ArticlePloS one2012
Interactions between amyloid-β and hemoglobin: implications for amyloid plaque formation in Alzheimer's disease.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 94 citations in OpenAlex.
- The role of neutrophils, red blood cells, and platelets in the pathology of Alzheimer's disease.Annals of medicine · 2025Review
- Amyloid β Peptide Modifies Membrane Architecture and Surface Electrostatic Properties of Human Red Blood Cells.International journal of molecular sciences · 2025Article
- Unraveling the Mystery of Hemoglobin in Hypoxia-Accelerated Neurodegenerative Diseases.Biomolecules · 2025Review
- Bidirectional relationship between anemia and cognitive function in middle-aged and older Chinese adults: a longitudinal study.Scientific reports · 2025Article
- Pro-Oxidative and Inflammatory Actions of Extracellular Hemoglobin and Heme: Molecular Events and Implications for Alzheimer's and Parkinson Disease.Biomolecules & therapeutics · 2025Review
- Fokker-Planck diffusion maps of microglial transcriptomes reveal radial differentiation into substates associated with Alzheimer's pathology.Communications biology · 2025Article
- Reevaluating the role of amyloidFrontiers in neurology · 2025Review
- LOU/c/jall rat as a model of resilience in the context of streptozotocin-induced cognitive impairment.Frontiers in aging neuroscience · 2025Article
- Key Proteins in Rat Cerebral Cortex: Application ofMolecules (Basel, Switzerland) · 2024Article
- A Triple Mystery of Insidious Organ Failure: Are the Lung, Kidney and Brain All Damaged by the Ageing Pulse?Biomedicines · 2024Review
- Iron Overload in Brain: Transport Mismatches, Microbleeding Events, and How Nanochelating Therapies May Counteract Their Effects.International journal of molecular sciences · 2024Review
- MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer's disease.Science (New York, N.Y.) · 2023Article
- Twelve protections evolved for the brain, and their roles in extending its functional life.Frontiers in neuroanatomy · 2023Review
- Iron Deposition in Brain: Does Aging Matter?International journal of molecular sciences · 2022Review
- Physiological and Pathological Functions of Neuronal Hemoglobin: A Key Underappreciated Protein in Parkinson's Disease.International journal of molecular sciences · 2022Review
- Proteomic Profiling of Cerebrum Mitochondria, Myelin Sheath, and Synaptosome Revealed Mitochondrial Damage and Synaptic Impairments in Association with 3 × Tg-AD Mice Model.Cellular and molecular neurobiology · 2022Article
- Article
- Extracellular protein components of amyloid plaques and their roles in Alzheimer's disease pathology.Molecular neurodegeneration · 2021Review
- Age, sex, and cerebral microbleeds in EFAD Alzheimer disease mice.Neurobiology of aging · 2021Article
- Interplay between stress-related genes may influence Alzheimer's disease development: The results of genetic interaction analyses of human data.Mechanisms of ageing and development · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of amyloid-β (Aβ) peptides in the brain is one of the central pathogenic events in Alzheimer's disease (AD). However, why and how Aβ aggregates within the brain of AD patients remains elusive. Previously, we demonstrated hemoglobin (Hb) binds to Aβ and co-localizes with the plaque and vascular amyloid deposits in post-mortem AD brains. In this study, we further characterize the interactions between Hb and Aβ in vitro and in vivo and report the following observations: 1) the binding of Hb to Aβ required iron-containing heme; 2) other heme-containing proteins, such as myoglobin and cytochrome C, also bound to Aβ; 3) hemin-induced cytotoxicity was reduced in neuroblastoma cells by low levels of Aβ; 4) Hb was detected in neurons and glial cells of post-mortem AD brains and was up-regulated in aging and APP/PS1 transgenic mice; 5) microinjection of human Hb into the dorsal hippocampi of the APP/PS1 transgenic mice induced the formation of an envelope-like structure composed of Aβ surrounding the Hb droplets. Our results reveal an enhanced endogenous expression of Hb in aging brain cells, probably serving as a compensatory mechanism against hypoxia. In addition, Aβ binds to Hb and other hemoproteins via the iron-containing heme moiety, thereby reducing Hb/heme/iron-induced cytotoxicity. As some of the brain Hb could be derived from the peripheral circulation due to a compromised blood-brain barrier frequently observed in aged and AD brains, our work also suggests the genesis of some plaques may be a consequence of sustained amyloid accretion at sites of vascular injury.
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.