ReviewFrontiers in neuroscience2019
The Brain NGF Metabolic Pathway in Health and in Alzheimer's Pathology.
Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 100 citations in OpenAlex.
- Stem cells and derived growth factors in Alzheimer's disease: mechanistic insights and translational perspectives.Inflammopharmacology · 2026Review
- Co-pathologies and biological processes beyond amyloid-beta and tau in people with Alzheimer's disease: Evidence from clinical cohort studies.Journal of internal medicine · 2026Review
- Taming the "death receptor": translating the first-in-class p75Journal of translational medicine · 2026Review
- A time-resolved RNA-sequencing dataset of transcriptional responses in PC12 cells to NGF withdrawal and replenishment.Data in brief · 2026Article
- Article
- 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
- Nerve growth factor responsive elements modulate immune cell inflammation and are dysregulated in an Alzheimer's disease mouse model.Frontiers in immunology · 2026Article
- Targeting autophagy and programmed cell death in neurological diseases via probiotic intervention.Gut pathogens · 2025Review
- Cholinergic system in patients with chronic kidney disease: cognitive and renal implications.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia.iScience · 2025Article
- Review
- Identification of novel benzothiazole-thiadiazole-based thiazolidinone derivative:Future medicinal chemistry · 2024Article
- The Use of Neurotrophic Factors as a Promising Strategy for the Treatment of Neurodegenerative Diseases (Review).Bulletin of experimental biology and medicine · 2024Review
- Innovation at the Intersection: Emerging Translational Research in Neurology and Psychiatry.Cells · 2024Article
- Article
- Nerve Growth Factor and the Role of Inflammation in Tumor Development.Current issues in molecular biology · 2024Review
- Neurotrophin growth factors and their receptors as promising blood biomarkers for Alzheimer's Disease: a gene expression analysis study.Molecular biology reports · 2024Article
- Cognitive Alterations in Addictive Disorders: A Translational Approach.Biomedicines · 2023Review
- Profiling the autoantibody repertoire reveals autoantibodies associated with mild cognitive impairment and dementia.Frontiers in neurology · 2023Article
- Reduced levels of NGF shift astrocytes toward a neurotoxic phenotype.Frontiers in cell and developmental biology · 2023Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Emerging research has re-emphasized the role of the cortical cholinergic system in the symptomology and progression of Alzheimer's disease (AD). Basal forebrain (BF) cholinergic nuclei depend on target-derived NGF for survival during development and for the maintenance of a classical cholinergic phenotype during adulthood. In AD, BF cholinergic neurons lose their cholinergic phenotype and function, suggesting an impairment in NGF-mediated trophic support. We propose that alterations to the enzymatic pathway that controls the maturation of proNGF to mature NGF and the latter's ulterior degradation underlie this pathological process. Indeed, the NGF metabolic pathway has been demonstrated to be impaired in AD and other amyloid pathologies, and pharmacological manipulation of NGF metabolism has consequences
Indexed as
Identifiers
What OpenQuestion holds
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.