A Population Study of Alzheimer’s Disease: Findings From the Cache County Study on Memory, Health, and Aging

2005 ◽  
Vol 6 (2) ◽  
pp. 107-114 ◽  
Author(s):  
Joann T. Tschanz ◽  
Katherine Treiber ◽  
Maria C. Norton ◽  
Kathleen A. Welsh-Bohmer ◽  
Leslie Toone ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Oldest Old ◽  
Population Based ◽  
Apolipoprotein E Gene ◽  
Initial Cohort ◽  
Males And Females ◽  
Cache County

There are several population-based studies of aging, memory, and dementia being conducted worldwide. Of these, the Cache County Study on Memory, Health and Aging is noteworthy for its large number of “oldest-old” members. This study, which has been following an initial cohort of 5,092 seniors since 1995, has reported among its major findings the role of the Apolipoprotein E gene on modifying the risk for Alzheimer’s disease (AD) in males and females and identifying pharmacologic compounds that may act to reduce AD risk. This article summarizes the major findings of the Cache County study to date, describes ongoing investigations, and reports preliminary analyses on the outcome of the oldest-old in this population, the subgroup of participants who were over age 84 at the study’s inception.

Apolipoprotein E Phenotype Alone Does Not Influence Survival in Alzheimer’s Disease: A Population-Based Longitudinal Study

2000 ◽  
Vol 19 (6) ◽  
pp. 327-332 ◽  
Author(s):  
Anne M. Koivisto ◽  
Päivi Lempiäinen ◽  
Keijo Koivisto ◽  
Eeva-Liisa Helkala ◽  
Leena Mykkänen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Longitudinal Study ◽  
Apolipoprotein E ◽  
Population Based

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

2001 ◽  
Vol 67 ◽  
pp. 111-120 ◽  
Author(s):  
Simon Lovestone ◽  
Brian Anderton ◽  
Joanna Betts ◽  
Rejith Dayanandan ◽  
Graham Gibb ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Significant Advance ◽  
Cholesterol Transport ◽  
Vascular Risk ◽  
Polymorphic Variation ◽  
Gene Encoding ◽  
Single Mechanism ◽  
Apolipoprotein E Gene

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.

scholarly journals Cross‐omics studies of the role of apolipoprotein E in Alzheimer’s disease and dementia: Searching common pathways in patients, populations and cellular models

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Cornelia M. van Duijn ◽  
Shahzad Ahmad ◽  
María Eugenia Sáez ◽  
Keiryn Bennett ◽  
Alfredo Cabrera Socorro ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Apolipoprotein E ◽  
Cellular Models

scholarly journals Revisiting the Role of Insulin-Like Growth Factor-I Receptor Stimulating Activity and the Apolipoprotein E in Alzheimer’s Disease

2019 ◽  
Vol 11 ◽  
Author(s):  
Sara A. Galle ◽  
Ashley van der Spek ◽  
Madeleine L. Drent ◽  
Michael P. Brugts ◽  
Erik J. A. Scherder ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Growth Factor ◽  
Apolipoprotein E ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I
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