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

A hypothalamic digoxin-mediated model for autism.

Ravi Kumar Kurup1, Parameswara Achutha Kurup

  • 1Department of Neurology, Medical College Hospital, Trivandrum, Kerala, India.

The International Journal of Neuroscience
|October 31, 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

Hypothalamic digoxin-mediated model for epileptogenesis.

Acta neuropsychiatrica·2016
Same author

Isoprenoid pathway dysfunction in chronic fatigue syndrome.

Acta neuropsychiatrica·2016
Same author

Hypothalamic digoxin, hemispheric chemical dominance and sarcoidosis.

Acta neuropsychiatrica·2016
Same author

A cholesterol and actinide dependent shadow biosphere of archaea and viroids in autoimmune diseases.

Immunobiology·2011
Same author

Familial hypothalamic digoxin deficiency syndrome.

The Journal of neuropsychiatry and clinical neurosciences·2004
Same author

Hypothalamic digoxin-mediated model for trisomy 21.

Pediatric pathology & molecular medicine·2003
Same journal

Thoracic paravertebral nerve block combined with general anesthesia for patients undergoing minimally invasive vertebroplasty: effects on pain and lumbar function.

The International journal of neuroscience·2026
Same journal

Recurrence associated IGFBP2 promotes malignant progression and epithelial mesenchymal transition in glioma cells via the AKT mTOR pathway.

The International journal of neuroscience·2026
Same journal

Decreased miR-1305 expression is associated with tumour invasiveness and poor prognosis in glioma patients.

The International journal of neuroscience·2026
Same journal

Astaxanthin alleviates ischemia-reperfusion injury by regulating the JAK2/STAT3 signaling pathway.

The International journal of neuroscience·2026
Same journal

Clinical efficacy of cryopreserved autologous bone flaps versus titanium plates for cranioplasty: A retrospective comparative study.

The International journal of neuroscience·2026
Same journal

Sericin improves diabetic cognitive impairment in rats by inhibiting TXNIP/NLRP3 neuroinflammation through SIRT1.

The International journal of neuroscience·2026
See all related articles

Autism is linked to an overactive isoprenoid pathway, leading to elevated digoxin levels and reduced Na+-K+ ATPase activity. This biochemical imbalance, particularly right hemispheric dominance, may contribute to autism development.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Autism Research

Background:

  • The isoprenoid pathway is crucial for cellular functions, producing metabolites like digoxin, dolichol, and ubiquinone.
  • Dysregulation in this pathway has been implicated in various neurological conditions.
  • Cerebral dominance may play a role in the neurodevelopmental aspects of autism.

Purpose of the Study:

  • To investigate the isoprenoid pathway and its metabolites in individuals with autism.
  • To explore the relationship between digoxin levels, Na+-K+ ATPase activity, and cerebral dominance in autism.
  • To elucidate the biochemical mechanisms underlying autism pathogenesis.

Main Methods:

  • Assessed isoprenoid pathway metabolites (digoxin, dolichol, ubiquinone) in autism.

Related Experiment Videos

  • Measured HMG CoA reductase activity as an indicator of isoprenoid pathway upregulation.
  • Evaluated red blood cell (RBC) membrane Na+-K+ ATPase activity and digoxin levels.
  • Compared biochemical profiles with hemispheric dominance.
  • Main Results:

    • Upregulation of the isoprenoid pathway with elevated HMG CoA reductase activity observed in autism.
    • Increased digoxin levels and reduced RBC membrane Na+-K+ ATPase activity found in autism.
    • Hypothalamic digoxin dysfunction linked to altered neurotransmitter precursor transport (tryptophan vs. tyrosine).
    • Biochemical patterns in autism correlated with right hemispheric chemical dominance.

    Conclusions:

    • Autism may be characterized by hypothalamic digoxin hypersecretion due to an upregulated isoprenoid pathway.
    • Na+-K+ ATPase inhibition, hypomagnesemia, and altered metabolite levels contribute to neuroinflammation, excitotoxicity, and synaptic dysfunction.
    • Right hemispheric chemical dominance is identified as a potential predisposing factor for autism.