Serum high density lipoprotein cholesterol in patients with abnormal coronary arteries

Tan, Meng H.; Macintosh, Wayne; Weldon, K. Laurence; Kapoor, Amar S.; Chandler, Brian M.; Hindmarsh, T

doi:10.1016/0021-9150(80)90004-0

Cited by 27 publications

(2 citation statements)

References 34 publications

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“…APOE is the ligand for the LDL receptor, LRP (LDL-related protein), and VLDL-receptor, all of which are preferentially expressed by neurons. Given its involvement in lipid transport, it is perhaps not surprising that the role for APOE as a disease gene was first recognized with respect to cardiovascular disease [ 64 – 66 ].…”

Section: Load Genesmentioning

confidence: 99%

The Genetics of Alzheimer’s Disease

Barber

2012

Scientifica

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Alzheimer's disease is a progressive, neurodegenerative disease that represents a growing global health crisis. Two major forms of the disease exist: early onset (familial) and late onset (sporadic). Early onset Alzheimer's is rare, accounting for less than 5% of disease burden. It is inherited in Mendelian dominant fashion and is caused by mutations in three genes (APP, PSEN1, and PSEN2). Late onset Alzheimer's is common among individuals over 65 years of age. Heritability of this form of the disease is high (79%), but the etiology is driven by a combination of genetic and environmental factors. A large number of genes have been implicated in the development of late onset Alzheimer's. Examples that have been confirmed by multiple studies include ABCA7, APOE, BIN1, CD2AP, CD33, CLU, CR1, EPHA1, MS4A4A/MS4A4E/MS4A6E, PICALM, and SORL1. Despite tremendous progress over the past three decades, roughly half of the heritability for the late onset of the disease remains unidentified. Finding the remaining genetic factors that contribute to the development of late onset Alzheimer's disease holds the potential to provide novel targets for treatment and prevention, leading to the development of effective strategies to combat this devastating disease.

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Section: Load Genesmentioning

confidence: 99%

The Genetics of Alzheimer’s Disease

Barber

2012

Scientifica

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“…Epidemiological studies in Western communities have suggested that the prevalence of clinical coronary artery disease in Western civilisation correlates positively with the plasma concentration of low density lipoproteins 1 , and negatively with high density lipoprotein concentration 2 . Assessment of coronary artery disease by angiographic studies has shown that the severity of lesions also correlates with increasing low density lipoprotein levels and decreasing high density lipoprotein levels 3 , 4 . There is heterogeneity within these classes of lipoproteins.…”

Section: Introductionmentioning

confidence: 99%

HDL subfractions and angiographically defined coronary artery disease

Thomas

Milne

Stocks

et al. 1987

Int J Clinical Practice

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Ninety eight patients (68 male, 30 female) were assessed with coronary angiography for suspected coronary artery disease. Total cholesterol, triglyceride, total HDL and the subfractions HDL2 and HDL3 and LDL were measured. A coronary index was derived to assess the severity of coronary artery disease. This was used to divide the patients into quartiles. In the quartile with the most severe disease the HDL2 level was lower (0.39 ± 0.3 compared to 0.65 ± 0.6 mmolll, p<0.04) and the LDL level was higher (5.25 ± 1.4 compared to 4.04 ± 1.32 mmolll, p < 0.002) in the quartile with the least severe disease.There was no relationship between the severity of coronary artery disease and HDL3 levels. Patterns of smoking behaviour, arterial blood pressure and body weight were all similar in each of the quartiles studied. It is concluded that high HDL2 levels are protective against the development of coronary artery disease.

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Symptomatic Coronary Artery Disease in a Marathon Runner

Gurewich¹

1983

JAMA

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Serum high density lipoprotein cholesterol in patients with abnormal coronary arteries

Cited by 27 publications

References 34 publications

The Genetics of Alzheimer’s Disease

The Genetics of Alzheimer’s Disease

HDL subfractions and angiographically defined coronary artery disease

Symptomatic Coronary Artery Disease in a Marathon Runner

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