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

Enzyme-linked Receptors01:00

Enzyme-linked Receptors

64.6K
Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
64.6K
Notch Signaling Pathway03:14

Notch Signaling Pathway

4.6K
The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...
4.6K

You might also read

Related Articles

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

Sort by
Same author

Overcoming the diagnostic gap in mild cognitive impairment in Parkinson's disease: a pilot study employing a machine learning-/augmented reality-based digital biomarker.

Frontiers in aging neuroscience·2026
Same author

Stem Cell Therapy for Parkinson's Disease: A Mechanistically Distinct Role for Muse Cells.

Journal of clinical medicine·2026
Same author

Promoting Research Excellence in Down Syndrome: Proceedings of the 5th International Conference of the Trisomy 21 Research Society.

Neuromolecular medicine·2026
Same author

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

Acta neuropathologica·2026
Same author

Associations of plasma biomarkers with age in the presenilin-1 E280A autosomal dominant Alzheimer's disease kindred.

The journal of prevention of Alzheimer's disease·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

Related Experiment Video

Updated: May 3, 2026

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells
06:38

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

Published on: March 7, 2025

1.1K

Nerve growth factor metabolic dysfunction in Down's syndrome brains.

M Florencia Iulita1, Sonia Do Carmo, Alison K Ower

  • 11 Department of Pharmacology and Therapeutics, McGill University, 3655 Sir-William-Osler Promenade, Montreal, H3G1Y6, Canada.

Brain : a Journal of Neurology
|February 13, 2014
PubMed
Summary

Down syndrome brains show impaired Nerve Growth Factor (NGF) precursor maturation and increased degradation, impacting cholinergic neuron support. These NGF metabolic issues may be treatable in fetal Down syndrome cortex cultures.

Keywords:
Alzheimer’s diseaseDown’s syndromebasal forebrain cholinergic neuronsmatrix metallo-protease 9proNGF

More Related Videos

Generation of Neural Stem Cells from Discarded Human Fetal Cortical Tissue
07:29

Generation of Neural Stem Cells from Discarded Human Fetal Cortical Tissue

Published on: May 25, 2011

15.1K
Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
07:43

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Published on: May 12, 2015

11.2K

Related Experiment Videos

Last Updated: May 3, 2026

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells
06:38

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

Published on: March 7, 2025

1.1K
Generation of Neural Stem Cells from Discarded Human Fetal Cortical Tissue
07:29

Generation of Neural Stem Cells from Discarded Human Fetal Cortical Tissue

Published on: May 25, 2011

15.1K
Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
07:43

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

Published on: May 12, 2015

11.2K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Basal forebrain cholinergic neurons are crucial for cognition and depend on Nerve Growth Factor (NGF) for integrity.
  • Degeneration of these neurons contributes to dementia in Alzheimer's disease (AD) and Down syndrome (DS).
  • AD brains show abundant NGF precursor (proNGF) due to impaired extracellular metabolism, not reduced synthesis.

Purpose of the Study:

  • To investigate if a similar NGF metabolic imbalance, characterized by impaired proNGF maturation, exists in Down syndrome.
  • To examine NGF metabolic dysfunction in post-mortem human DS brains, fetal DS cortical cultures, and a mouse model of DS.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR)
  • Enzyme-linked immunosorbent assay (ELISA)
  • Western blotting
  • Zymography
  • Analysis of post-mortem human DS and control brains (temporal, frontal, parietal cortex)
  • Primary cultures of human fetal DS cortex
  • Brains from Ts65Dn mice (a DS model)

Main Results:

  • Significant increase in proNGF levels in human and mouse DS brains.
  • Reduced messenger RNA (mRNA) levels of plasminogen and tissue plasminogen activator (tPA), key enzymes in proNGF maturation.
  • Increased neuroserpin expression and elevated matrix metalloproteinase-9 (MMP9) activity, indicating impaired NGF maturation and enhanced degradation.

Conclusions:

  • Down syndrome brains exhibit a failure in NGF precursor maturation and likely enhanced NGF degradation, compromising cholinergic neuron support.
  • Alterations in proNGF and MMP9 were also observed in fetal DS cortical cultures, suggesting potential for early therapeutic intervention.
  • This study offers a new perspective on cholinergic neuroprotection strategies for Alzheimer's disease and Down syndrome.