ReviewBiomedicines2021
Alzheimer's Disease: A Molecular View of β-Amyloid Induced Morbific Events.
Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Current Landscape of Glycogen Synthase Kinase-3β PET Tracers: Progress, Limitations, and Perspectives-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The Brown Algal Phlorotannin Dieckol Attenuates Amyloid-β Oligomer-Induced Oxidative DNA Damage and Senescence-like Stress in Human Neuron-like Cells.Marine drugs · 2026Article
- Computational Repurposing of Janus Kinase Inhibitors as Potential Therapeutic Candidates for Alzheimer's Disease.Medicina (Kaunas, Lithuania) · 2026Article
- Unmasking the hidden catalyst: How infections trigger Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- Tau Protein Aggregation Inhibitors-Therapeutic Strategy for Concurrent Tau and Amyloid Aggregation Inhibition.Biomedicines · 2026Review
- Induced Microglial-like Cells Derived from Familial and Sporadic Alzheimer's Disease Peripheral Blood Monocytes Show Abnormal Phagocytosis and Inflammatory Response to PSEN1 E280A Cholinergic-like Neurons.International journal of molecular sciences · 2025Article
- Structure and function of therapeutic antibodies approved by the US FDA in 2024.Antibody therapeutics · 2025Review
- Age-related p53 SUMOylation accelerates senescence and tau pathology in Alzheimer's disease.Cell death and differentiation · 2025Article
- IL-17 A Exacerbated Neuroinflammatory and Neurodegenerative Biomarkers in Intranasal Amyloid-Beta Model of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Role of PIM Kinase Inhibitor in the Treatment of Alzheimer's Disease.Molecular neurobiology · 2024Review
- Amyloid-Beta, Tau, and Microglial Activation in Aged Felid Brains.The Journal of comparative neurology · 2024Article
- Preconditioning of Mesenchymal Stem Cells Enhances the Neuroprotective Effects of Their Conditioned Medium in an Alzheimer's Disease In Vitro Model.Biomedicines · 2024Article
- Anthocyanin-Rich Fraction of Black Rice Bran Extract Protects against Amyloid β-Induced Oxidative Stress, Endoplasmic Reticulum Stress, and Neuronal Apoptosis in SK-N-SH Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Structure and function of therapeutic antibodies approved by the US FDA in 2023.Antibody therapeutics · 2024Review
- Emerging Evidence of Golgi Stress Signaling for Neuropathies.Neurology international · 2024Review
- Stem cell therapy in Alzheimer's disease: current status and perspectives.Frontiers in neuroscience · 2024Review
- Advancing Alzheimer's Therapeutics: Exploring the Impact of Physical Exercise in Animal Models and Patients.Cells · 2023Review
- Modulation of LPS-Induced Neurodegeneration by Intestinal Helminth Infection in Ageing Mice.International journal of molecular sciences · 2023Article
- Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach.Biomedicines · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Amyloid-β (Aβ) is a dynamic peptide of Alzheimer's disease (AD) which accelerates the disease progression. At the cell membrane and cell compartments, the amyloid precursor protein (APP) undergoes amyloidogenic cleavage by β- and γ-secretases and engenders the Aβ. In addition, externally produced Aβ gets inside the cells by receptors mediated internalization. An elevated amount of Aβ yields spontaneous aggregation which causes organelles impairment. Aβ stimulates the hyperphosphorylation of tau protein via acceleration by several kinases. Aβ travels to the mitochondria and interacts with its functional complexes, which impairs the mitochondrial function leading to the activation of apoptotic signaling cascade. Aβ disrupts the Ca
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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.