Role of apolipoprotein E in neurodegenerative diseases

Giau, Vo Van; Bagyinszky, Eva; An, Seong Soo A.; Kim, SangYun

doi:10.2147/ndt.s84266

Cited by 138 publications

(73 citation statements)

References 173 publications

(136 reference statements)

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“…This causes delayed clearance of remnant lipoproteins and results in increased triglyceride and cholesterol levels (Havel and Kane 1973; Mahley and Rall 2000). Hyperlipoproteinemia III (HLP III), a genetic lipid disorder, is characterised by an accumulation of remnant lipoproteins in the plasma, leading to the development of premature atherosclerosis, and virtually all patients with HLP III are ε2 homozygotes (Giau et al 2015). Despite causing increased cholesterol levels, ApoE2 may be protective in atherosclerosis as it is associated with lower LDL levels (Davignon et al 1988; Elosua et al 2004; Huang 2010).…”

Section: Biological Function Of Apoementioning

confidence: 99%

The Neurobiology and Age-Related Prevalence of the ε4 Allele of Apolipoprotein E in Alzheimer’s Disease Cohorts

et al. 2016

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterised by amyloid beta (Aβ) plaques and tau neurofibrillary tangles in the brain. Human apolipoprotein E (ApoE) is a lipid transport protein coded by the polymorphic APOE gene, with three major alleles: ε2, ε3 and ε4. After age, the ε4 allele is the greatest risk factor for developing sporadic AD, conferring an increased risk of 3–4 and 8–12 times for one or two copies of the allele, respectively. This risk is reported to vary by demographic factors including sex, ethnicity and geography. In order to understand the risk of ApoE ε4 in relation to age, the primary risk factor for developing AD, we need to understand how the prevalence of APOE genotypes changes with age. Here, we present the first data on age-related prevalence of APOE ε4 in AD in three AD cohorts in Australia and the USA. There is a significant association between age and ε4 prevalence, particularly for ε4 homozygotes, such that as age increases the prevalence of ε4 decreases. Further studies on a random, population-based sample of the population are needed to provide more generalizable data, particularly in the >90-year-old age group.

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Section: Biological Function Of Apoementioning

confidence: 99%

The Neurobiology and Age-Related Prevalence of the ε4 Allele of Apolipoprotein E in Alzheimer’s Disease Cohorts

et al. 2016

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“…Previously it has been reported that in many NDs, oxidative damage to protein-coding or non-coding RNA potentially causes dysregulation of gene expression and oxidative RNA damage described in many NDs including AD and PD [63]. The apolipoprotein E (APOE) gene, encodes a 299 amino acids long glycoprotein and located on chromosome 19 is estimated to be the major genetic factor in AD (up to 50%) and also reported in case of PD [64]. The similarities in the pathogenesis of NDs suggest that certain genes can be targeted for intervention of multiple NDs [65].…”

Section: Commonalities In Neurodegenerative Diseasesmentioning

confidence: 99%

Commonalities in Biological Pathways, Genetics, and Cellular Mechanism between Alzheimer Disease and Other Neurodegenerative Diseases: An In Silico-Updated Overview

Ahmad

Baig

Mushtaq

et al. 2017

CAR

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Background Alzheimer's disease (AD) is the most common and well-studied neurodegenerative disease (ND). Biological pathways, pathophysiology and genetics of AD show commonalities with other NDs viz. Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), Prion disease and Dentatorubral-pallidoluysian atrophy (DRPLA). Many of the NDs, sharing the common features and molecular mechanisms suggest that pathology may be directly comparable and be implicated in disease prevention and development of highly effective therapies. Method In this review, a brief description of pathophysiology, clinical symptoms and available treatment of various NDs have been explored with special emphasis on AD. Commonalities in these fatal NDs provide support for therapeutic advancements and enhance the understanding of disease manifestation. Conclusion The studies concentrating on the commonalities in biological pathways, cellular mechanisms and genetics may provide the scope to researchers to identify few novel common target(s) for disease prevention and development of effective common drugs for multi-neurodegenerative diseases.

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“…In addition to its important role in lipid and cholesterol metabolism (Wang and Eckel, 2014), apoE has also been implicated in the physiopathology of many neurological diseases (Giau et al, 2015; Mahley, 2016). For example, the gene dosage of the APOE4 allele is associated with increasing risk and early onset of Alzheimer's disease (Toops et al, 2016; Zhu et al, 2015; Huang et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein E as a novel therapeutic neuroprotection target after traumatic spinal cord injury

Cheng

Zheng

et al. 2018

Experimental Neurology

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Apolipoprotein E (apoE), a plasma lipoprotein well known for its important role in lipid and cholesterol metabolism, has also been implicated in many neurological diseases. In this study, we examined the effect of apoE on the pathophysiology of traumatic spinal cord injury (SCI). ApoE-deficient mutant (apoE−/−) and wild-type mice received a T9 moderate contusion SCI and were evaluated using histological and behavioral analyses after injury. At 3 days after injury, the permeability of spinal cord-blood-barrier, measured by extravasation of Evans blue dye, was significantly increased in apoE−/− mice compared to wild type. The inflammation and spared white matter was also significantly increased and decreased, respectively, in apoE−/− mice compared to the wild type ones. The apoptosis of both neurons and oligodendrocytes was also significantly increased in apoE−/− mice. At 42 days after injury, the inflammation was still robust in the injured spinal cord in apoE−/− but not wild type mice. CD45+ leukocytes from peripheral blood persisted in the injured spinal cord of apoE−/− mice. The spared white matter was significantly decreased in apoE−/− mice compared to wild type ones. Locomotor function was significantly decreased in apoE−/− mice compared to wild type ones from week 1 to week 8 after contusion. Treatment of exogenous apoE mimetic peptides partially restored the permeability of spinal cord-blood-barrier in apoE−/− mice after SCI. Importantly, the exogenous apoE peptides decreased inflammation, increased spared white matter and promoted locomotor recovery in apoE−/− mice after SCI. Our results indicate that endogenous apoE plays important roles in maintaining the spinal cord-blood-barrier and decreasing inflammation and spinal cord tissue loss after SCI, suggesting its important neuroprotective function after SCI. Our results further suggest that exogenous apoE mimetic peptides could be a novel and promising neuroprotective reagent for SCI.

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Role of apolipoprotein E in neurodegenerative diseases

Cited by 138 publications

References 173 publications

The Neurobiology and Age-Related Prevalence of the ε4 Allele of Apolipoprotein E in Alzheimer’s Disease Cohorts

The Neurobiology and Age-Related Prevalence of the ε4 Allele of Apolipoprotein E in Alzheimer’s Disease Cohorts

Commonalities in Biological Pathways, Genetics, and Cellular Mechanism between Alzheimer Disease and Other Neurodegenerative Diseases: An In Silico-Updated Overview

Apolipoprotein E as a novel therapeutic neuroprotection target after traumatic spinal cord injury

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