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 alpha2-macroglobulin: genotype-phenotype relation.

G Birkenmeier1, R Müller, K Huse

  • 1Institute for Biochemistry, University of Leipzig, Liebigstrasse 16, Leipzig, Germany. birg@medizin.uni-leipzig.de

Experimental Neurology
|November 26, 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

Evidence for a Spectral Break or Curvature in the Spectrum of Astrophysical Neutrinos from 5 TeV to 10 PeV.

Physical review letters·2026
Same author

Search for Extremely-High-Energy Neutrinos and First Constraints on the Ultrahigh-Energy Cosmic-Ray Proton Fraction with IceCube.

Physical review letters·2025
Same author

Measurement of Atmospheric Neutrino Oscillation Parameters Using Convolutional Neural Networks with 9.3 Years of Data in IceCube DeepCore.

Physical review letters·2025
Same author

Search for an eV-Scale Sterile Neutrino Using Improved High-Energy ν_{μ} Event Reconstruction in IceCube.

Physical review letters·2024
Same author

Validation of the synthetic model for the imaging heavy ion beam probe at the ASDEX Upgrade tokamak (invited).

The Review of scientific instruments·2024
Same author

Observation of Seven Astrophysical Tau Neutrino Candidates with IceCube.

Physical review letters·2024
Same journal

Neuropathological and functional impact of astrocyte-derived extracellular vesicles in an aged model of Alzheimer's disease.

Experimental neurology·2026
Same journal

PI3K/Akt pathway in ischemic stroke: A central regulator of neuronal survival and repair.

Experimental neurology·2026
Same journal

Hepatokines and stellakines in liver and neurological diseases: The liver-brain axis.

Experimental neurology·2026
Same journal

Structural dynamics of α-Synuclein: Multi-scale imaging insights into pathological progression across Synucleinopathies.

Experimental neurology·2026
Same journal

Retraction notice to 'Mitochondrial ferritin upregulation reduced oxidative stress and blood-brain-barrier disruption by maintaining cellular iron homeostasis in a neonatal rat model of germinal matrix hemorrhage' [Experimental Neurology 374 (2024) 114703].

Experimental neurology·2026
Same journal

Sivelestat sodium alleviates blood-brain barrier dysfunction after traumatic brain injury by reduction of NETs formation.

Experimental neurology·2026
See all related articles

The alpha-2-macroglobulin (alpha2-M) deletion polymorphism is not linked to Alzheimer's disease (AD) risk. However, age-related decreases in alpha2-M may contribute to amyloid-beta accumulation in AD.

Area of Science:

  • Genetics
  • Neuroscience
  • Biochemistry

Background:

  • A pentanucleotide deletion polymorphism in the alpha2-macroglobulin (alpha2-M) gene is controversially linked to late-onset Alzheimer's disease (AD).
  • The hypothesis suggests this deletion impacts alpha2-M quantity and function, potentially contributing to AD pathology.

Purpose of the Study:

  • To investigate the association between the alpha2-M deletion polymorphism and Alzheimer's disease.
  • To determine the effect of the polymorphism on alpha2-M plasma concentrations and functional properties.

Main Methods:

  • Genotyping of the alpha2-M deletion polymorphism in 227 healthy Caucasians.
  • Measurement of plasma concentrations of total and transformed alpha2-M.
  • Analysis of alpha2-M subunit structure and binding properties.

Related Experiment Videos

Main Results:

  • No significant correlation was found between age and alpha2-M genotypes.
  • The alpha2-M genotype did not significantly affect total or transformed alpha2-M concentrations.
  • Functional analyses revealed no genotype-specific alterations in alpha2-M properties.
  • A significant age-related decrease in total alpha2-M was observed, with higher levels in females.

Conclusions:

  • The alpha2-M deletion polymorphism is unlikely to be a major risk factor for AD.
  • Age-related decline in alpha2-M may promote amyloid-beta accumulation, a potential mechanism in AD pathogenesis.