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

Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

1.9K
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...
1.9K
Neural Regulation01:37

Neural Regulation

44.0K
Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
44.0K
Alzheimer's Disease: Treatment01:22

Alzheimer'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
Amyloid Fibrils03:03

Amyloid Fibrils

12.5K
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,...
12.5K
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

2.8K
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...
2.8K

You might also read

Related Articles

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

Sort by
Same author

Therapeutic targeting of fibrin-microglia interactions ameliorates Alzheimer's disease-related hyperexcitability and brain network dysfunction.

bioRxiv : the preprint server for biology·2026
Same author

Resilience to neuronal hyperactivity and restoration of the neuroimmune interactome by blocking fibrin-induced microglia activation in Alzheimers disease.

bioRxiv : the preprint server for biology·2026
Same author

Parvalbumin Neuron-Targeted Loss of Alzheimer's Disease Risk Gene <i>BIN1</i> Is Insufficient to Drive Cognitive or Network Excitability Changes.

eNeuro·2026
Same author

cGAS-mediated IFN-I signaling contributes to disease progression in drug-refractory epilepsy.

bioRxiv : the preprint server for biology·2026
Same author

Sleep-Wake Transitions Are Impaired in the <i>App</i> <sup>NL-G-F</sup> Mouse Model of Early Onset Alzheimer's Disease.

bioRxiv : the preprint server for biology·2026
Same author

Basic Science and Pathogenesis.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same journal

Boundary issues for multidimensional frameworks of representation.

Nature reviews. Neuroscience·2026
Same journal

Reply to 'Boundary issues for multidimensional frameworks of representation'.

Nature reviews. Neuroscience·2026
Same journal

Brain-spleen axis regulates learned fear.

Nature reviews. Neuroscience·2026
Same journal

Acetylcholine: a candidate substrate for hippocampal predictive learning?

Nature reviews. Neuroscience·2026
Same journal

Astrocytes viewed through the lens of their proteomes and subproteomes.

Nature reviews. Neuroscience·2026
Same journal

m<sup>6</sup>A in RNA: a key regulator of brain development, function and disease.

Nature reviews. Neuroscience·2026
See all related articles

Related Experiment Video

Updated: Mar 12, 2026

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
07:57

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

7.4K

Network abnormalities and interneuron dysfunction in Alzheimer disease.

Jorge J Palop1,2, Lennart Mucke1,2

  • 1Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, California 94158, USA.

Nature Reviews. Neuroscience
|November 11, 2016
PubMed
Summary
This summary is machine-generated.

Altered brain network activity and hypersynchrony are early indicators of Alzheimer disease (AD), appearing decades before symptoms. Modulating interneuron dysfunction may offer a therapeutic strategy for cognitive decline in AD.

More Related Videos

Visualizing Axonal Growth Cone Collapse and Early Amyloid &#946; Effects in Cultured Mouse Neurons
06:23

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

Published on: October 30, 2018

8.6K
Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

8.5K

Related Experiment Videos

Last Updated: Mar 12, 2026

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
07:57

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

7.4K
Visualizing Axonal Growth Cone Collapse and Early Amyloid &#946; Effects in Cultured Mouse Neurons
06:23

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

Published on: October 30, 2018

8.6K
Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
09:33

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

Published on: December 26, 2016

8.5K

Area of Science:

  • Neuroscience
  • Cognitive Science
  • Neurology

Background:

  • Neural circuit function relies on synchronized activity.
  • Hypersynchrony and altered rhythms are implicated in Alzheimer disease (AD) cognitive deficits.
  • Cognitive network alterations precede clinical AD onset by decades, predicting pathology.

Purpose of the Study:

  • To explore the role of interneuron dysfunction in AD-related cognitive abnormalities.
  • To investigate the potential of modulating network mechanisms for improving brain function in AD.

Main Methods:

  • Review of existing literature on neural synchrony, AD, and interneuron function.
  • Conceptual exploration of therapeutic targets for cognitive dysfunction in AD.

Main Results:

  • Network hypersynchrony and altered oscillatory activity are linked to cognitive impairment in AD.
  • Interneuron dysfunction is a potential mechanism underlying cognitive deficits in AD and related disorders.

Conclusions:

  • Modulating interneuron dysfunction and network abnormalities presents a potential therapeutic avenue for AD.
  • Early network alterations in AD offer insights into disease progression and potential interventions.