APOE status and its association to learning and memory performance in middle aged and older Norwegians seeking assessment for memory deficits

Wehling Eike, Lundervold, Standnes Brit, Gjerstad Leif, Reinvang, Reinvang Ivar

Description

We examined the hypothesis that deficits in learning, memory, and other cognitive functions are associated with the ε4 allele of the Apolipoprotein E (APOE) gene in a non-demented sample with memory complaints recruited from a population with a high prevalence of this allele. Methods The study group comprised 70 consecutively referred patients aged 50–75 seeking assessment due to memory complaints. They were screened for dementia, for neurological and psychiatric disease, and for cerebral infarction using Magnet Resonance Imaging (MRI). Participants were classified as non-demented based on clinical evaluation and results on cognitive tests. Results APOE ε4 carriers (56% of the sample) showed poorer performance than non-carriers on the Mini Mental State Examination, a number of measures of verbal memory function from the California Verbal Learning Test, and visual recall. In 46% of the participants, psychometric criteria for amnestic Mild Cognitive Impairment (aMCI) were satisfied. Conclusion Findings may be partly explained by a significant number of participants being in a preclinical phase of Alzheimer's disease. The observed deficits in learning performance and the lack of significant age modulation of the genetic association suggest a more general genetic effect. The findings are consistent with known neurobiological function of APOE ε4, including both increased risk of neurodegenerative disease and reduced synaptic integrity in older age.

Informations

• Publié par: biomed
• Publié le: 01 janvier 2007
• Nombre de lectures: 9
• Langue: English

Extrait

BioMed CentralBehavioral and Brain Functions
Open AccessResearch
APOE status and its association to learning and memory
performance in middle aged and older Norwegians seeking
assessment for memory deficits
1 1 3 4Eike Wehling* , Astri J Lundervold , Brit Standnes , Leif Gjerstad and
2Ivar Reinvang
1 2Address: Department of Biological and Medical Psychology, University of Bergen, Norway, Center for the study of human cognition, Department
3 4of Psychology, University of Oslo, Norway, Department of Neurology, Buskerud Hospital, Drammen, Norway and Department of Neurology,
Rikshospitalet University Hospital, Oslo, Norway
Email: Eike Wehling* - [e-mail]; Astri J Lundervold - [e-mail]; Brit Standnes -
[e-mail]; Leif Gjerstad - [e-mail]; Ivar Reinvang - [e-mail]
* Corresponding author
Published: 31 October 2007 Received: 24 January 2007
Accepted: 31 October 2007
Behavioral and Brain Functions 2007, 3:57 doi:10.1186/1744-9081-3-57
This article is available from: http://www.behavioralandbrainfunctions.com/content/3/1/57
© 2007 Wehling et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Background: We examined the hypothesis that deficits in learning, memory, and other cognitive
functions are associated with the ε4 allele of the Apolipoprotein E (APOE) gene in a non-demented
sample with memory complaints recruited from a population with a high prevalence of this allele.
Methods: The study group comprised 70 consecutively referred patients aged 50–75 seeking
assessment due to memory complaints. They were screened for dementia, for neurological and
psychiatric disease, and for cerebral infarction using Magnet Resonance Imaging (MRI). Participants
were classified as non-demented based on clinical evaluation and results on cognitive tests.
Results: APOE ε4 carriers (56% of the sample) showed poorer performance than non-carriers on
the Mini Mental State Examination, a number of measures of verbal memory function from the
California Verbal Learning Test, and visual recall. In 46% of the participants, psychometric criteria
for amnestic Mild Cognitive Impairment (aMCI) were satisfied.
Conclusion: Findings may be partly explained by a significant number of participants being in a
preclinical phase of Alzheimer's disease. The observed deficits in learning performance and the lack
of significant age modulation of the genetic association suggest a more general genetic effect. The
findings are consistent with known neurobiological function of APOE ε4, including both increased
risk of neurodegenerative disease and reduced synaptic integrity in older age.
which has been characterized by subjective memory com-Background
Alzheimer's disease (AD) is the most prevalent form of plaints and clinical criteria of cognitive impairment
withdementia in all age groups, with less than 1% incidence out being demented [2,3]. Memory may be the only
before age 65, but with an exponential increase with age cognitive function affected (amnestic MCI), but MCI may
[1]. Prior to diagnosis of AD many patients go through a also affect other cognitive domains in isolation or in
comclinical phase termed mild cognitive impairment (MCI), bination with memory impairment [3]. Patients with MCI
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