Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Revision of the apolipoprotein E compensatory mechanism recruitment hypothesis.

Alzheimer's & dementia : the journal of the Alzheimer's Association - 1 Jul 2008

Han S Duke, Bondi Mark W

Abstract excerpt

The association between the apolipoprotein E epsilon4 allele and Alzheimer's disease (AD) is well-established. Functional neuroimaging research has supported a compensatory mechanism recruitment hypothesis whereby nondemented epsilon4 participants use additional cognitive resources to buffer against episodic memory declines in older age, a mechanism that is presumably associated with encroaching disease. However,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer Disease
Share to Apolipoprotein E4
Share to Brain

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genetic Predisposition to Disease

Source

Identifiers

PMID: 18631975
DOI: 10.1016/j.jalz.2008.02.006

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Revision of the apolipoprotein E compensatory mechanism recruitment hypothesis.PMID 18631975Read ↗

APOE moderates compensatory recruitment of neuronal resources during working memory processing in healthy older adults.Semantic proximity Read ↗

Cognitive and neural signatures of the APOE E4 allele in mid-aged adults.Semantic proximity Read ↗

Cognitive domain decline in healthy apolipoprotein E epsilon4 homozygotes before the diagnosis of mild cognitive impairment.Semantic proximity Read ↗

Better memory and neural efficiency in young apolipoprotein E epsilon4 carriers.Semantic proximity Read ↗

Genetic risk for Alzheimer's disease alters the five-year trajectory of semantic memory activation in cognitively intact elders.Semantic proximity Read ↗

Reduced functional brain activity response in cognitively intact apolipoprotein E epsilon4 carriers.Semantic proximity Read ↗

Increased brain activation during working memory in cognitively intact adults with the APOE epsilon4 allele.Semantic proximity Read ↗

Accelerated decline in apolipoprotein E-epsilon4 homozygotes with Alzheimer's disease.Semantic proximity Read ↗

fMRI evidence of compensatory mechanisms in older adults at genetic risk for Alzheimer disease.Semantic proximity Read ↗

Altered PET functional brain responses in cognitively intact elderly persons at risk for Alzheimer disease (carriers of the epsilon4 allele).Semantic proximity Read ↗

Working memory deficits in healthy APOE epsilon 4 carriers.Semantic proximity Read ↗

Verbal paired-associate learning by APOE genotype in non-demented older adults: fMRI evidence of a right hemispheric compensatory response.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.