ReviewMolecular neurobiology2012
Nerve growth factor and Alzheimer's disease: new facts for an old hypothesis.
Review in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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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.
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Who cites it
54 citing papers in PubMed.
- From the Scientific Underground to the Height of Recognition: The 40th Anniversary of Rita Levi-Montalcini's Nobel Prize and the Promising Horizon in Psychiatry.Neurochemical research · 2026Article
- Decoding the Role of Neurotrophins in Glycogen Synthase Kinase 3-Beta Regulation in Alzheimer's Disease.Molecular neurobiology · 2025Review
- Alzheimer's Disease and Frontotemporal Dementia: A Review of Pathophysiology and Therapeutic Approaches.Journal of neuroscience research · 2025Review
- New BDNF and NT-3 Cyclic Mimetics Concur with Copper to Activate Trophic Signaling Pathways as Potential Molecular Entities to Protect Old Brains from Neurodegeneration.Biomolecules · 2024Article
- Reversal of neurological deficits by painless nerve growth factor in a mouse model of Rett syndrome.Brain : a journal of neurology · 2024Article
- Fraction ofThe journal of venomous animals and toxins including tropical diseases · 2024Article
- The Drosophila homolog of APP promotes Dscam expression to drive axon terminal growth, revealing interaction between Down syndrome genes.Disease models & mechanisms · 2023Article
- New perspectives on the basal forebrain cholinergic system in Alzheimer's disease.Neuroscience and biobehavioral reviews · 2023Review
- Analysis of β-nerve growth factor and its precursor during human pregnancy by immunoaffinity-liquid chromatography tandem mass spectrometry.Scientific reports · 2023Article
- Direct Enhancement Effect of Hippocampal Cholinergic Neurostimulating Peptide on Cholinergic Activity in the Hippocampus.International journal of molecular sciences · 2023Article
- Enhanced TrkA signaling impairs basal forebrain-dependent behavior.Frontiers in molecular neuroscience · 2023Article
- Neurotrophic Factors in Health and Disease.Cells · 2022Article
- Review
- TrkA-cholinergic signaling modulates fear encoding and extinction learning in PTSD-like behavior.Translational psychiatry · 2022Article
- Peripheral Pathways to Neurovascular Unit Dysfunction, Cognitive Impairment, and Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- 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
- Pharmacokinetic Modelling of Human Recombinant Protein, p75ECD-Fc: A Novel Therapeutic Approach for Treatment of Alzheimer's Disease, in Serum and Tissue of Sprague Dawley Rats.European journal of drug metabolism and pharmacokinetics · 2021Article
- Nerve Growth Factor-Based Therapy in Alzheimer's Disease and Age-Related Macular Degeneration.Frontiers in neuroscience · 2021Review
- Anti-Neurodegenerative Benefits of Acetylcholinesterase Inhibitors in Alzheimer's Disease: Nexus of Cholinergic and Nerve Growth Factor Dysfunction.Current Alzheimer research · 2021Review
- Microcontact Printing of Cholinergic Neurons in Organotypic Brain Slices.Frontiers in neurology · 2021Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding sporadic Alzheimer's disease (AD) onset and progression requires an explanation of what triggers the common core of abnormal processing of the amyloid precursor protein and tau processing. In the quest for upstream drivers of sporadic, late-onset AD neurodegeneration, nerve growth factor (NGF) has a central role. Initially connected to AD on a purely correlative basis, because of its neurotrophic actions on basal forebrain cholinergic neurons, two independent lines of research, reviewed in this article, place alterations of NGF processing and signaling at the center stage of a new mechanism, leading to the activation of amyloidogenesis and tau processing. Thus, experimental studies on NGF deficit induced neurodegeneration in transgenic mice, as well as the mechanistic studies on the anti-amyloidogenic actions of NGF/TrkA signaling in primary neuronal cultures demonstrated a novel causal link between neurotrophic signaling deficits and Alzheimer's neurodegeneration. Around these results, a new NGF hypothesis can be built, with neurotrophic deficits of various types representing an upstream driver of the core AD triad pathology. According to the new NGF hypothesis for AD, therapies aimed at reestablishing a correct homeostatic balance between ligands (and receptors) of the NGF pathway appear to have a clear and strong rationale, not just as long-term cholinergic neuroprotection, but also as a truly disease-modifying approach.
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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.