2020
DOI: 10.1002/cne.24955
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Differential temporal and spatial post‐injury alterations in cerebral cell morphology and viability

Abstract: Combination of ischemia and β-amyloid (Aβ) toxicity has been shown to simultaneously increase neuro-inflammation, endogenous Aβ deposition, and neurodegeneration. However, studies on the evolution of infarct and panorama of cellular degeneration as a synergistic or overlapping mechanism between ischemia and Aβ toxicity are lacking. Here, we compared fluorojade B (FJB) and hematoxylin and eosin (H&E) stains primarily to examine the chronology of infarct, and the viability and morphological changes in neuroglia … Show more

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Cited by 3 publications
(1 citation statement)
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“…The defective blood-brain barrier (BBB) function (Amtul et al., 2018 ) or vascular phenotype or both leads to dysregulated cerebral blood flow (CBF) (Yang et al., 2014 ) resulting in proteinaceous storage disorders in the brain and cerebral vessels (Amtul et al., 2019 ; 2020 ) of Alzheimer’s patients (Zlokovic, 2008 ). Aggregation of monomeric amyloid β-peptide (Aβ) into Aβ fibrils/oligomeric species of Aβ plaques is a critical step in the pathophysiology of Alzheimer’s disease (AD) (Meinhardt et al., 2009 ).…”
Section: Introductionmentioning
confidence: 99%
“…The defective blood-brain barrier (BBB) function (Amtul et al., 2018 ) or vascular phenotype or both leads to dysregulated cerebral blood flow (CBF) (Yang et al., 2014 ) resulting in proteinaceous storage disorders in the brain and cerebral vessels (Amtul et al., 2019 ; 2020 ) of Alzheimer’s patients (Zlokovic, 2008 ). Aggregation of monomeric amyloid β-peptide (Aβ) into Aβ fibrils/oligomeric species of Aβ plaques is a critical step in the pathophysiology of Alzheimer’s disease (AD) (Meinhardt et al., 2009 ).…”
Section: Introductionmentioning
confidence: 99%