Amyloid precursor protein accumulates in white matter at the margin of a focal ischaemic lesion

Yam, P.S.; Takasago, Teiichi; Dewar, Deborah; Graham, David I.; McCulloch, James

doi:10.1016/s0006-8993(97)00290-4

Cited by 83 publications

(52 citation statements)

References 38 publications

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“…Pathological amyloid precursor protein staining especially for -amyloid peptide and C-terminal has been observed in periventricular and subcortical white matter after ischemic brain injury . The more intense postischemic brain injury of white matter is, the more extensive is the staining of different parts of amyloid precursor protein in this region (Yam et al, 1997). In contrast, in our unpublished studies, the data are opposite.…”

Section: Amyloid Precursor Protein and β-Amyloid Peptide After Ischemiacontrasting

confidence: 59%

Alzheimer's Factors in Ischemic Brain Injury

Pluta¹,

Jabłoński²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Section: Amyloid Precursor Protein and β-Amyloid Peptide After Ischemiacontrasting

confidence: 59%

Alzheimer's Factors in Ischemic Brain Injury

Pluta¹,

Jabłoński²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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“…Therefore, the SMI-32 antibody can be used to detect axonal injury under many conditions (Gresle et al, 2006). Although many authors have detected axonal injury by amyloid precursor protein immunohistochemistry, assessment of axonal injury with an amyloid precursor protein antibody is limited, because the immunostaining is restricted mainly to the margins of the ischemic lesion, and hence is largely absent from the ischemic core (Gresle et al, 2006;Yam et al, 1997). Therefore, we used SMI-32 immunohistochemistry, and clearly detected axonal injury.…”

Section: Fig 7 (A and B)mentioning

confidence: 99%

“…White matter injury was evaluated only by immunostaining, which is difficult to quantify. Some authors have evaluated white matter injury after focal ischemia using an amyloid precursor protein immunoreactivity score (Imai et al, 2001;Yam et al, 1997); however, such scoring systems are not quantitative. We need to develop a quantitative evaluating method in a future study.…”

Section: Fig 7 (A and B)mentioning

confidence: 99%

Consistent Injury to Medium Spiny Neurons and White Matter in the Mouse Striatum after Prolonged Transient Global Cerebral Ischemia

Yoshioka

Niizuma

Katsu

et al. 2011

Journal of Neurotrauma

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A reproducible transient global cerebral ischemia (tGCI) mouse model has not been fully established. Although striatal neurons and white matter are recognized to be vulnerable to ischemia, their injury after tGCI in mice has not been elucidated. The purpose of this study was to evaluate injuries to striatal neurons and white matter after tGCI in C57BL/6 mice, and to develop a reproducible tGCI model. Male C57BL/6 mice were subjected to tGCI by bilateral common carotid artery occlusion (BCCAO). Mice whose cortical cerebral blood flow after BCCAO decreased to less than 13% of the pre-ischemic value were used. Histological analysis showed that at 3 days after 22 min of BCCAO, striatal neurons were injured more consistently than those in other brain regions. Quantitative analysis of cytochrome c release into the cytosol and DNA fragmentation in the striatum showed consistent injury to the striatum. Immunohistochemistry and Western blot analysis revealed that DARPP-32-positive medium spiny neurons, the majority of striatal neurons, were the most vulnerable among the striatal neuronal subpopulations. The striatum (especially medium spiny neurons) was susceptible to oxidative stress after tGCI, which is probably one of the mechanisms of vulnerability. SMI-32 immunostaining showed that white matter in the striatum was also consistently injured 3 days after 22 min of BCCAO. We thus suggest that this is a tGCI model using C57BL/6 mice that consistently produces neuronal and white matter injury in the striatum by a simple technique. This model can be highly applicable for elucidating molecular mechanisms in the brain after global ischemia.

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“…Oligodendrocytes are the most vulnerable glial cell, followed by microglia and then astrocytes, to combined glucose and oxygen deprivation in vitro (Lyons and Kettenmann, 1998;McDonald et al, 1998). Global and focal ischemia can damage white matter (Kurumatani et al, 1998;Pantoni et al, 1996;Valeriani et al, 2000;Yam et al, 1997). Death of oligodendrocytes has been documented at the margins of the infarct and some of the dying oligodendrocytes are TUNEL positive (Mandai et al, 1997).…”

Section: White Matter Injury Can Stimulate Microglial/macrophage Prolmentioning

confidence: 99%

Microglia/Macrophages Proliferate in Striatum and Neocortex but Not in Hippocampus after Brief Global Ischemia That Produces Ischemic Tolerance in Gerbil Brain

Liu

Bartels

et al. 2001

J Cereb Blood Flow Metab

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Summary:The current study determined whether short durations of ischemia that produce ischemia-induced tolerance stimulate glial proliferation in brain. Adult male gerbils were injected with BrdU (50 mg/kg) and dividing cells were detected using immunocytochemistry after sham operations, 2.5 or 5 minutes of global ischemia, or ischemia-induced tolerance. The 2.5-minute ischemia and the ischemia-induced tolerance did not kill hippocampal CA1 pyramidal neurons, whereas the 5-minute ischemia did kill the neurons. At 4 days after 2.5-minute global ischemia, when cell proliferation was maximal, BrdU-labeled cells increased in striatum and in neocortex, but not in hippocampus. The majority of the BrdU-labeled cells were double-labeled with isolectin B4, showing that these dividing cells were primarily microglia or macrophages, or both. Similarly, BrdU-labeled microglia/macrophages were found in striatum and neocortex but not in hippocampus of most animals 4 days after ischemia-induced tolerance (2.5 minutes of global ischemia followed 3 days later by 5 minutes of global ischemia). No detectable neuronal cell death existed in striatal and cortical regions where the microglia/macrophage proliferation occurred. Though 3 of 7 animals subjected to 2.5 minutes of ischemia showed decreased myelin-associated glycoprotein (MAG) immunostaining and increased numbers of adenomatous polyposis coli-stained oligodendrocytes in lateral striatum, this did not explain the microglia/macrophage proliferation. Data show that ischemia-induced tolerance in the gerbil is associated with proliferation of microglia/macrophages in striatum and cortex but not in hippocampus. Because there is no apparent neuronal death, it is postulated that the microglia/ macrophage proliferation occurs in response to an unknown nonlethal injury to neurons or glia and may be beneficial.

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Amyloid precursor protein accumulates in white matter at the margin of a focal ischaemic lesion

Cited by 83 publications

References 38 publications

Alzheimer's Factors in Ischemic Brain Injury

Alzheimer's Factors in Ischemic Brain Injury

Consistent Injury to Medium Spiny Neurons and White Matter in the Mouse Striatum after Prolonged Transient Global Cerebral Ischemia

Microglia/Macrophages Proliferate in Striatum and Neocortex but Not in Hippocampus after Brief Global Ischemia That Produces Ischemic Tolerance in Gerbil Brain

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