This paper aims to give further insights into Alzheimer's disease (AD), a devastating neurodegenerative disorder which accounts for 60‐80 per cent of late‐onset dementia. AD is genetically complex where three genes are known to cause the early‐onset familial form of disease and ten genes have been identified to contribute to the risk of developing late‐onset sporadic AD.
The paper discusses the recently identified AD susceptibility loci and outlines the various hypotheses of how these loci and the pathways in which they function may elucidate the aetiology and pathogenesis of sporadic late‐onset AD.
The loci identified to increase susceptibility to sporadic AD are not random, but instead point to defects in specific biological processes and pathways that contribute to the development of the disease. These include impairments in: innate/adaptive immunity, specifically inflammation and the complement system; endocytosis/intracellualar trafficking, which includes the internalisation of material from the cell surface and the mechanisms by which molecules are transported; and lipid processing. High levels of lipids such as cholesterol have been associated with development of AD in later life.
The paper highlights that determining the function of the known susceptibility loci, and establishing how they increase risk for AD will aid in the development of new treatments.
CitationDownload as .RIS
Emerald Group Publishing Limited
Copyright © 2012, Emerald Group Publishing Limited