ReviewNeurotoxicity research2020
β-Amyloid Peptide: the Cell Compartment Multi-faceted Interaction in Alzheimer's Disease.
Review in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 48 citations in OpenAlex.
- Lysosomal protease-mediated APP degradation is pH-dependent, mutation-sensitive, and facilitates tau proteolysis.Molecular neurodegeneration advances · 2026Article
- Phosphatidate phosphatase Lipin1 alters mitochondria-associated endoplasmic reticulum membranes (MAMs) homeostasis: effects which contribute to the development of diabetic encephalopathy.Journal of neuroinflammation · 2025Article
- Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.Cellular and molecular neurobiology · 2024Review
- Updates on Aβ Processing by Hsp90, BRICHOS, and Newly Reported Distinctive Chaperones.Biomolecules · 2023Review
- Dendrimers and Derivatives as Multifunctional Nanotherapeutics for Alzheimer's Disease.Pharmaceutics · 2023Review
- Metabolomic Footprint of Disrupted Energetics and Amino Acid Metabolism in Neurodegenerative Diseases: Perspectives for Early Diagnosis and Monitoring of Therapy.Metabolites · 2023Review
- Flow Synthesis of Nature-Inspired Mitochondria-Targeted Phenolic Derivatives as Potential Neuroprotective Agents.Antioxidants (Basel, Switzerland) · 2022Article
- Nanobiotechnology: A New Frontier for Brain Disorders.International journal of molecular sciences · 2022Article
- Epidermal Growth Factor Receptor Kinase Inhibitor Ameliorates β-Amyloid Oligomer-Induced Alzheimer Disease in Swiss Albino Mice.Molecules (Basel, Switzerland) · 2022Article
- Review
- Hibiscus, Rooibos, and Yerba Mate for Healthy Aging: A Review on the Attenuation of In Vitro and In Vivo Markers Related to Oxidative Stress, Glycoxidation, and Neurodegeneration.Foods (Basel, Switzerland) · 2022Review
- Tricyclodecan-9-yl-Xanthogenate (D609): Mechanism of Action and Pharmacological Applications.International journal of molecular sciences · 2022Review
- Promising Treatment for Multiple Sclerosis: Mitochondrial Transplantation.International journal of molecular sciences · 2022Review
- Regulation of Neurodegeneration-associated Protein Fragments by the N-degron Pathways.Neurotoxicity research · 2022Review
- Protective, Antioxidant and Antiproliferative Activity of Grapefruit IntegroPectin on SH-SY5Y Cells.International journal of molecular sciences · 2021Article
- Adlay hull extracts attenuate β-amyloid-induced neurotoxicity and oxidative stress in PC12 cells through antioxidative, anti-inflammatory, and antiapoptotic activities.Biochemistry and biophysics reports · 2021Article
- Interactions of Amyloid-β with Membrane Proteins.International journal of molecular sciences · 2021Review
- Phytochemical Analysis and Evaluation of Biological Activity ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Adiponectin Role in Neurodegenerative Diseases: Focus on Nutrition Review.International journal of molecular sciences · 2020Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most widespread form of dementia, characterized by memory loss and reduction of cognitive functions that strongly interfere with normal daily life. Numerous evidences show that aggregates of the amyloid beta peptide, formed by 39 to 42 amino acid residues (Aβ39-43), from soluble small oligomers to large fibrils are characteristic markers of this pathology. However, AD is a complex disease and its neurodegenerative molecular mechanism is not yet fully understood. Growing evidence suggests a link between Aβ polymorphic nature, oligomers and fibrils, and specific mechanisms of neurodegeneration. The Aβ variable nature and its multiplicity of interactions with different proteins and organelles reflect the complexity of this pathology. In this review, we analyze the effects of the interaction between Aβ peptide and different cellular compartments in relation to the different kinds and sizes of amyloid aggregates. In particular, Aβ interaction with different cell structures such as the plasma membrane, mitochondria, lysosomes, nucleus, and endoplasmic reticulum is discussed. Further, we analyze the Aβ peptide ability to modify the structure and function of the target organelle, inducing alteration of its physiological role thus contributing to the pathological event. Dysfunction of cellular components terminating with the activation of the cellular death mechanism and subsequent neurodegeneration is also taken into consideration.
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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.