Apolipoprotein E gene and Alzheimer's disease: is tau the link?

TY - CHAP

T1 - Apolipoprotein E gene and Alzheimer's disease: is tau the link?

AU - ONeill, C

AU - Betts, J

AU - Dayanadan, R

AU - Gibb, G

AU - Ljungberg, C

AU - Pearce, J

A2 - Anderton, B

PY - 2001

Y1 - 2001

N2 - The finding that APOE (the gene encoding apolipoprotein E) polymorphic variation was associated with an altered risk of developing Alzheimer's disease (AD) was a significant advance and immediately prompted a search for the mechanisms responsible for this alteration. Some 6 years later, a number of different hypotheses remain that might account for this influence on pathogenesis with no single mechanism being unequivocally accepted. The different approaches to understanding these mechanisms can be broadly categorized as: those suggesting a remote effect, such as different rates of vascular risk factors in those with the different APOE alleles; those proposing altered neuronal vulnerability, perhaps due to apolipoprotein E (ApoE)-isoform-specific differences in local cholesterol transport; and those hypotheses postulating an ApoE interaction with the two key lesions of AD, plaques and tangles. In this chapter we will review the evidence for and against an interaction between ApoE and the neuronal cytoskeleton, in particular with the microtubule-associated protein tau.

AB - The finding that APOE (the gene encoding apolipoprotein E) polymorphic variation was associated with an altered risk of developing Alzheimer's disease (AD) was a significant advance and immediately prompted a search for the mechanisms responsible for this alteration. Some 6 years later, a number of different hypotheses remain that might account for this influence on pathogenesis with no single mechanism being unequivocally accepted. The different approaches to understanding these mechanisms can be broadly categorized as: those suggesting a remote effect, such as different rates of vascular risk factors in those with the different APOE alleles; those proposing altered neuronal vulnerability, perhaps due to apolipoprotein E (ApoE)-isoform-specific differences in local cholesterol transport; and those hypotheses postulating an ApoE interaction with the two key lesions of AD, plaques and tangles. In this chapter we will review the evidence for and against an interaction between ApoE and the neuronal cytoskeleton, in particular with the microtubule-associated protein tau.

M3 - Conference paper

SN - 1-85578-133-6

T3 - BIOCHEMICAL SOCIETY SYMPOSIUM

SP - 111

EP - 120

BT - BIOCHEM SOC SYMPOSIUM

PB - PORTLAND PRESS LTD

CY - LONDON

T2 - Annual Symposium of the Biochemical-Society

Y2 - 1 January 2001

ER -