ArticleNature medicine2014
Longitudinal PET-MRI reveals β-amyloid deposition and rCBF dynamics and connects vascular amyloidosis to quantitative loss of perfusion.
Article in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 126 citations in OpenAlex.
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- Bidirectional crusher gradient method to estimate the labeling efficiency of pseudo-continuous arterial spin labeling MRI in mice.Magnetic resonance in medicine · 2026Article
- ZCCHC17: a target for synaptic dysfunction and neuronal excitability in Alzheimer's disease.Frontiers in aging neuroscience · 2026Review
- Vascular smooth muscle cell loss, but not neuroinflammation, drives cerebrovascular reactivity impairment in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Transferrin receptor-binding blood-brain barrier shuttle enhances brain delivery and plaque-clearing efficacy of a therapeutic anti-Aβ antibody.Fluids and barriers of the CNS · 2025Article
- Abnormal calcium activity and CREB phosphorylation are associated with motor memory impairment in presenilin-1 mutant knock-in mice.Cell calcium · 2025Article
- Assessing blood-brain barrier (BBB) integrity in an Alzheimer's disease mouse model: is the BBB globally or locally disrupted?Fluids and barriers of the CNS · 2025Article
- Alzheimer's Disease-Thrombosis Comorbidity: A Growing Body of Evidence from Patients and Animal Models.Cells · 2025Review
- Unveiling blood biomarkers for neuronal hyperplasticity: Insights from AD molecular subtyping, a comprehensive review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Associations of plasma biomarkers with cerebral perfusion and structure in Alzheimer's disease.Translational psychiatry · 2025Article
- Vasomotion loss precedes impaired cerebrovascular reactivity and microbleeds in cerebral amyloid angiopathy.Brain communications · 2025Article
- Western diet increases brain metabolism and adaptive immune responses in a mouse model of amyloidosis.Journal of neuroinflammation · 2024Article
- Metabolic and vascular imaging markers for investigating Alzheimer's disease complicated by sleep fragmentation in mice.Frontiers in physiology · 2024Article
- Oscillatory characteristics of resting-state magnetoencephalography reflect pathological and symptomatic conditions of cognitive impairment.Frontiers in aging neuroscience · 2024Article
- A 3D pseudo-continuous arterial spin labeling study of altered cerebral blood flow correlation networks in mild cognitive impairment and Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
- Neurophysiological alterations in mice and humans carrying mutations in APP and PSEN1 genes.Alzheimer's research & therapy · 2023Article
- Cerebrovascular GMolecular imaging and biology · 2023Article
- Magnetic Resonance Imaging Studies of Neurodegenerative Disease: From Methods to Translational Research.Neuroscience bulletin · 2023Review
- Aberrant protein S-nitrosylation contributes to hyperexcitability-induced synaptic damage in Alzheimer's disease: Mechanistic insights and potential therapies.Frontiers in neural circuits · 2023Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dynamics of β-amyloid deposition and related second-order physiological effects, such as regional cerebral blood flow (rCBF), are key factors for a deeper understanding of Alzheimer's disease (AD). We present longitudinal in vivo data on the dynamics of β-amyloid deposition and the decline of rCBF in two different amyloid precursor protein (APP) transgenic mouse models of AD. Using a multiparametric positron emission tomography and magnetic resonance imaging approach, we demonstrate that in the presence of cerebral β-amyloid angiopathy (CAA), β-amyloid deposition is accompanied by a decline of rCBF. Loss of perfusion correlates with the growth of β-amyloid plaque burden but is not related to the number of CAA-induced microhemorrhages. However, in a mouse model of parenchymal β-amyloidosis and negligible CAA, rCBF is unchanged. Because synaptically driven spontaneous network activity is similar in both transgenic mouse strains, we conclude that the disease-related decline of rCBF is caused by CAA.
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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.