Articles: apolipoproteins-e.
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Journal of neurotrauma · Sep 2012
Administration of COG1410 reduces axonal amyloid precursor protein immunoreactivity and microglial activation after controlled cortical impact in mice.
Traumatic axonal injury (TAI) accounts for at least 35% of the morbidity and mortality in traumatic brain injury (TBI) patients without space-occupying lesions. It is also believed to be a key determinant of adverse outcomes such as cognitive dysfunction across the spectrum of TBI severity. Previous studies have shown that COG1410, a synthetic peptide derived from the apolipoprotein E (apoE) receptor binding region, has anti-inflammatory effects after experimental TBI, with improvements in cognitive recovery. ⋯ There was no effect of COG1410 on pericontusional white matter volume or silver staining at any time point. This indicates a possible effect of COG1410 on delayed but not immediate TAI. Future studies are needed to investigate the underlying mechanisms, therapeutic time window, and physiological implications of this effect.
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The CT angiography (CTA) spot sign predicts hematoma expansion and poor outcome in patients with primary intracerebral hemorrhage (ICH). The biological underpinnings of the spot sign remain poorly understood; it may be that the underlying vasculopathy influences its presence. Therefore, we conducted a study to identify genetic predictors of the spot sign. ⋯ Patients with ICH on warfarin are more likely to present with a spot sign regardless of ICH location. Among patients with lobar ICH, those who possess the apolipoprotein E ε2 allele are more likely to have a spot sign. Given the established relationship between apolipoprotein E ε2 and vasculopathic changes in cerebral amyloid angiopathy, our findings suggest that both hemostatic factors and vessel pathology influence spot sign presence.
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We investigated suspected longitudinal interaction effects of apolipoprotein E (APOE) genotype and educational attainment on cognitive decline in normal aging. ⋯ We conclude that the combination of APOE-ε4 allele and high educational attainment may be a risk factor for accelerated cognitive decline in older age, as has been reported before, but only to a very limited extent. Moreover, we conclude that, within the cognitive reserve framework, education does not have significant protective power against age-related cognitive decline.
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Microvascular research · Jul 2012
Radial pressure waves mediate apoptosis and functional angiogenesis during wound repair in ApoE deficient mice.
This study aims to quantify by intravital microscopy and histological wound scoring the effect of radial pressure wave treatment (RPWT) on murine incisional wound healing. The dorsal skinfold chamber in mice was used for intravital microscopy, whereby an incisional wound was created within the chamber. RPWT to the wound was carried out using a ballistic pressure wave source (EMS Swiss DolorClast). ⋯ Following RPWT, on day three we observed enhanced expression of capase-3 (2-fold), proliferating cell nuclear antibody (PCNA, 1,6-fold), and endothelial nitric oxide synthase (eNOS, 2.6-fold), all P<0.05. In conclusion repetitive RPWT accelerated wound healing in ApoE(-/-) mice by increasing functional neovascular density. In addition our findings strongly suggest that RPW may facilitate the linear progression of wound healing phases by fostering apoptosis.
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Clinical Trial
Apolipoprotein E genotype predicts hematoma expansion in lobar intracerebral hemorrhage.
Hematoma volume is the most potent predictor of outcome in spontaneous intracerebral hemorrhage (ICH), and hematoma expansion after hospital presentation occurs in up to 40% of individuals. Among patients with lobar ICH, the apolipoprotein E (APOE) ε2 allele predicts larger hematoma volumes at presentation. We investigated whether the ε2 allele also identifies individuals at increased risk of hematoma expansion. ⋯ Possession of APOE ε2 predisposes individuals with lobar ICH to hematoma expansion. This effect is even more pronounced in patients with amyloid angiopathy-related ICH, consistent with the ε2 allele's role in vascular amyloid deposition and vessel fragility.