Application of magnetic resonance imaging to the measurement of neurodegeneration in rat brain: MRI data correlate strongly with histology and enzymatic analysis

Allegrini, Peter R.; Sauer, Dirk

doi:10.1016/0730-725x(92)90411-r

Cited by 83 publications

(31 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have demonstrated that the volume of hyperintense area in T 2 -weighted images correlates well with the lesion size determined by histological staining methods, 32,33 justifying MRI as a quantification method of infarcts. A 4.7-T horizontal magnet (Magnex Scientific) equipped with actively shielded field gradients (Magnex Scientific) interfaced to an SMIS console (Surrey Medical Imaging Systems) was used for MRI experiments.…”

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

Expression of Human Apolipoprotein E Downregulates Amyloid Precursor Protein–Induced Ischemic Susceptibility

Koistinaho

Kettunen²,

Holtzman³

et al. 2002

Stroke

View full text Add to dashboard Cite

Background and Purpose-Epidemiological findings and experimental data on transgenic mice show that Alzheimer's disease-related changes render the brain more susceptible to ischemic damage. We studied whether the previously observed vulnerability in mice overexpressing the 751-amino-acid isoform of human amyloid precursor protein (APP751) is regulated by human apolipoprotein E (apoE) alleles, which determine the relative risk for Alzheimer's disease and the susceptibility to various forms of acute brain damage. Methods-Aged apoE knock out (KO) mice, mice overexpressing APP751 in the apoE KO background and mice expressing either human apoE3 or apoE4 and APP751 in the apoE KO background were exposed to permanent occlusion of the middle cerebral artery (MCA). Infarct volumes were quantified from T 2 -weighted magnetic resonance images 24 hours after the MCA occlusion. Local cortical blood flow was monitored by laser Doppler flowmetry. Ischemia-induced microgliosis was detected by immunohistochemistry. Results-Overexpression of human APP751 significantly increased the infarct volumes in apoE KO mice. Furthermore, this APP751-induced ischemic vulnerability was attenuated by the coexpression of either human apoE isoform. MCA occlusion resulted in a similar relative reduction in cortical blood flow in all mouse groups. Vascular anatomy showed no variation in the MCA territory between the groups. Instead, the expression of human apoE isoforms reduced the ischemia-induced microgliosis. Conclusions-Expression of either the human apoE3 or apoE4 isoform protects against the increased ischemic vulnerability observed in aged mice overexpressing human APP751, probably by modulating the inflammatory response induced by MCA occlusion.

show abstract

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

Expression of Human Apolipoprotein E Downregulates Amyloid Precursor Protein–Induced Ischemic Susceptibility

Koistinaho

Kettunen²,

Holtzman³

et al. 2002

Stroke

View full text Add to dashboard Cite

show abstract

“…Indeed, in vivo MRI has been employed to identify structural degradation in several experimental rodent models (Assaf et al, 1997;Baba et al, 1990;Bouilleret et al, 2000;Norman et al, 1991;Saunders et al, 1989;Wolf et al, 2002). In addition, some studies even reported an agreement between their MRI and histological observations (Allegrini and Sauer, 1992;Ben Horin et al, 1996;Minematsu et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

The aging hippocampus: A multi-level analysis in the rat

et al. 2006

View full text Add to dashboard Cite

The purpose of the current thesis was twofold: (1) to examine various factors that might be contributing to age-related learning and memory deficits specifically related to the hippocampus, and (2) to validate our rat model of aging, employing a multilevel analysis. We found age-related deficits on both spatial and non-spatial hippocampus-dependent tasks that were accompanied by structural alterations observed both in vivo (volume, but not neuronal metabolic function) and post mortem (neuronal density and neurogenesis, but not synaptic or mitochondrial density). Furthermore, our results suggest that the observed hippocampal structural changes, namely decreased volume and neurogenesis, predict learning and memory deficits, and both can be accounted for by neurogenic reduction. In addition, the above-mentioned pattern of age-related deficits closely resembles that seen in humans, suggesting the present rat version of aging to be a very useful model for investigating hippocampal aging in humans.

show abstract

“…Infarct volume was determined 24 hours after PCI or MCAO by means of quantitative in vivo magnetic resonance imaging (MRI). Measurements were performed on a 4.7-T 30-cm-bore Spectrospin DBX (Bruker, Karlsruhe, Germany) equipped with a 20-cm gradient coil as described in detail elsewhere (Allegrini and Sauer, 1992;Wiessner et al, 2000). Briefly, rats were anesthetized with isoflurane (see preceding paragraphs) and the head was positioned in a 35-mm resonator.…”

Section: Characterization Of Monoclonal Antibody 7b12mentioning

confidence: 99%

Anti—Nogo-A Antibody Infusion 24 Hours after Experimental Stroke Improved Behavioral Outcome and Corticospinal Plasticity in Normotensive and Spontaneously Hypertensive Rats

Wiessner¹,

Bareyre

Allegrini

et al. 2003

J Cereb Blood Flow Metab

Self Cite

143

View full text Add to dashboard Cite

Summary:Nogo-A is a myelin-associated neurite outgrowth inhibitory protein limiting recovery and plasticity after central nervous system injury. In this study, a purified monoclonal anti-Nogo-A antibody (7B12) was evaluated in two rat stroke models with a time-to-treatment of 24 hours after injury. After photothrombotic cortical injury (PCI) and intraventricular infusion of a control mouse immunoglobulin G for 2 weeks, long-term contralateral forepaw function was reduced to about 55% of prelesion performance until the latest time point investigated (9 weeks). Forepaw function was significantly better in the 7B12-treated group 6 to 9 weeks after PCI, and reached about 70% of prelesion levels. Cortical infarcts were also produced in spontaneously hypertensive rats (SHR) by permanent middle cerebral artery occlusion (MCAO). In the control group, forepaw function remained between 40% and 50% of prelesion levels 4 to 12 weeks after MCAO. In contrast, 7B12-treated groups showed significant improvement between 4 and 7 weeks after MCAO from around 40% of prelesion levels at week 4 to about 60% to 70% at 7 to 12 weeks after MCAO. Treatment in both models was efficacious without influencing infarct volume or brain atrophy. Neuroanatomically in the spinal cord, a significant increase of midline crossing corticospinal fibers originating in the unlesioned sensorimotor cortex was found in 7B12-treated groups, reaching 2.3 ± 1.5% after PCI (control group: 1.1 ± 0.5%) and 4.5 ± 2.2% after MCAO in SHR rats (control group: 1.8 ± 0.8%). Behavioral outcome and the presence of midline crossing fibers in the cervical spinal cord correlated significantly, suggesting a possible contribution of the crossing fibers for forepaw function after PCI and MCAO. The results suggest that specific anti-Nogo-A antibodies bear potential as a new rehabilitative treatment approach for ischemic stroke with a prolonged time-to-treatment window.

show abstract

Application of magnetic resonance imaging to the measurement of neurodegeneration in rat brain: MRI data correlate strongly with histology and enzymatic analysis

Cited by 83 publications

References 14 publications

Expression of Human Apolipoprotein E Downregulates Amyloid Precursor Protein–Induced Ischemic Susceptibility

Expression of Human Apolipoprotein E Downregulates Amyloid Precursor Protein–Induced Ischemic Susceptibility

The aging hippocampus: A multi-level analysis in the rat

Anti—Nogo-A Antibody Infusion 24 Hours after Experimental Stroke Improved Behavioral Outcome and Corticospinal Plasticity in Normotensive and Spontaneously Hypertensive Rats

Contact Info

Product

Resources

About