Related Experiment Video
Updated: Feb 23, 2026
07:44
Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
Published on: October 6, 2017
18.2K
Role of BACE1 in Alzheimer's synaptic function.
1Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue/NC30, Cleveland, OH 44195 USA.
Translational Neurodegeneration
|September 1, 2017
Summary
This review explores beta-secretase 1 (BACE1) synaptic functions. Understanding BACE1
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid plaques and neurofibrillary tangles.
- Accumulation of beta-amyloid peptides (Aβ) is a key early event in AD pathogenesis.
- Beta-site APP cleaving enzyme 1 (BACE1) is responsible for generating Aβ from amyloid precursor protein (APP).
Purpose of the Study:
- To review recent studies investigating the role of BACE1 in synaptic functions.
- To assess the potential impact of BACE1 inhibition on cognitive functions in Alzheimer's disease patients.
Main Methods:
- Literature review of recent scientific studies.
- Analysis of research on BACE1's physiological and pathological roles at synapses.
Main Results:
- BACE1 plays a significant role in normal synaptic function.
- Inhibition of BACE1 may have unintended consequences on cognition due to its role in synaptic plasticity.
Conclusions:
- BACE1 inhibition, while reducing Aβ, may affect cognitive functions.
- Further research is needed to understand the complex role of BACE1 at synapses to guide safe therapeutic strategies for Alzheimer's disease.
Related Concept Videos
01:26Alzheimer's Disease: Overview
1.8K
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...
1.8K
01:23Role of Neurotransmitters in Memory
2.7K
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...
2.7K
01:22Alzheimer's Disease: Treatment
1.1K
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...
1.1K
01:30Ligand-Gated Ion Channel Receptor: Gating Mechanism
4.3K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
4.3K
01:03Long-term Depression
3.5K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
Calcium Ion Concentration Mechanism
If over...
3.5K