Related Experiment Video
Updated: Aug 6, 2026
07:44
Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
Published on: October 6, 2017
Synaptic vulnerability in neurodegenerative disease
Thomas M Wishart1, Simon H Parson, Thomas H Gillingwater
1Centre for Integrative Physiology & Centre for Neuroscience Research, University of Edinburgh Medical School, UK.
Journal of Neuropathology and Experimental Neurology
|August 10, 2006
Summary
Synapses are crucial in neurodegenerative diseases. Protecting these vital neuronal connections offers a promising therapeutic target for slowing disease progression and managing symptoms.
Area of Science:
- Neuroscience
- Pathophysiology
- Synaptic Biology
Background:
- Neurodegenerative diseases involve neuronal loss in central and peripheral nervous systems.
- Synaptic compartments are increasingly recognized as critical in disease initiation and progression.
- Previous therapeutic strategies may have failed due to insufficient synaptic protection.
Purpose of the Study:
- To highlight the synapse as a key target for neuroprotection.
- To review evidence of common synaptic vulnerability across neurodegenerative diseases.
- To explore novel synaptoprotective strategies.
Main Methods:
- Review of human studies and animal models.
- Analysis of pathophysiological mechanisms at the synaptic level.
- Synthesis of current understanding of synaptic degeneration.
Main Results:
- Synaptic vulnerability is a common feature across multiple neurodegenerative diseases.
- Degenerative mechanisms are often localized to synapses.
- Understanding synaptic pathology is key to developing effective treatments.
Conclusions:
- The synapse is a critical therapeutic target for neurodegenerative diseases.
- Developing synaptoprotective strategies is essential for slowing disease progression.
- Targeting synaptic mechanisms offers a promising avenue for future treatments.
Related Concept Videos
01:24Parkinson Disease ll: Pathophysiology
Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
01:29Excitatory and Inhibitory Effects of Neurotransmitters
When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
01:26Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
01:26Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling 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...
01:15Parkinson's Disease: Overview
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...