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

Human cholinergic basal forebrain: chemoanatomy and neurologic dysfunction.

Elliott J Mufson1, Stephen D Ginsberg, Milos D Ikonomovic

  • 1Department of Neurological Sciences and Alzheimer's Disease Center, Rush Presbyterian-St. Luke's Medical Center, Tech 2000, 2242 West Harrison St., Suite 200, Chicago, IL 60612, USA. emufson@rush.edu

Journal of Chemical Neuroanatomy
|January 20, 2004
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

An open-source stereotaxic container with an integrated cutting guide for human brain fixation during magnetic resonance imaging and sectioning for histology.

bioRxiv : the preprint server for biology·2026
Same author

CNS-selective plasma p-tau217 accurately captures Alzheimer's disease pathology and progression.

medRxiv : the preprint server for health sciences·2026
Same author

Complex interplay of astrogliosis and pathology in preclinical Alzheimer's disease.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026
Same author

Frequency of mixed neuropathologies in individuals with down syndrome with and without Alzheimer's dementia.

Acta neuropathologica·2026
Same author

Psychometric criteria for superior cognitive performance in very old adults.

Journal of Alzheimer's disease : JAD·2026
Same author

Cerebrospinal fluid and frontal cortex TMPRSS2 and ACE2 protein levels differ in Down syndrome and Alzheimer's disease.

Acta neuropathologica communications·2026

The human cholinergic basal forebrain (CBF) is complex, with aging and Alzheimer's disease (AD) causing distinct cellular changes. Understanding these neurochemical alterations is key to addressing cognitive and attentional dysfunctions.

Area of Science:

  • Neuroscience
  • Neuroanatomy
  • Alzheimer's Disease Research

Background:

  • The human cholinergic basal forebrain (CBF) innervates key brain regions involved in cognition and attention.
  • Dysfunction of the CBF is implicated in Alzheimer's disease (AD).
  • CBF neurons exhibit diverse neurochemical phenotypes, including cholinergic markers, neurotrophic factors, and receptors.

Purpose of the Study:

  • To investigate the complex chemoanatomy of the human CBF.
  • To understand the role of various molecules within CBF neurons in aging and AD.
  • To elucidate the specific cellular changes occurring in the CBF during the progression of AD.

Main Methods:

  • Analysis of human autopsy material.
  • Examination of cholinergic markers, nerve growth factor (NGF) and its receptors, calbindin, glutamate receptors, and estrogen receptors (ERalpha, ERbeta).

Related Experiment Videos

  • Assessment of m2 muscarinic acetylcholine receptor (mAChRs), NADPH-diaphorase, GABA, calcium binding proteins, and galanin (GAL).

    • Main Results:

    • Age-related dissociation of calbindin and GluR2 suggests excitotoxic cell death mechanisms.
    • Choline acetyltransferase (ChAT) activity and neuron number are preserved/upregulated in early AD.
    • Reduced NGF receptor-containing neurons occur early in AD, indicating phenotypic changes rather than cell loss.
    • End-stage AD shows reduced trkA mRNA, suggesting a neurotrophic defect.

    Conclusions:

    • The human CBF exhibits complex chemoanatomy with diverse neuronal phenotypes.
    • Multiple factors contribute differentially to CBF dysfunction in aging and AD.
    • Neurotrophic defects and excitotoxicity are implicated in CBF alterations during AD progression.