Fat and lipid metabolism and the involvement of apolipoprotein E in Alzheimer's disease

Document Type

Book Chapter

Publication Title

Neurodegeneration and Alzheimer's Disease: The Role of Diabetes, Genetics, Hormones and Lifestyle


John Wiley and Sons


School of Medical and Health Sciences / Centre of Excellence for Alzheimer's Disease Research and Care




Hone, E., Lim, F., & Martins, I. J. (2019). Fat and lipid metabolism and the involvement of apolipoprotein E in Alzheimer's disease. In R. N. Martins, C. S. Brennan, B. Fernando, M. A. Brennan, & S. J. Fuller (Eds.), Neurodegeneration and Alzheimer's disease: The role of diabetes, genetics, hormones, and lifestyle (pp. 189-231). Available here


Cholesterol including lipids have been shunned in diets for many decades, due to the evidence that high cholesterol levels and a high intake of saturated fats are linked to cardiovascular disease. However, there are certain essential lipids such as the omega‐3 and omega‐6 fatty acids which the human body cannot synthesise and must be obtained through dietary means. Cholesterol is also an essential lipid, and the liver can produce more cholesterol when dietary intake is low. It is now known that dyslipidaemia, which can result from a number of factors, is associated with increased risk of Alzheimer's disease (AD). There is also a large body of evidence that the greatest genetic risk factor for developing AD is carriage of the ϵ4 allele of the apolipoprotein E gene(APOE), whereas carriage of the ϵ2 form is mildly protective. This is of relevance here as the apolipoprotein E protein (apoE) is not only a major lipid carrier, it is also involved in the clearance of the amyloid‐beta (Aβ) peptide from the brain. Disruptions to Aβ clearance are thought to be part of the initiating steps of AD pathogenesis. Following a brief description of lipid absorption and transport systems, the links between dietary lipid intake, dyslipidaemia, apoE function, and AD are discussed in this chapter.



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