ArticleFrontiers in aging neuroscience2013
β-Amyloid oligomers in aging and Alzheimer's disease.
Article in Frontiers in aging neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses that pooled it.
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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
33 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Insights into Pharmacological Activities of Nicotine and 6-Hydroxy-L-nicotine, a Bacterial Nicotine Derivative: A Systematic Review.Biomolecules · 2023Pooled it
- The Amyloid-β Pathway in Alzheimer's Disease.Molecular psychiatry · 2021Pooled it
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- Chronic administration of XBD173 ameliorates cognitive deficits and neuropathology via 18 kDa translocator protein (TSPO) in a mouse model of Alzheimer's disease.Translational psychiatry · 2023Article
- Aβ and Tau Prions Causing Alzheimer's Disease.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Aβ and tau prions feature in the neuropathogenesis of Down syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Chronic oral administration of adipoRon reverses cognitive impairments and ameliorates neuropathology in an Alzheimer's disease mouse model.Molecular psychiatry · 2021Article
- Rhein Relieves Oxidative Stress in an AβFrontiers in pharmacology · 2021Article
- Neuropathological and Biomarker Findings in Parkinson's Disease and Alzheimer's Disease: From Protein Aggregates to Synaptic Dysfunction.Journal of Parkinson's disease · 2021Review
- α-Sheet secondary structure in amyloid β-peptide drives aggregation and toxicity in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Plasma amyloid-β levels, cerebral atrophy and risk of dementia: a population-based study.Alzheimer's research & therapy · 2018Article
- PPAR Gamma Coactivator 1 Beta (PGC-1β) Reduces Mammalian Target of Rapamycin (mTOR) Expression via a SIRT1-Dependent Mechanism in Neurons.Cellular and molecular neurobiology · 2017Article
- YXQN Reduces Alzheimer's Disease-Like Pathology and Cognitive Decline in APPswePS1dE9 Transgenic Mice.Frontiers in aging neuroscience · 2017Article
- A Novel Aβ B-Cell Epitope Vaccine (rCV01) for Alzheimer's Disease Improved Synaptic and Cognitive Functions in 3 × Tg-AD Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016Article
- Prophylactic immunotherapy of Alzheimer's disease using recombinant amyloid-β B-cell epitope chimeric protein as subunit vaccine.Human vaccines & immunotherapeutics · 2016Article
- Overcoming translational barriers impeding development of Alzheimer's disease modifying therapies.Journal of neurochemistry · 2016Review
- A novel recombinant 6Aβ15-THc-C chimeric vaccine (rCV02) mitigates Alzheimer's disease-like pathology, cognitive decline and synaptic loss in aged 3 × Tg-AD mice.Scientific reports · 2016Article
- Toward more predictive genetic mouse models of Alzheimer's disease.Brain research bulletin · 2016Review
- The Role of Amyloid-β Oligomers in Toxicity, Propagation, and Immunotherapy.EBioMedicine · 2016Review
- Mesenchymal Stem Cells Preserve Working Memory in the 3xTg-AD Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2016Article
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2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a fatal neurodegenerative disorder, and the most common cause of dementia in the elderly. The cause of AD is not known, but genetic evidence strongly supports the hypothesis that pathological aggregation of the β-amyloid protein (Aβ) triggers the disease process. AD has a long preclinical phase, lasting a decade or more. It is during this preclinical phase, before the irreversible neuron loss that characterizes the dementia phase of the disease, that therapies are most likely to be effective. If we are to block AD during the preclinical phase, we must identify the Aβ species that are present before there are overt symptoms and that are associated with downstream markers of pathology. A specific soluble Aβ assembly, the putative dodecamer "Aβ*56," is present in the brains and cerebrospinal fluid of cognitively intact individuals and correlates with markers of synaptic dysfunction and neuronal injury. This assembly also correlates with memory dysfunction in multiple lines of transgenic mice that model the preclinical phase of AD. We suggest that Aβ*56 has a critical role during the earliest phase of AD and might serve as a molecular trigger of the disease.
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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.