Related Experiment Video
Updated: Jun 22, 2026
09:38
Generalized Psychophysiological Interaction (PPI) Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease
Published on: November 14, 2017
Association between ApoE epsilon4 and cognitive impairment after stroke
Jørgen Wagle1, Lasse Farner, Kjell Flekkøy
1Faculty of Medicine, University of Oslo, Oslo, Norway. jowagle@gmail.com
Dementia and Geriatric Cognitive Disorders
|June 5, 2009
Summary
The apolipoprotein E epsilon4 allele (ApoE ε4) is a significant risk factor for early cognitive impairment following a stroke. This genetic factor, along with stroke severity and pre-existing cognitive decline, contributes to post-stroke cognitive deficits.
Area of Science:
- Neurology
- Genetics
- Cognitive Science
Background:
- Understanding genetic contributions to post-stroke cognitive impairment remains incomplete.
- The apolipoprotein E epsilon4 allele (ApoE ε4) is investigated as a potential genetic risk factor.
Purpose of the Study:
- To determine if the ApoE ε4 allele is a risk factor for cognitive impairment in the early stages after stroke.
- To identify independent risk factors for post-stroke cognitive impairment.
Main Methods:
- 152 Norwegian stroke patients were assessed for cognitive impairment using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS).
- ApoE genotype, demographics, pre-stroke cognitive decline (IQCODE), stroke characteristics, and neurological impairment (NIHSS) were analyzed as potential risk factors.
- Multiple logistic regression was used to identify independent risk factors for cognitive impairment.
Main Results:
- ApoE ε4 was identified as an independent risk factor for post-stroke cognitive impairment (OR = 3.7).
- Other significant risk factors included pre-stroke cognitive reduction (IQCODE > 3.44, OR = 9.2), anterior stroke syndromes (OR = 3.2), and stroke severity (NIHSS > 5, OR = 7.3).
- No association was found between ApoE ε4 and pre-stroke cognitive decline (IQCODE).
Conclusions:
- The presence of one or two ApoE ε4 alleles is a significant independent risk factor for early cognitive impairment after stroke.
- Early identification of ApoE ε4 carriers may aid in predicting cognitive outcomes post-stroke.
Related Concept Videos
01:29Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
01:15Ischemic Stroke l: Introduction
Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
01:15Ischemic Stroke ll: Pathophysiology
An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
01:23Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
01:22Dementia l: Introduction
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
01:26Alzheimer's Disease: Overview
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...