ReviewNeural regeneration research2019
Physiological and pathological effects of amyloid-β species in neural stem cell biology.
Review in Neural regeneration research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 33 citations in OpenAlex.
- Growth hormone-releasing hormone attenuates amyloid deposition and neuroinflammation in Alzheimer's disease models.Cell death & disease · 2026Article
- The 2024 NIA-AA biological definition of Alzheimer's disease: linking biomarkers to clinical practice.Frontiers in dementia · 2026Review
- Preexisting Genetic Background Primes the Responses of Human Neurons to Amyloid β.International journal of molecular sciences · 2025Article
- Potential use of iPSCs for disease modeling, drug screening, and cell-based therapy for Alzheimer's disease.Cellular & molecular biology letters · 2023Review
- Amyloid-β: A potential mediator of aging-related vascular pathologies.Vascular pharmacology · 2023Review
- The Role of cAMP-Dependent Intracellular Signaling Pathways in the Regulation of the Functions of Neural Stem Cells and Neuroglial Cells in Amyloid-β-Induced Neurodegeneration.Bulletin of experimental biology and medicine · 2023Article
- Molecular Insights into Cell Type-specific Roles in Alzheimer's Disease: Human Induced Pluripotent Stem Cell-based Disease Modelling.Neuroscience · 2023Review
- The Roles of the Amyloid Beta Monomers in Physiological and Pathological Conditions.Biomedicines · 2023Review
- Cellular response to β-amyloid neurotoxicity in Alzheimer's disease and implications in new therapeutics.Animal models and experimental medicine · 2023Review
- The Role of JAKs and STAT3 in Regulation of Regenerative-Competent Cells of the Nervous Tissue in β-Amyloid-Induced Neurodegeneration.Bulletin of experimental biology and medicine · 2022Article
- Article
- Impact of Two Neuronal Sigma-1 Receptor Modulators, PRE084 and DMT, on Neurogenesis and Neuroinflammation in an AβInternational journal of molecular sciences · 2022Article
- Inhibition of Amyloid β-Induced Lipid Membrane Permeation and Amyloid β Aggregation by K162.ACS chemical neuroscience · 2021Article
- A Review of Techniques for Biodelivery of Nerve Growth Factor (NGF) to the Brain in Relation to Alzheimer's Disease.Advances in experimental medicine and biology · 2021Review
- Using NMR spectroscopy to investigate the role played by copper in prion diseases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020Review
- Aggregation of biologically important peptides and proteins: inhibition or acceleration depending on protein and metal ion concentrations.RSC advances · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although amyloid-β peptide is considered neurotoxic, it may mediate several physiological processes during embryonic development and in the adult brain. The pathological function of amyloid-β peptide has been extensively studied due to its implication in Alzheimer's disease, but its physiological function remains poorly understood. Amyloid-β peptide can be detected in non-aggregated (monomeric) and aggregated (oligomeric and fibrillary) forms. Each form has different cytotoxic and/or physiological properties, so amyloid-β peptide and its role in Alzheimer's disease need to be studied further. Neural stem cells and neural precursor cells are good tools for the study on neurodegenerative diseases and can provide future therapeutic applications in diseases such as Alzheimer's disease. In this review, we provide an outline of the effects of amyloid-β peptide, in monomeric and aggregated forms, on the biology of neural stem cells/neural precursor cells, and discuss the controversies. We also describe the possible molecular targets that could be implicated in these effects, especially GSK3β. A better understanding of amyloid-β peptide (both physiological and pathological), and the signaling pathways involved are essential to advance the field of Alzheimer's disease.
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.