ArticleActa neuropathologica communications2014
In vivo imaging reveals sigmoidal growth kinetic of β-amyloid plaques.
Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 63 citations in OpenAlex.
- Amyloid-Induced Network Resilience and Collapse in Alzheimer's Disease: Insights From Computational Modeling.The European journal of neuroscience · 2026Article
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Particulate matter and co-occurring genetic risk induce oxidative stress and cardiac and brain Alzheimer's pathology.Communications biology · 2025Article
- Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer's disease model mice.Nature neuroscience · 2024Article
- APOE4 genotype and aging impair injury-induced microglial behavior in brain slices, including toward Aβ, through P2RY12.Molecular neurodegeneration · 2024Article
- Few-shot prediction of amyloid β accumulation from mainly unpaired data on biomarker candidates.NPJ systems biology and applications · 2023Article
- Role of the caspase-8/RIPK3 axis in Alzheimer's disease pathogenesis and Aβ-induced NLRP3 inflammasome activation.JCI insight · 2023Article
- Immune-mediated platelet depletion augments Alzheimer's disease neuropathological hallmarks in APP-PS1 mice.Aging · 2023Article
- Whole-brain microscopy reveals distinct temporal and spatial efficacy of anti-Aβ therapies.EMBO molecular medicine · 2023Article
- Experimental evidence for temporal uncoupling of brain Aβ deposition and neurodegenerative sequelae.Nature communications · 2022Article
- Potential for Ketotherapies as Amyloid-Regulating Treatment in Individuals at Risk for Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- The Prion-Like Spreading of Alpha-Synuclein in Parkinson's Disease: Update on Models and Hypotheses.International journal of molecular sciences · 2021Review
- Modeling the Inhibition Kinetics of Curcumin, Orange G, and Resveratrol with Amyloid-β Peptide.ACS omega · 2021Article
- Article
- High Glycemic Diet Is Related to Brain Amyloid Accumulation Over One Year in Preclinical Alzheimer's Disease.Frontiers in nutrition · 2021Article
- Microvessel occlusions alter amyloid-beta plaque morphology in a mouse model of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Staging Alzheimer's Disease in the Brain and Retina of B6.APP/PS1 Mice by Transcriptional Profiling.Journal of Alzheimer's disease : JAD · 2020Article
- Synaptic Loss in Alzheimer's Disease: Mechanistic Insights Provided by Two-PhotonFrontiers in cellular neuroscience · 2020Review
- Tau deletion reduces plaque-associated BACE1 accumulation and decelerates plaque formation in a mouse model of Alzheimer's disease.The EMBO journal · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major neuropathological hallmark of Alzheimer's disease is the deposition of amyloid plaques in the brains of affected individuals. Amyloid plaques mainly consist of fibrillar β-amyloid, which is a cleavage product of the amyloid precursor protein. The amyloid-cascade-hypothesis postulates Aβ accumulation as the central event in initiating a toxic cascade leading to Alzheimer's disease pathology and, ultimately, loss of cognitive function. We studied the kinetics of β-amyloid deposition in Tg2576 mice, which overexpress human amyloid precursor protein with the Swedish mutation. Utilizing long-term two-photon imaging we were able to observe the entire kinetics of plaque growth in vivo. Essentially, we observed that plaque growth follows a sigmoid-shaped curve comprising a cubic growth phase, followed by saturation. In contrast, plaque density kinetics exhibited an asymptotic progression. Taking into account the fact that a critical concentration of Aβ is required to seed new plaques, we can propose the following kinetic model of β-amyloid deposition in vivo. In the early cubic phase, plaque growth is not limited by Aβ concentration and plaque density increases very fast. During the transition phase, plaque density stabilizes whereas plaque volume increases strongly reflecting a robust growth of the plaques. In the late asymptotic phase, Aβ peptide production becomes rate-limiting for plaque growth. In conclusion, the present study offers a direct link between in vitro and in vivo studies facilitating the translation of Aβ-lowering strategies from laboratory models to patients.
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