ArticleActa neuropathologica2013
Clustering of plaques contributes to plaque growth in a mouse model of Alzheimer's disease.
Article in Acta neuropathologica, 2013. 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.
- Meningeal vascular Aβ deposition associates with cerebral hypoperfusion and compensatory collateral remodeling.Alzheimer's research & therapy · 2025Article
- ProSAAS is preferentially up-regulated during homeostatic scaling and reduces amyloid plaque burden in the 5xFAD mouse hippocampus.Journal of neurochemistry · 2024Article
- ProSAAS is Preferentially Secreted from Neurons During Homeostatic Scaling and Reduces Amyloid Plaque Size in the 5xFAD Mouse Hippocampus.bioRxiv : the preprint server for biology · 2024Article
- The Role of the JAK/STAT Signaling Pathway in the Pathogenesis of Alzheimer's Disease: New Potential Treatment Target.International journal of molecular sciences · 2023Review
- Isoflurane has no effect on cognitive or behavioral performance in a mouse model of early-stage Alzheimer's disease.Frontiers in neuroscience · 2022Article
- Long-term dynamics of aberrant neuronal activity in awake Alzheimer's disease transgenic mice.Communications biology · 2021Article
- Neurotoxicity of different amyloid beta subspecies in mice and their interaction with isoflurane anaesthesia.PloS one · 2020Article
- Tau deletion reduces plaque-associated BACE1 accumulation and decelerates plaque formation in a mouse model of Alzheimer's disease.The EMBO journal · 2019Article
- Imbalance in the response of pre- and post-synaptic components to amyloidopathy.Scientific reports · 2019Article
- The association between hypertensive arteriopathy and cerebral amyloid angiopathy in spontaneously hypertensive stroke-prone rats.Brain pathology (Zurich, Switzerland) · 2018Article
- Microglial priming in Alzheimer's disease.Annals of translational medicine · 2018Review
- BACE1 inhibition more effectively suppresses initiation than progression of β-amyloid pathology.Acta neuropathologica · 2018Article
- The Cyanthin Diterpenoid and Sesterterpene Constituents of Hericium erinaceus Mycelium Ameliorate Alzheimer's Disease-Related Pathologies in APP/PS1 Transgenic Mice.International journal of molecular sciences · 2018Article
- Novel botanical drug DA-9803 prevents deficits in Alzheimer's mouse models.Alzheimer's research & therapy · 2018Article
- The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer's Disease.Frontiers in cellular neuroscience · 2018Review
- Close Correlation of Monoamine Oxidase Activity with Progress of Alzheimer's Disease in Mice, Observed byACS central science · 2016Article
- Defining the earliest pathological changes of Alzheimer's disease.Current Alzheimer research · 2016Review
- Inhibition of amyloid-β plaque formation by α-synuclein.Nature medicine · 2015Article
- Microglia as a critical player in both developmental and late-life CNS pathologies.Acta neuropathologica · 2014Review
- Early-onset formation of parenchymal plaque amyloid abrogates cerebral microvascular amyloid accumulation in transgenic mice.The Journal of biological chemistry · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Amyloid-β (Aβ) plaque deposition plays a central role in the pathogenesis of Alzheimer's disease (AD). Post-mortem analysis of plaque development in mouse models of AD revealed that plaques are initially small, but then increase in size and become more numerous with age. There is evidence that plaques can grow uniformly over time; however, a complementary hypothesis of plaque development is that small plaques cluster and grow together thereby forming larger plaques. To investigate the latter hypothesis, we studied plaque formation in APPPS1 mice using in vivo two-photon microscopy and immunohistochemical analysis. We used sequential pre- and post-mortem staining techniques to label plaques at different stages of development and to detect newly emerged plaques. Post-mortem analysis revealed that a subset (22 %) of newly formed plaques appeared very close (<40 μm) to pre-existing plaques and that many close plaques (25 %) that were initially separate merged over time to form one single large plaque. Our results suggest that small plaques can cluster together, thus forming larger plaques as a complementary mechanism to simple uniform plaque growth from a single initial plaque. This study deepens our understanding of Aβ deposition and demonstrates that there are multiple mechanisms at play in plaque development.
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.