Cited by 82Alzheimer's disease research and treatmentsBarrier Structure and Function StudiesNeurological Disease Mechanisms and Treatments

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Imaging of cerebrovascular pathology in animal models of Alzheimer's disease

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Klohs, Jan, Rudin, Markus, Shimshek, Derya R., Beckmann, Nicolau·2014·Frontiers in Aging Neuroscience

DOI 10.3389/fnagi.2014.00032PMC PMC3952109

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Abstract

In Alzheimer's disease (AD), vascular pathology may interact with neurodegeneration and thus aggravate cognitive decline. As the relationship between these two processes is poorly understood, research has been increasingly focused on understanding the link between cerebrovascular alterations and AD. This has at last been spurred by the engineering of transgenic animals, which display pathological features of AD and develop cerebral amyloid angiopathy to various degrees. Transgenic models are versatile for investigating the role of amyloid deposition and vascular dysfunction, and for evaluating novel therapeutic concepts. In addition, research has benefited from the development of novel imaging techniques, which are capable of characterizing vascular pathology in vivo. They provide vascular structural read-outs and have the ability to assess the functional consequences of vascular dysfunction as well as to visualize and monitor the molecular processes underlying these pathological alterations. This article focusses on recent in vivo small animal imaging studies addressing vascular aspects related to AD. With the technical advances of imaging modalities such as magnetic resonance, nuclear and microscopic imaging, molecular, functional and structural information related to vascular pathology can now be visualized in vivo in small rodents. Imaging vascular and parenchymal amyloid-β (Aβ) deposition as well as Aβ transport pathways have been shown to be useful to characterize their dynamics and to elucidate their role in the development of cerebral amyloid angiopathy and AD. Structural and functional imaging read-outs have been employed to describe the deleterious affects of Aβ on vessel morphology, hemodynamics and vascular integrity. More recent imaging studies have also addressed how inflammatory processes partake in the pathogenesis of the disease. Moreover, imaging can be pivotal in the search for novel therapies targeting the vasculature.

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Aβ40 Inhibits Amyloid Deposition In Vivo
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“Other reports suggested that Aβ40 can inhibit fibril formation and even inhibit amyloid deposition (Jarrett et al., 1993; Kim et al., 2007).”
Background
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Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein
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Pathological alterations of the cerebral microvasculature in Alzheimer's disease and related dementing disorders
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Novel Therapeutic Approach for the Treatment of Alzheimer's Disease by Peripheral Administration of Agents with an Affinity to β-Amyloid
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Neuroinflammation and Neuronal Loss Precede Aβ Plaque Deposition in the hAPP-J20 Mouse Model of Alzheimer’s Disease
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Fibrin deposition accelerates neurovascular damage and neuroinflammation in mouse models of Alzheimer's disease
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Blood–brain barrier P-glycoprotein function in Alzheimer's disease
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Passive Amyloid Immunotherapy Clears Amyloid and Transiently Activates Microglia in a Transgenic Mouse Model of Amyloid Deposition
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Spontaneous Hemorrhagic Stroke in a Mouse Model of Cerebral Amyloid Angiopathy
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Novel 18F-Labeled Arylquinoline Derivatives for Noninvasive Imaging of Tau Pathology in Alzheimer Disease
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Cerebrovascular autoregulation is profoundly impaired in mice overexpressing amyloid precursor protein
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Time sequence of maturation of dystrophic neurites associated with Aβ deposits in APP/PS1 transgenic mice
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Hippocampal Neuron Loss Exceeds Amyloid Plaque Load in a Transgenic Mouse Model of Alzheimer's Disease
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Circle of Willis Atherosclerosis Is a Risk Factor for Sporadic Alzheimer’s Disease
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Characterization of Pathology in Transgenic Mice Over-Expressing Human Genomic and cDNA Tau Transgenes
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Microbleed Topography, Leukoaraiosis, and Cognition in Probable Alzheimer Disease From the Sunnybrook Dementia Study
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Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementias
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Interstitial fluid drainage is impaired in ischemic stroke and Alzheimer’s disease mouse models
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ASL Perfusion MRI Predicts Cognitive Decline and Conversion From MCI to Dementia
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Voxel-level comparison of arterial spin-labeled perfusion MRI and FDG-PET in Alzheimer disease
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Altered morphology and 3D architecture of brain vasculature in a mouse model for Alzheimer's disease
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The Arctic Alzheimer mutation facilitates early intraneuronal Aβ aggregation and senile plaque formation in transgenic mice
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Intracellular Aβ and cognitive deficits precede β-amyloid deposition in transgenic arcAβ mice
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Does vascular pathology contribute to Alzheimer changes?
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Cerebral hypoperfusion accelerates cerebral amyloid angiopathy and promotes cortical microinfarcts
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Florbetapir PET analysis of amyloid-β deposition in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional study
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Simultaneous BOLD fMRI and fiber-optic calcium recording in rat neocortex
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Persistent Amyloidosis following Suppression of Aβ Production in a Transgenic Model of Alzheimer Disease
Jankowsky, J. L., Slunt, H. H., Gonzales, V., Savonenko, A. V., Wen, J. C., Jenkins, N. A., Copeland, N. G., Younkin, L. H., Lester, H. A., Younkin, S. G., et al. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020355 · Cited by 237
Circle of Willis atherosclerosis: association with Alzheimer’s disease, neuritic plaques and neurofibrillary tangles
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MDR1‐P‐Glycoprotein (ABCB1) Mediates Transport of Alzheimer’s Amyloid‐β Peptides—Implications for the Mechanisms of Aβ Clearance at the Blood–Brain Barrier
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Functional Connectivity fMRI of the Rodent Brain: Comparison of Functional Connectivity Networks in Rat and Mouse
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Vascular β-amyloid and early astrocyte alterations impair cerebrovascular function and cerebral metabolism in transgenic arcAβ mice
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Prominent Cerebral Amyloid Angiopathy in Transgenic Mice Overexpressing the London Mutant of Human APP in Neurons
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Early formation of mature amyloid‐β protein deposits in a mutant APP transgenic model depends on levels of Aβ1–42
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ABCG2 Is Upregulated in Alzheimer's Brain with Cerebral Amyloid Angiopathy and May Act as a Gatekeeper at the Blood–Brain Barrier for Aβ 1–40 Peptides
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Arterial Spin Labeling Blood Flow MRI: Its Role in the Early Characterization of Alzheimer's Disease
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Behavioral disturbances in transgenic mice overexpressing the V717F Β-amyloid precursor protein.
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Dentate gyrus volume is reduced before onset of plaque formation in PDAPP mice: A magnetic resonance microscopy and stereologic analysis
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PS2APP Transgenic Mice, Coexpressing hPS2mut and hAPPswe, Show Age-Related Cognitive Deficits Associated with Discrete Brain Amyloid Deposition and Inflammation
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Aβ-peptides enhance vasoconstriction in cerebral circulation
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Cerebral Microvascular Amyloid β Protein Deposition Induces Vascular Degeneration and Neuroinflammation in Transgenic Mice Expressing Human Vasculotropic Mutant Amyloid β Precursor Protein
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Demonstration of poly-N-acetyl lactosamine residues in ameboid and ramified microglial cells in rat brain by tomato lectin binding.
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The Role of the Cell Surface LRP and Soluble LRP in Blood-Brain Barrier Aβ Clearance in Alzheimers Disease
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Astrocyte-mediated control of cerebral microcirculation
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Cognitive Deficits and Delayed Neuronal Loss in a Mouse Model of Multiple Microinfarcts
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Dense-Core Plaques in Tg2576 and PSAPP Mouse Models of Alzheimer's Disease Are Centered on Vessel Walls
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Two‐Photon Imaging of Astrocytic Ca2+ Signaling and the Microvasculature in Experimental Mice Models of Alzheimer's Disease
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Reduced Spine Density in Specific Regions of CA1 Pyramidal Neurons in Two Transgenic Mouse Models of Alzheimer's Disease
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Mechanism of Cerebral β-Amyloid Angiopathy: Murine and Cellular Models
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Diffusion tensor imaging detects age-dependent white matter changes in a transgenic mouse model with amyloid deposition
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Behavioral disturbances in transgenic mice overexpressing the V717F Β-amyloid precursor protein.
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Electrophysiological properties of microglial cells in normal and pathologic rat brain slices
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Angiotensin Receptor Blocker Prevented β-Amyloid-Induced Cognitive Impairment Associated With Recovery of Neurovascular Coupling
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Scavenger receptor class B type I (SR-BI) regulates perivascular macrophages and modifies amyloid pathology in an Alzheimer mouse model
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Age-dependent rescue by simvastatin of Alzheimer’s disease cerebrovascular and memory deficits
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Apolipoprotein E Markedly Facilitates Age-Dependent Cerebral Amyloid Angiopathy and Spontaneous Hemorrhage in Amyloid Precursor Protein Transgenic Mice
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Imaging of Atherosclerosis
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Amyloid-β-dependent compromise of microvascular structure and function in a model of Alzheimer’s disease
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Deglycosylated Anti-Amyloid-β Antibodies Eliminate Cognitive Deficits and Reduce Parenchymal Amyloid with Minimal Vascular Consequences in Aged Amyloid Precursor Protein Transgenic Mice
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Vascular Remodeling versus Amyloid β-Induced Oxidative Stress in the Cerebrovascular Dysfunctions Associated with Alzheimer's Disease
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Changes in cerebral blood volume and amyloid pathology in aged Alzheimer APP/PS1 mice on a docosahexaenoic acid (DHA) diet or cholesterol enriched Typical Western Diet (TWD)
Hooijmans, C. R., Rutters, F., Dederen, P. J. W. C., Gambarota, G., Veltien, A. A., Groen, T. V., Broersen, L. M., Lütjohann, D., Heerschap, A., Tanila, H., et al. (2007) · Neurobiology of Disease · doi:10.1016/j.nbd.2007.06.007 · Cited by 154
In vivo axonal transport rates decrease in a mouse model of Alzheimer's disease
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Beckmann, 2000, High resolution magnetic resonance angiography non-invasively reveals mouse strain differences in the cerebrovascular anatomy in vivo, Magn. Reson. Med, 44, 252, 10.1002/1522-2594(200008)44:2252::AID-MRM123.0.CO;2-G · DOI
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Authors: Klohs, J., Rudin, M., Shimshek, D. R., & Beckmann, N.
Affiliations: University of Zurich (CH)
Novartis (Switzerland) (CH)
Corresponding author: Beckmann, Nicolau
ORCID: Klohs, Jan
Rudin, Markus
Shimshek, Derya R.
Beckmann, Nicolau
Venue: Frontiers in Aging Neuroscience
Publisher: Frontiers Media SA
Published: 2014-03-13
Volume: 6
Pages: 32-32
ISSN: 1663-4365 (ISSN-L)
DOI: 10.3389/fnagi.2014.00032
PMC: PMC3952109
OpenAlex: W2150972825
Cited by: 82
References: 281
Citations by year: 2026: 1 · 2025: 4 · 2024: 3 · 2023: 5 · 2022: 4 · 2021: 10 · 2020: 16 · 2019: 10 · 2018: 6 · 2017: 8 · 2016: 7 · 2015: 7 · 2014: 1
FWCI: 0.90
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Frontiers in Aging Neuroscience (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Zurich Open Repository and Archive (University of Zurich) (submittedVersion, cc-by)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by)
ETH Zürich Research Collection (cc-by)
Zurich Open Repository and Archive (University of Zurich)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords: Alzheimer's disease, cerebrovascular pathology, cerebral amyloid angiopathy, amyloid-beta deposition, amyloid-beta transport, vascular dysfunction, transgenic animal models, in vivo imaging, small animal imaging, hemodynamics, vascular inflammation, vascular integrity, neurovascular unit

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Imaging of cerebrovascular pathology in animal models of Alzheimer's disease

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