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 Experiment Videos

Nicotinic treatment for cognitive dysfunction.

E D Levin1, A H Rezvani

  • 1Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710, USA. edlevin@duke.edu

Current Drug Targets. CNS and Neurological Disorders
|May 29, 2003
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Corrigendum to "Stickler A, Hawkey AB, Gondal A, Natarajan S, Mead M, Levin ED. Embryonic exposures to cadmium and PAHs cause long-term and interacting neurobehavioral effects in zebrafish" [Neurotoxicol Teratol. 2024 Mar-Apr;102:107339. doi: 10.1016/j.ntt.2024.107339. Epub 2024 Mar 6].

Neurotoxicology and teratology·2024
Same author

Corrigendum to "Paternal cannabis extract exposure in rats: Preconception timing effects on neurobehavioral effects in offspring" [Neurotoxicology 81 (2020) 180-188].

Neurotoxicology·2021
Same author

Long-term characterization of the Flinders Sensitive Line rodent model of human depression: Behavioral and PET evidence of a dysfunctional entorhinal cortex.

Behavioural brain research·2015
Same author

Developmental exposure to a complex PAH mixture causes persistent behavioral effects in naive Fundulus heteroclitus (killifish) but not in a population of PAH-adapted killifish.

Neurotoxicology and teratology·2015
Same author

Developmental exposure to organophosphate flame retardants causes behavioral effects in larval and adult zebrafish.

Neurotoxicology and teratology·2015
Same author

Neurotoxicity of FireMaster 550® in zebrafish (Danio rerio): Chronic developmental and acute adolescent exposures.

Neurotoxicology and teratology·2015
Same journal

Partial QSAR analysis of some selected natural inhibitors of FAAH suggests a working hypothesis for the development of endocannabinoid-based drugs.

Current drug targets. CNS and neurological disorders·2005
Same journal

Therapeutic perspectives of inhibitors of endocannabinoid degradation.

Current drug targets. CNS and neurological disorders·2005
Same journal

Pharmacological properties and therapeutic possibilities for drugs acting upon endocannabinoid receptors.

Current drug targets. CNS and neurological disorders·2005
Same journal

Cannabinoids: between neuroprotection and neurotoxicity.

Current drug targets. CNS and neurological disorders·2005
Same journal

From cannabis to endocannabinoids in multiple sclerosis: a paradigm of central nervous system autoimmune diseases.

Current drug targets. CNS and neurological disorders·2005
Same journal

Endocannabinoids in neuroimmunology and stress.

Current drug targets. CNS and neurological disorders·2005
See all related articles

Nicotinic medications, like transdermal nicotine, show promise for improving cognitive dysfunction in conditions such as Alzheimer's disease and ADHD. Animal studies reveal key brain regions and receptors involved in these cognitive benefits.

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Cognitive dysfunction, seen in Alzheimer's disease, schizophrenia, and ADHD, presents a significant therapeutic challenge.
  • Nicotine, a well-characterized compound, is being investigated for its potential in treating cognitive deficits.
  • Transdermal nicotine patches offer a safer alternative to traditional nicotine administration for therapeutic purposes.

Purpose of the Study:

  • To evaluate the efficacy of transdermal nicotine in improving attentional function in individuals with cognitive disorders and healthy adults.
  • To investigate the neurobehavioral mechanisms underlying nicotinic treatment of cognitive dysfunction using animal models.
  • To identify specific nicotinic receptors and neural pathways involved in working memory.

Main Methods:

  • Clinical trials assessing attentional function with transdermal nicotine in patients with Alzheimer's disease, schizophrenia, ADHD, and healthy controls.

Related Experiment Videos

  • Rat studies involving local infusions into the hippocampus and amygdala to examine effects on working memory.
  • Neurotransmitter system analysis, focusing on interactions between nicotinic, dopaminergic, and glutaminergic systems.
  • Main Results:

    • Transdermal nicotine significantly improved attentional function across all studied groups.
    • The hippocampus and amygdala were identified as critical brain regions mediating nicotinic effects on working memory.
    • Both alpha7 and alpha4beta2 nicotinic receptors were found to play a role in working memory function.

    Conclusions:

    • Nicotinic medications, particularly delivered via transdermal patches, demonstrate therapeutic potential for cognitive dysfunction.
    • Understanding the neural underpinnings, including specific receptors and brain regions, is crucial for developing targeted nicotinic treatments.
    • Further research into nicotinic mechanisms may lead to safer and more effective therapies for cognitive disorders.