ReviewMetabolic brain disease2020
Mechanisms of action of amyloid-beta and its precursor protein in neuronal cell death.
Review in Metabolic brain disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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
45 citing papers in PubMed, 75 citations in OpenAlex.
- Crosstalk between death-associated protein kinase 1-regulated mechanisms and dysfunctions in alzheimer's disease.Molecular biology reports · 2026Review
- Amyloid Beta Oligomers as Early Triggers of Neuronal Cytoskeleton Dysfunction in Alzheimer's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Gut microbiota-derived extracellular vesicles in Alzheimer's disease - Immunomodulatory mechanisms, biomarkers, and therapeutic opportunities: A review.Biomolecules & biomedicine · 2025Review
- Insights into Biomarkers of Alzheimer's Disease: From Core Markers to Emerging Directions.Aging and disease · 2025Review
- The potential link between the development of Alzheimer's disease and osteoporosis.Biogerontology · 2025Review
- Inhibition of Aβ Aggregation by Cholesterol-End-Modified PEG Vesicles and Micelles.Pharmaceutics · 2024Article
- Understanding the Molecular Impact of Physical Exercise on Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Multispectroscopic and computational insights into amyloid fibril formation of alpha lactalbumin induced by sodium hexametaphosphate.Scientific reports · 2024Article
- Phytoactive drugs used in the treatment of Alzheimer's disease and dementia.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Five percent CONeuroprotection (Chichester, England) · 2024Article
- BetaZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- The beneficial effects of vortioxetine on BDNF, CREB, S100B, β amyloid, and glutamate NR2b receptors in chronic unpredictable mild stress model of depression.Psychopharmacology · 2023Article
- Primary Hypothyroidism and Alzheimer's Disease: A Tale of Two.Cellular and molecular neurobiology · 2023Review
- Article
- Micromotion Derived Fluid Shear Stress Mediates Peri-Electrode Gliosis through Mechanosensitive Ion Channels.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Exploring the Role of Glycolytic Enzymes PFKFB3 and GAPDH in the Modulation of Aβ and Neurodegeneration and Their Potential of Therapeutic Targets in Alzheimer's Disease.Applied biochemistry and biotechnology · 2023Review
- Article
- Therapeutic Potential of Natural Compounds in Neurodegenerative Diseases: Insights from Clinical Trials.Pharmaceutics · 2023Review
- Controllable membrane damage by tunable peptide aggregation with albumin.AIChE journal. American Institute of Chemical Engineers · 2022Article
- Intranasally Co-administered Berberine and Curcumin Loaded in Transfersomal Vesicles Improved Inhibition of Amyloid Formation and BACE-1.ACS omega · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular senile plaques and intracellular neurofibrillary tangles are the neuropathological findings of the Alzheimer's disease (AD). Based on the amyloid cascade hypothesis, the main component of senile plaques, the amyloid-beta (Aβ) peptide, and its derivative called amyloid precursor protein (APP) both have been found to place their central roles in AD development for years. However, the recent therapeutics have yet to reverse or halt this disease. Previous evidence demonstrates that the accumulation of Aβ peptides and APP can exert neurotoxicity and ultimately neuronal cell death. Hence, we discuss the mechanisms of excessive production of Aβ peptides and APP serving as pathophysiologic stimuli for the initiation of various cell signalling pathways including apoptosis, necrosis, necroptosis and autophagy which lead to neuronal cell death. Conversely, the activation of such pathways could also result in the abnormal generation of APP and Aβ peptides. An elucidation of actions of APP and its metabolite, Aβ, could be vital in suggesting novel therapeutic opportunities.
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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.