Related Experiment Video
Updated: Jun 14, 2025

07:55
Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
Published on: October 17, 2015
11.8K
Apolipoprotein E in Alzheimer's Disease: Focus on Synaptic Function and Therapeutic Strategy
Longjie Qu1, Shuai Xu2, Zhen Lan1
1Department of Neurology, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, 210008, China.
Molecular Neurobiology
|August 30, 2024
Summary
Alzheimer
Area of Science:
- Neuroscience
- Genetics
- Pathology
Background:
- Synaptic dysfunction is an early indicator of Alzheimer's disease (AD), preceding amyloid plaques and neurofibrillary tangles.
- The apolipoprotein E (APOE) gene, particularly the ε4 allele, is the primary genetic risk factor for sporadic AD.
- APOE4 is known to accelerate the progression of beta-amyloid and tau pathologies in AD.
Purpose of the Study:
- To elucidate the mechanisms by which APOE isoforms modulate synaptic function.
- To explore the therapeutic potential of targeting APOE4 for Alzheimer's disease treatment.
Main Methods:
- Review and synthesis of recent studies on APOE and synaptic function.
- Analysis of pathways affected by different APOE isoforms.
Main Results:
- APOE isoforms differentially affect synaptic function through various molecular pathways.
- Targeting APOE4 presents a promising therapeutic strategy for AD.
Conclusions:
- Understanding APOE's role in synaptic modulation is crucial for AD pathogenesis.
- Interventions targeting APOE4 may offer a novel approach to treating Alzheimer's disease.
Related Concept Videos
Alzheimer's Disease: Treatment
170
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...
170
Alzheimer's Disease: Overview
454
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...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
454
Role of Neurotransmitters in Memory
485
Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
485
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
110
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
110
Amyloid Fibrils
9.3K
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,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
9.3K

