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

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.

You might also read

Related Articles

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

Sort by

Same author

Synucleins in Neural Physiology: Understanding Endogenous Function to Better Contextualize Pathology.

Annual review of neuroscience·2026

Same author

Two-photon 3D imaging of optically stimulated neural activity at 100 Hz.

Light, science & applications·2026

Same author

Targeting immune cells in the aged brain reveals that engineered cytokine IL-10 enhances neurogenesis and improves cognition.

Immunity·2026

Same author

Aged circulating CD8<sup>+</sup> T cells and their secreted factors drive cognitive decline.

Immunity·2026

Same author

Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Same author

Ultrasensitive measurement of brain penetration mechanics and blood vessel rupture with microscale probes.

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

Search research articles

Related Experiment Video

Updated: Jan 6, 2026

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

Neuronal O-GlcNAcylation Improves Cognitive Function in the Aged Mouse Brain.

Elizabeth G Wheatley¹, Eddy Albarran², Charles W White¹

¹Department of Anatomy, University of California, San Francisco, San Francisco, CA 94143, USA; Developmental and Stem Cell Biology Graduate Program, University of California, San Francisco, San Francisco, CA 94143, USA.

Current Biology : CB

|October 8, 2019

Summary

Boosting O-linked N-Acetylglucosamine (O-GlcNAc) levels rejuvenates cognitive function in aging brains. This study identifies O-GlcNAcylation as a key molecular target for reversing age-related cognitive decline.

Keywords:

O-GlcNAcylation OGT aging brain cognition hippocampus rejuvenation synaptic plasticity

More Related Videos

A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration

A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration

Published on: February 27, 2018

Barnes Maze Testing Strategies with Small and Large Rodent Models

Barnes Maze Testing Strategies with Small and Large Rodent Models

Published on: February 26, 2014

Related Experiment Videos

Last Updated: Jan 6, 2026

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

A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration

A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration

Published on: February 27, 2018

Barnes Maze Testing Strategies with Small and Large Rodent Models

Barnes Maze Testing Strategies with Small and Large Rodent Models

Published on: February 26, 2014

Area of Science:

Neuroscience
Molecular Biology
Aging Research

Background:

The aging brain exhibits cellular and cognitive decline, particularly in regions like the hippocampus.
O-linked N-Acetylglucosamine (O-GlcNAc) is a post-translational modification implicated in synaptic function and neurodegeneration.
The role of O-GlcNAc in physiological brain aging is not well understood.

Purpose of the Study:

To investigate the role of O-GlcNAc transferase (OGT) and O-GlcNAcylation in age-related cognitive impairments.
To determine if modulating O-GlcNAc levels can reverse cognitive decline in aged mice.

Main Methods:

Utilized a neuron-specific conditional knockout mouse model to abrogate OGT expression, mimicking aging.
Employed viral-mediated gene transfer to overexpress OGT in hippocampal neurons of young and aged mice.
Assessed cognitive functions including spatial learning, memory, and associative fear memory.

Main Results:

Decreased OGT expression and O-GlcNAcylation correlate with cognitive impairments in aged mice.
Abrogating OGT in young mice recapitulated age-related cognitive and cellular deficits.
Overexpressing OGT in aged mice partially rescued spatial learning, memory, and associative fear memory deficits.

Conclusions:

O-GlcNAcylation is a critical molecular mediator of cognitive function in the aging brain.
Modulating OGT expression and O-GlcNAc levels offers a potential therapeutic strategy for cognitive rejuvenation.