Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

381
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
381
Biological Causes of Schizophrenia01:29

Biological Causes of Schizophrenia

111
Schizophrenia, a severe psychiatric disorder, arises from a complex interplay of biological factors, including genetic predisposition, structural brain abnormalities, neurotransmitter dysregulation, and developmental irregularities. These factors collectively contribute to the onset and progression of the disorder, which typically manifests in late adolescence or early adulthood.
Genetic Factors in Schizophrenia
The genetic basis of schizophrenia is strongly supported by family and twin...
111
Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

801
Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within...
801
Negative and Cognitive Symptoms of Schizophrenia01:30

Negative and Cognitive Symptoms of Schizophrenia

104
Negative symptoms of schizophrenia indicate a reduction or absence of typical behaviors and emotional responses found in healthy individuals, while positive symptoms reflect an excess or distortion of normal functioning.
Negative Symptoms
Negative symptoms of schizophrenia manifest as deficits in normal emotional and behavioral functioning, profoundly impacting daily life. Individuals with schizophrenia often display a flat affect, characterized by a near-total absence of emotional expression,...
104
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

1.5K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
1.5K
Schizophrenia01:17

Schizophrenia

177
Schizophrenia, a term introduced by Swiss psychiatrist Eugen Bleuler in 1911, describes a severe psychological disorder marked by profound disruptions in attention, thought processes, language, emotion, and interpersonal relationships. The core feature of schizophrenia is psychosis — a state characterized by a fundamental detachment from reality. This disconnection manifests through distorted logic, impaired perception, and atypical behavior, severely affecting the lives of those...
177

You might also read

Related Articles

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

Sort by
Same author

A Qualitative Study of Family Experiences of the Peer Supported Family Intervention, Psychosis Recovery by Enabling Adult Carers at Home (Psychosis REACH), in an Early Psychosis Clinic.

Early intervention in psychiatry·2026
Same author

Comparison of adenoma and gland hyperplasia on bone mineral density in primary hyperparathyroidism.

Journal of clinical densitometry : the official journal of the International Society for Clinical Densitometry·2026
Same author

Combining post-mortem and neuroimaging measures of brain amyloidosis to accelerate genomic discovery.

Brain : a journal of neurology·2026
Same author

Co-expression-based models improve eQTL predictions for transcriptome-wide association studies and highlight new schizophrenia-associated genes.

Nature genetics·2026
Same author

Peripheral complement C4 protein in schizophrenia: Association with gene copy number and immune cell subtypes.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Latent brain state dynamics predict early amyloid accumulation and cognitive impairment.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Aug 6, 2025

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra
05:14

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra

Published on: September 8, 2021

3.6K

Reductions in synaptic marker SV2A in early-course Schizophrenia.

Jong H Yoon1, Zhener Zhang1, Elizabeth Mormino2

  • 1Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine and VA Palo Alto Health Care System, Palo Alto, CA, USA.

Journal of Psychiatric Research
|March 19, 2023
PubMed
Summary
This summary is machine-generated.

Early-stage schizophrenia patients show significant synaptic deficits, mirroring findings in chronic cases. This supports excess synaptic pruning as a key mechanism in schizophrenia development and progression.

Keywords:
PET ImagingSchizophreniaSynapses

More Related Videos

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density
09:10

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density

Published on: July 22, 2022

3.4K
An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
09:33

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

Published on: June 26, 2018

7.6K

Related Experiment Videos

Last Updated: Aug 6, 2025

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra
05:14

Standardized Data Acquisition for Neuromelanin-Sensitive Magnetic Resonance Imaging of the Substantia Nigra

Published on: September 8, 2021

3.6K
DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density
09:10

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density

Published on: July 22, 2022

3.4K
An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins
09:33

An Optical Assay for Synaptic Vesicle Recycling in Cultured Neurons Overexpressing Presynaptic Proteins

Published on: June 26, 2018

7.6K

Area of Science:

  • Neuroscience
  • Psychiatry
  • Radiology

Background:

  • Excessive synaptic pruning during neurodevelopment is a leading hypothesis for schizophrenia.
  • Synaptic deficits may be present early in schizophrenia, before formal diagnosis.
  • The novel synaptic marker [11C]UCB-J allows in vivo assessment of synaptic density.

Purpose of the Study:

  • To investigate synaptic density in early-course schizophrenia using [11C]UCB-J positron emission tomography (PET).
  • To determine if synaptic deficits observed in chronic schizophrenia patients are also present in early stages of the illness.

Main Methods:

  • 18 subjects (9 early-course schizophrenia, 9 healthy controls) underwent [11C]UCB-J PET scans.
  • Non-displaceable specific binding (BPND) was quantified in predefined brain regions of interest (ROIs).
  • Statistical analyses compared BPND between groups and correlated findings with cognitive performance and delusion severity.

Main Results:

  • Significant reductions in [11C]UCB-J binding were observed in multiple brain regions in early-course schizophrenia patients.
  • These reductions were widespread, confirmed by atlas-wide analyses.
  • Higher synaptic binding correlated positively with cognitive function and negatively with delusion severity.

Conclusions:

  • Extensive synaptic binding deficits are present in early-course schizophrenia, replicating findings in chronic patients.
  • These results reinforce the role of excess synaptic pruning as a core mechanism in schizophrenia.
  • Synaptic deficits are a reliable and reproducible biomarker in schizophrenia across illness stages.