Decreased Cerebrospinal Fluid Apolipoprotein E After Subarachnoid Hemorrhage

Kay, Andrew D.; Petzold, Axel; Kerr, Mary Margaret; Keir, Geoff; Thompson, E. D.; Nicoll, James

doi:10.1161/01.str.0000057579.25430.16

Cited by 48 publications

(39 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…9 We speculated that possible mechanisms for the depletion of apoE from SAH CSF include increased receptor-mediated uptake of apoE containing lipoproteins and/or interactions between apoE and other hydrophobic molecules such as A␤. The findings in the present study provide indirect evidence for interactions between A␤ and apoE in vivo after SAH.…”

Section: Discussionmentioning

confidence: 99%

“…9 The control group comprised 13 patients (mean age, 36 years; range, 16 to 61 years) with suspected shunt dysfunction or compensated chronic hydrocephalus with no history of acute brain injury or impaired level of consciousness, who required drainage/examination of ventricular CSF. Only patients with CSF found to have a normal cell count, albumin, total protein concentration, and no xanthochromia were included, so that ventricular CSF parameters were as "normal" as was feasible.…”

Section: Patients and Control Subjectsmentioning

confidence: 99%

“…9 Total (Innogenetics), A␤ , and A␤ (BioSource International) were assayed with commercial kits according to the manufacturers' instructions.…”

Section: Csf Analysismentioning

confidence: 99%

See 2 more Smart Citations

Temporal Alterations in Cerebrospinal Fluid Amyloid β-Protein and Apolipoprotein E After Subarachnoid Hemorrhage

Kay

Petzold

Kerr

et al. 2003

Stroke

Self Cite

View full text Add to dashboard Cite

Background and Purpose-The mechanism underlying the association between possession of the APOE⑀4 allele and less favorable outcome after subarachnoid hemorrhage (SAH) remains to be determined. After SAH the level of apolipoprotein E (apoE) in the cerebrospinal fluid (CSF) is decreased, and lower levels are associated with more severe injury and less favorable outcome. This study examined serial CSF samples to determine the time course for the decrease in CSF apoE and the relationship between CSF apoE and amyloid ␤-protein (A␤), testing the hypothesis that apoE-A␤ interactions occur in vivo after SAH. Methods-Enzyme-linked immunosorbent assay was used to assay apoE, A␤ 1-40 , and A␤ 1-42 in serial ventricular CSF samples from 19 patients with SAH and 13 controls. CSF S100B and were assayed as surrogate markers of brain injury. Results-There was a sustained decrease in CSF apoE (PϽ0.001) and A␤ (PϽ0.001) after SAH in contrast to the observed elevation in CSF S100B (PϽ0.001) and (PϽ0.001) concentration. There was significant correlation between CSF A␤ concentration and clinical outcome (rϭ0.65, PϽ0.01), and the decrease in CSF A␤ concentration correlated significantly with that of apoE (rϭ0.85, PϽ0.0001). Conclusions-After SAH both apoE and A␤ levels decrease in the CSF, supporting the concept that interactions between these proteins occur in vivo. The possibility that apoE and A␤ influence outcome after SAH warrants further investigation. (Stroke. 2003;34:e240-e243.)

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Patients and Control Subjectsmentioning

confidence: 99%

See 1 more Smart Citation

Temporal Alterations in Cerebrospinal Fluid Amyloid β-Protein and Apolipoprotein E After Subarachnoid Hemorrhage

Kay

Petzold

Kerr

et al. 2003

Stroke

Self Cite

View full text Add to dashboard Cite

show abstract

“…32 Furthermore, a poorer outcome has been shown to be related to increased blood S100B concentrations. 33 In contrast it has been reported that there is no direct correlation between CSF and serum levels of S100B, however it must be noted that this was in patients following either SAH or traumatic brain injury.…”

Section: S100bmentioning

confidence: 99%

Subarachnoid haemorrhage: Early clinical indicators and biomarkers

Kaura

Bonner

2012

Trends in Anaesthesia and Critical Care

View full text Add to dashboard Cite

“…ApoE and S100B, a marker of brain injury, were measured in the cerebrospinal fluid (CSF) of SAH patients. 24 Concentrations of S100B increased but those of ApoE decreased, suggesting that ApoE is retained in the brain after injury in response to injury and leading the authors to speculate that this is a protective mechanism. Other compounds examined for their ability to predict outcome after SAH include C-type natriuretic peptide (CNP).…”

Section: Ruptured Aneurysmsmentioning

confidence: 99%

Advances in Vascular Surgery

Macdonald

2004

Stroke

View full text Add to dashboard Cite

The first report of the International Study of Unruptured Intracranial Aneurysms (ISUIA) cited very low rates of subarachnoid hemorrhage (SAH) for previously unruptured aneurysms. 1 Data were collected retrospectively. It was difficult to reconcile these rates with those reported from prior studies, with the known sizes of ruptured aneurysms and with clinical experience. Prior reports including prospective studies suggested that unruptured aneurysms carried a 1% to 2% risk of hemorrhage per year. [2][3][4] The second report from the ISUIA prospectively enrolled 4060 patients with unruptured aneurysms. 5 Of these, 1692 had no intervention for their aneurysm, 1917 had open surgery, and 451 had endovascular procedures. The rupture rates were more in agreement with prior studies (Table). Risk factors for SAH were increasing aneurysm size and aneurysm location at the basilar apex or posterior communicating artery. The risk of surgical repair increased significantly with increasing patient age, posterior circulation location of the aneurysm, history of ischemic cerebrovascular disease, and presence of symptoms from the aneurysm. Thirty-day mortality occurred in 1.5%, morbidity in 3%, poor cognitive function plus morbidity (a Rankin score of 3 to 5) in 4%, and overall total morbidity and mortality in 13%. The data indicate that the decision to treat a ruptured aneurysm needs to include a careful analysis of the patient, their risk factors for poor outcome, and the features of the aneurysm. Endovascular treatment is an option, although overall complete obliteration rates were only about 50% in this study, and risk of treatment was similar to but lower than with surgery, although the groups were not randomized to treatment and are thus not comparable. The findings of the initial results of ISUIA that were at variance with prior assumptions about unruptured aneurysms prompted an exhaustive review of the literature that suggested some explanations for the findings. 6 Numerous assumptions and biases inherent in the retrospective design of the first study were cited. An important one is that selection bias could account for the finding that 10 mm seemed to be the cutoff for rupture, yet this is at odds with the fact that the average size of a ruptured aneurysm is 8 mm. The distribution of cases included in the initial cohort will strongly influence the size cutoff for rupture that is found. To take an extreme example, if one collects only aneurysms Ͼ10 mm in diameter, then one will necessarily conclude that the cutoff for rupture is some value Ͼ10 mm. The author recommended that unruptured aneurysms with clinical pathological profiles resembling those of ruptured lesions be considered for treatment at a smaller size than unruptured lesions with profiles typical of intact aneurysms. The question of whether and how to follow patients with unruptured aneurysms that are not treated is unanswered, but it was felt that periodic radiological imaging might be wise. Screening for aneurysms in asymptomatic patients is only recommended...

show abstract

Decreased Cerebrospinal Fluid Apolipoprotein E After Subarachnoid Hemorrhage

Cited by 48 publications

References 45 publications

Temporal Alterations in Cerebrospinal Fluid Amyloid β-Protein and Apolipoprotein E After Subarachnoid Hemorrhage

Temporal Alterations in Cerebrospinal Fluid Amyloid β-Protein and Apolipoprotein E After Subarachnoid Hemorrhage

Subarachnoid haemorrhage: Early clinical indicators and biomarkers

Advances in Vascular Surgery

Contact Info

Product

Resources

About