Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Alzheimer Disease ll: Pathophysiology

Alzheimer 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...

Parkinson Disease ll: Pathophysiology

Parkinson 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...

Alzheimer Disease l: Introduction

Alzheimer 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...

Excitatory and Inhibitory Effects of Neurotransmitters

Excitatory 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...

Parkinson's Disease: Overview

Parkinson'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...

Long-term Depression

Long-term Depression

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 time, all...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Conformational Switch in the Alpha-Synuclein C-Terminal Domain Directs Its Fibril Polymorphs.

Chemistry (Weinheim an der Bergstrasse, Germany)·2025

Same author

Decreased hepatic enzymes reflect the decreased vitamin B6 levels in Parkinson's disease patients.

Pharmacology research & perspectives·2024

Same author

Lysophagy protects against propagation of α-synuclein aggregation through ruptured lysosomal vesicles.

Proceedings of the National Academy of Sciences of the United States of America·2023

Same author

Involvement of Mitochondria in Parkinson's Disease.

International journal of molecular sciences·2023

Same author

Phosphatidylinositol-3,4,5-trisphosphate interacts with alpha-synuclein and initiates its aggregation and formation of Parkinson's disease-related fibril polymorphism.

Acta neuropathologica·2023

Same author

A Cross-Trait Genetic Correlation Study Identified Eight Diseases and Traits Associated with Psoriasis.

The Journal of investigative dermatology·2023

Search research articles

Related Experiment Video

Updated: May 9, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Neurodegenerative changes initiated by presynaptic dysfunction.

Toru Yasuda¹, Yasuto Nakata, Chi-Jing Choong

¹Department of Neurology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. hmochizuki@neurol.med.osaka-u.ac.jp.

Translational Neurodegeneration

|August 8, 2013

Summary

Presynaptic dysfunction may initiate neurodegenerative diseases like Parkinson's and dementia with Lewy bodies. Abnormal alpha-synuclein (αSyn) accumulation in presynaptic terminals could trigger neuronal death.

More Related Videos

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Published on: August 16, 2020

Related Experiment Videos

Last Updated: May 9, 2026

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Studying Pre-formed Fibril Induced α-Synuclein Accumulation in Primary Embryonic Mouse Midbrain Dopamine Neurons

Published on: August 16, 2020

Area of Science:

Neuroscience
Neuropathology
Molecular Biology

Background:

α-Synucleinopathies, including Parkinson's disease (PD) and dementia with Lewy bodies (DLB), are characterized by α-synuclein (αSyn) aggregates.
Over 90% of αSyn aggregates in DLB occur as small deposits in presynaptic terminals.
Mechanisms driving abnormal αSyn presynaptic accumulation remain largely unknown.

Purpose of the Study:

To review recent findings on the role of presynaptic dysfunction in initiating neuronal changes.
To explore the potential of presynaptic failure as a trigger for neurodegenerative processes.

Main Methods:

Literature review of recent research findings.
Analysis of studies focusing on α-synuclein aggregation and neuronal pathways.

Main Results:

Presynaptic terminals are a primary site for αSyn aggregation in DLB.
Evidence suggests presynaptic dysfunction precedes broader neuronal degeneration.
αSyn accumulation at presynapses may disrupt normal neuronal function.

Conclusions:

Presynaptic dysfunction is implicated in the early stages of α-synucleinopathies.
Failure at the presynapse may act as a critical trigger for dying-back neuronal death.
Targeting presynaptic mechanisms could offer new therapeutic strategies for neurodegenerative diseases.