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

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...

Amyloid Fibrils

Amyloid Fibrils

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,...

You might also read

Related Articles

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

Sort by

Same author

Mitochondrial oxidative stress promotes the accumulation of advanced glycation end products.

PloS one·2026

Same author

How Do Amyloid Pathology and Aberrant Neuronal Activity Disrupt Plasticity and Memory in Alzheimer's Disease?

The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry·2026

Same author

PINK1-dependent NFKB signaling contributes to amyloid pathology in Alzheimer disease.

Autophagy·2025

Same author

Functional Connectivity Favors Aberrant Visual Network c-Fos Expression Accompanied by Cortical Synapse Loss in a Mouse Model of Alzheimer's Disease.

Journal of Alzheimer's disease : JAD·2024

Same author

Synaptic mitochondria glycation contributes to mitochondrial stress and cognitive dysfunction.

Brain : a journal of neurology·2024

Same author

Methionine oxidation of clusterin in Alzheimer's disease and its effect on clusterin's binding to beta-amyloid.

Neuroscience letters·2024

Same journal

Vestibular function drives gaze stability in locomoting macaques.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026

Same journal

Region- and layer-specific glutamatergic synapse development in the nascent cortical hierarchy.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026

Same journal

Endogenous peptide derived from c-Cbl-associated protein counteracts its inhibitory effect on enteric neural crest cell colonization in Hirschsprung disease.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026

Same journal

Drowsiness alters the neural dynamics but not the core computations of multisensory integration.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026

Same journal

A Matter of Parameters: Tailored Transcranial Focused Ultrasound Enhances Cortico-Thalamo-Cortical Circuit Resonance.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026

Same journal

Proactive visual and motor prioritization differentially scale with cue reliability.

The Journal of neuroscience : the official journal of the Society for Neuroscience·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Jul 9, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

Amyloid Pathology Impairs Experience-Dependent Inhibitory Synaptic Plasticity.

Suraj Niraula¹, Shirley ShiDu Yan^1,2, Jaichandar Subramanian³

¹Department of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, Kansas 66045.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|December 5, 2023

Summary

This summary is machine-generated.

Alzheimer's disease impairs inhibitory synapse adaptation to visual changes, unlike in healthy brains. Synapse loss patterns differ, indicating altered responses to neuronal activity shifts in amyloidosis.

Keywords:

Alzheimer’s disease clustered synaptic plasticity homeostatic plasticity in vivo imaging inhibitory synapse neuronal hyperactivity

More Related Videos

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

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

Related Experiment Videos

Last Updated: Jul 9, 2025

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

Published on: October 30, 2018

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

Area of Science:

Neuroscience
Synaptic Plasticity
Alzheimer's Disease Research

Background:

Alzheimer's disease (AD) is linked to abnormal brain activity and imbalanced neuronal connections.
Amyloid pathology, a hallmark of AD, may affect synaptic structure and function.
Understanding how AD impacts synaptic adaptation to experience is crucial for therapeutic development.

Purpose of the Study:

To investigate how amyloid pathology affects the structural dynamics of excitatory and inhibitory synapses.
To determine if amyloid pathology alters synaptic adaptation to changes in visual experience in vivo.
To compare synaptic adaptation mechanisms in amyloidosis models versus nonpathological conditions.

Main Methods:

Utilized multicolor two-photon microscopy for in vivo imaging of synapses.
Studied synaptic structural dynamics in mouse models of amyloidosis.
Assessed synaptic adaptation to visual deprivation in both pathological and nonpathological states.

Main Results:

Baseline dynamics of mature excitatory and inhibitory synapses were unaffected by amyloidosis.
Amyloidosis prevented the typical loss of inhibitory synapses during visual deprivation.
Synapse loss distribution differed, with non-clustered loss observed in amyloidosis, suggesting impaired adaptation.

Conclusions:

Amyloid pathology does not alter baseline synaptic dynamics or adaptation of excitatory synapses to visual deprivation.
Visual deprivation fails to induce inhibitory synapse loss in the amyloidosis model, unlike in controls.
Amyloidosis impairs the adaptive response of inhibitory synapses to altered excitatory activity, evidenced by non-clustered synapse loss.