ accumulation during AD progression.
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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.