Related Experiment Video
Updated: Aug 5, 2026
07:55
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
Published on: October 17, 2015
Apolipoprotein E, amyloid, and Alzheimer disease
K R Bales1, J C Dodart, R B DeMattos
1Neuroscience Discovery Research, Lilly Research Laboratories Indianapolis, IN 46285, USA.
Molecular Interventions
|March 3, 2004
Summary
Alzheimer disease research identifies apolipoprotein E (apoE) as a key factor. Understanding apoE
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Alzheimer disease (AD) remains a significant challenge, with effective long-term treatments still lacking.
- The molecular pathology of AD is increasingly understood, highlighting various contributing factors.
- Apolipoprotein E (apoE) is recognized as a significant genetic factor influencing AD risk and progression.
Purpose of the Study:
- To investigate the role of apolipoprotein E (apoE) in the molecular pathology of Alzheimer disease.
- To elucidate how different isoforms of apoE influence Alzheimer disease risk.
- To establish the importance of apoE's function in the brain for developing effective AD therapies.
Main Methods:
- This study focuses on the known roles and varying risks associated with different apolipoprotein E (apoE) isoforms.
- The research synthesizes existing data on apoE's function in the central nervous system.
- No new experimental methods were employed; this is a review and synthesis of current knowledge.
Main Results:
- Specific isoforms of apolipoprotein E (apoE) are clearly associated with varying levels of risk for Alzheimer disease.
- The diverse roles of apoE in brain function are critical for understanding disease mechanisms.
- Apolipoprotein E's function is central to the development of potential therapeutic strategies.
Conclusions:
- Apolipoprotein E (apoE) is a critical determinant of Alzheimer disease risk.
- Further understanding of apoE's functions in the brain is essential for advancing Alzheimer disease treatment.
- Targeting apoE pathways may offer promising therapeutic avenues for Alzheimer disease.
More Related Videos
Related Concept Videos
03:03Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
03:03Amyloid Fibrils
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining, normally used to...
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...
01:22Alzheimer's Disease: Treatment
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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...
01:23Alzheimer 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...