gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 05 Mar 2015.

Apolipoprotein Ea

apolipoprotein E
Top mentioned proteins: apolipoprotein E, AGE, HAD, CAN, V1a
Papers on apolipoprotein E
APOE Genotype Alters Immunoglobulin Subtypes in Knock-In Mice.
Rebeck et al., Gainesville, United States. In J Alzheimers Dis, 03 Apr 2015
UNASSIGNED: Apolipoprotein E (APOE) alleles are strongly related to the risk of Alzheimer's disease (AD).
Clinical relevance of apolipoprotein E genotyping based on a family history of Alzheimer's disease.
Kotze et al., Tokyo, Japan. In Curr Alzheimer Res, 02 Apr 2015
UNASSIGNED: Having a family history of Alzheimer's disease (AD) may potentiate cumulative risk associated with phenotypic expression of the ε-4 allele of the apolipoprotein E (APOE) gene.
Apolipoprotein E isoforms 3/3 and 3/4 differentially interact with circulating stearic, palmitic, and oleic fatty acids and lipid levels in Alaskan Natives.
Tejero et al., Mexico. In Nutr Res, 14 Mar 2015
Variation of the apolipoprotein E (Apo E) genotype may contribute to the diverse response to diet in lipid metabolism and influence the association between fatty acids in plasma and risk factors for cardiovascular disease.
Apolipoprotein ε4 Is Associated with Lower Brain Volume in Cognitively Normal Chinese but Not White Older Adults.
Rosen et al., São Paulo, Brazil. In Plos One, Dec 2014
The ε4 allele of apolipoprotein E (APOE ε4) is a well-established risk factor for Alzheimer's disease (AD), and may confer anatomic and functional effects years before clinical signs of cognitive decline are observed.
Cholesterol and metal ions in Alzheimer's disease.
Lim et al., Ann Arbor, United States. In Chem Soc Rev, Nov 2014
For example, (a) cholesterol has been shown to be misregulated in AD-afflicted brains, and the aberrant activity of proteins (particularly, apolipoprotein E (ApoE) and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGR)) has been linked to cholesterol-related AD exacerbation; (b) dyshomeostasis of metal ions associated with misfolded proteins (i.e., amyloid-β (Aβ) aggregates) found in the brains of AD patients is shown to promote oxidative stress leading to the malfunction of multiple proteins, including cytochrome c oxidase (CcO), and Cu/Zn superoxide dismutase (SOD1); (c) metal ion misregulation has also been observed to disrupt the activity of proteins (e.g., HMGR, low-density lipoproteins (LDL)), required for cholesterol production and regulation.
Post-Traumatic Brain Injury: Genetic Susceptibility to Outcome.
Bendena et al., Toronto, Canada. In Neuroscientist, Aug 2014
To provide health care workers with the basic information for clinical management we summarize and compare the data on post-TBI outcome with regard to the impact of genetic variation: apolipoprotein E (APOE), brain-derived neurotrophic factor (BDNF), calcium channel, voltage dependent P/Q type, catechol-O-methyltransferase (COMT), dopamine receptor D2 and ankyrin repeat and kinase domain containing 1 (DRD2 and ANKK1), interleukin-1 (IL-1), interleukin-6 (IL-6), kidney and brain expressed protein (KIBRA), neurofilament, heavy polypeptide (NEFH), endothelial nitric oxide synthase 3 (NOS3), poly (ADP-ribose) polymerase-1 (PARP-1), protein phosphatase 3, catalytic subunit, gamma isozyme (PPP3CC), the serotonin transporter (5-HTT) gene solute carrier family 6 member (SLC6A4) and tumor protein 53 (TP53).
[Role of apolipoprotein E in the molecular pathomechanism of Alzheimer disease].
Michikawa, In Nihon Shinkei Seishin Yakurigaku Zasshi, Feb 2014
Apolipoprotein E (Apo-E) is a major cholesterol carrier regulating lipid transport and injury repair in the brain.
Two phase 3 trials of bapineuzumab in mild-to-moderate Alzheimer's disease.
Bapineuzumab 301 and 302 Clinical Trial Investigators et al., Jarash, Jordan. In N Engl J Med, Feb 2014
METHODS: We conducted two double-blind, randomized, placebo-controlled, phase 3 trials involving patients with mild-to-moderate Alzheimer's disease--one involving 1121 carriers of the apolipoprotein E (APOE) ε4 allele and the other involving 1331 noncarriers.
Histological structure of the thyroid gland in apolipoprotein E deficient female mice after levothyroxine application.
Kostovska et al., Скопје, Macedonia. In Prilozi, 2013
(Full text is available at
Apolipoprotein E in Alzheimer's disease: an update.
Hardy et al., Qingdao, China. In Annu Rev Neurosci, 2013
Apolipoprotein E (APOE) has been irrefutably recognized as the major genetic risk factor, with semidominant inheritance, for LOAD.
Herpes simplex virus type 1 and Alzheimer's disease: increasing evidence for a major role of the virus.
Itzhaki, Manchester, United Kingdom. In Front Aging Neurosci, 2013
Herpes simplex virus type 1 (HSV1), when present in brain of carriers of the type 4 allele of the apolipoprotein E gene (APOE), has been implicated as a major factor in Alzheimer's disease (AD).
The potential applications of Apolipoprotein E in personalized medicine.
Gaudet et al., Montréal, Canada. In Front Aging Neurosci, 2013
Personalized medicine uses various individual characteristics to guide medical decisions.
[Clinical and prognostic significance of genetic markers in craniocerebral injury (Part III)].
Potapov et al., In Vopr Neirokhir, 2013
The first part of the review by Potapov et al. (201 0) [2] was devoted to the role of apolipoprotein E (apoE) gene polymorphism in CCI, the second one [3]- to the role of inflammation and immune response genes in the course and outcome of CCI.
Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease.
Amouyel et al., In Nat Genet, 2013
In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10(-8)) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.
Integrative genomics identifies APOE ε4 effectors in Alzheimer's disease.
Abeliovich et al., New York City, United States. In Nature, 2013
Late-onset Alzheimer's disease (LOAD) risk is strongly influenced by genetic factors such as the presence of the apolipoprotein E ε4 allele (referred to here as APOE4), as well as non-genetic determinants including ageing.
share on facebooktweetadd +1mail to friends