ReviewNeural regeneration research2018
Amyloid β and free heme: bloody new insights into the pathogenesis of Alzheimer's disease.
Review in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 37 citations in OpenAlex.
- The Role of Cytochrome P450 Holoenzyme Metabolism in the Origin of Neuropathologies.International journal of molecular sciences · 2026Review
- The ligand preference of LRP1 is regulated by O-glycans.Science advances · 2026Article
- How Sodium Dodecyl Sulfate Micelles Affect the Coordination and Peroxidase-Like Activity of the Hemin-Aβ16 Complex.ChemPlusChem · 2025Article
- Mechanism of action and therapeutic potential of S100A8/A9 in neuroinflammation and cognitive impairment: From molecular target to clinical application (Review).International journal of molecular medicine · 2025Review
- Pro-Oxidative and Inflammatory Actions of Extracellular Hemoglobin and Heme: Molecular Events and Implications for Alzheimer's and Parkinson Disease.Biomolecules & therapeutics · 2025Review
- Spatial transcriptomics reveals an unexpected impact of tau and tau pathology on the expression of transthyretin.Frontiers in aging neuroscience · 2025Article
- The Neural Palette of Heme: Altered Heme Homeostasis Underlies Defective Neurotransmission, Increased Oxidative Stress, and Disease Pathogenesis.Antioxidants (Basel, Switzerland) · 2024Review
- Biological Oxidations and Nitrations Promoted by the Hemin-AβAntioxidants (Basel, Switzerland) · 2023Article
- Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Review
- Tripterygium glycoside ameliorates neuroinflammation in a mouse model of Aβ25-35-induced Alzheimer's disease by inhibiting the phosphorylation of IκBα and p38.Bioengineered · 2021Article
- Extracellular protein components of amyloid plaques and their roles in Alzheimer's disease pathology.Molecular neurodegeneration · 2021Review
- An Analysis of the Multifaceted Roles of Heme in the Pathogenesis of Cancer and Related Diseases.Cancers · 2021Review
- Biomarkers of Alzheimer's disease in severe obstructive sleep apnea-hypopnea syndrome in the Chinese population.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2021Article
- Article
- Plasma transferrin and hemopexin are associated with altered Aβ uptake and cognitive decline in Alzheimer's disease pathology.Alzheimer's research & therapy · 2020Article
- Amyloid β chaperone - lipocalin-type prostaglandin D synthase acts as a peroxidase in the presence of heme.The Biochemical journal · 2020Article
- DNAzymes as Catalysts for l-Tyrosine and Amyloid β Oxidation.ACS omega · 2020Article
- Low Cerebrospinal Fluid Levels of Hemopexin Are Associated With Increased Alzheimer's Pathology, Hippocampal Hypometabolism, and Cognitive Decline.Frontiers in molecular biosciences · 2020Article
- Protective Effect of Buyang Huanwu Decoction on Neurovascular Unit in Alzheimer's Disease Cell Model via Inflammation and RAGE/LRP1 Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cerebral formation of Amyloid β (Aβ) is a critical pathological feature of Alzheimer's disease (AD). An accumulation of this peptide as senile plaques (SP) was already reported by Alois Alzheimer, the discoverer of the disease. Yet the exact contribution of Aβ to AD development remains elusive. Moreover, while extensive cerebral Aβ formation leads to fibril formation in many species, AD-like symptoms apparently depend on the highly conserved N-terminal residues R5, Y10 and H13. The amino acids were also shown to lead to the formation of Aβ-heme complexes, which exhibit peroxidase activity in the presence of H
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.