ReviewMolecules (Basel, Switzerland)2020
The Positive Side of the Alzheimer's Disease Amyloid Cross-Interactions: The Case of the Aβ 1-42 Peptide with Tau, TTR, CysC, and ApoA1.
Review in Molecules (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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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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
37 citing papers in PubMed, 65 citations in OpenAlex.
- Serum cystatin C levels are independently correlated with cognitive impairment in individuals with cerebral small vessel disease.Frontiers in neuroscience · 2026Article
- Alterations of Apolipoprotein A1, E, and J Genes in the Frontal Cortex in an Ischemic Model of Alzheimer's Disease with 2-Year Survival.International journal of molecular sciences · 2025Article
- Synthetic chaperone based on Hsp90-Tau interaction inhibits Tau aggregation and rescues physiological Tau-Microtubule interaction.Nature communications · 2025Article
- Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025Review
- Developing non-invasive molecular markers for early risk assessment of Alzheimer's disease.Biomarkers in neuropsychiatry · 2025Article
- Lipidopathy disrupts peripheral and central amyloid clearance in Alzheimer's disease: Where are our knowledge.IBRO neuroscience reports · 2025Review
- The Role of APOA-I in Alzheimer's Disease: Bridging Peripheral Tissues and the Central Nervous System.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Transthyretin as a therapeutic target: the future of disease-modifying therapies for Alzheimer's disease.Molecular biology reports · 2025Review
- HDL-Apolipoprotein in Alzheimer's Disease Revisited: From Periphery to CNS.Aging medicine (Milton (N.S.W)) · 2025Review
- Extracellular PHF-tau modulates astrocyte mitochondrial dynamics and mediates neuronal connectivity.Translational neurodegeneration · 2025Article
- Molecular Simulation of the Binding of Amyloid Beta to Apolipoprotein A-I in High-Density Lipoproteins.International journal of molecular sciences · 2025Article
- Spatial transcriptomics reveals an unexpected impact of tau and tau pathology on the expression of transthyretin.Frontiers in aging neuroscience · 2025Article
- Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies.Signal transduction and targeted therapy · 2024Review
- New Hybrid Compounds Incorporating Natural Products as Multifunctional Agents against Alzheimer's Disease.Pharmaceutics · 2023Article
- Pomegranate: A Source of Multifunctional Bioactive Compounds Potentially Beneficial in Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Article
- Aggregation Limiting Cell-Penetrating Peptides Derived from Protein Signal Sequences.International journal of molecular sciences · 2023Article
- Proteostasis and neurodegeneration: a closer look at autophagy in Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Aβ and Tau Interact with Metal Ions, Lipid Membranes and Peptide-Based Amyloid Inhibitors: Are These Common Features Relevant in Alzheimer's Disease?Molecules (Basel, Switzerland) · 2022Review
- Potential neuroprotection byNeural regeneration research · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) represents a progressive amyloidogenic disorder whose advancement is widely recognized to be connected to amyloid-β peptides and Tau aggregation. However, several other processes likely contribute to the development of AD and some of them might be related to protein-protein interactions. Amyloid aggregates usually contain not only single type of amyloid protein, but also other type of proteins and this phenomenon can be rationally explained by the process of protein cross-seeding and co-assembly. Amyloid cross-interaction is ubiquitous in amyloid fibril formation and so a better knowledge of the amyloid interactome could help to further understand the mechanisms of amyloid related diseases. In this review, we discuss about the cross-interactions of amyloid-β peptides, and in particular Aβ1-42, with other amyloids, which have been presented either as integrated part of Aβ neurotoxicity process (such as Tau) or conversely with a preventive role in AD pathogenesis by directly binding to Aβ (such as transthyretin, cystatin C and apolipoprotein A1). Particularly, we will focus on all the possible therapeutic strategies aiming to rescue the Aβ toxicity by taking inspiration from these protein-protein interactions.
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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.