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Encephalitis l: Introduction01:19

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Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Experimental Autoimmune Encephalomyelitis Influences GH-Axis in Female Rats.

Anica Zivkovic1, Svetlana Trifunovic2, Danijela Savic1

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This study reveals altered growth hormone (GH) and insulin-like growth factor-1 (IGF-1) axis activity during experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis model. Findings suggest GH resistance, potentially impacting therapeutic strategies.

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Area of Science:

  • Neuroimmunology
  • Endocrinology
  • Autoimmune Diseases

Background:

  • Multiple sclerosis (MS) involves central nervous system (CNS) inflammation, demyelination, and axonal damage.
  • The growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis plays a role in immune regulation, but its connection to MS/EAE is unclear.

Purpose of the Study:

  • To investigate alterations in the GH axis during acute experimental autoimmune encephalomyelitis (EAE).
  • To explore the relationship between GH/IGF-1 axis changes and disease severity in EAE.

Main Methods:

  • Analysis of gene expression in the hypothalamus and pituitary gland during EAE.
  • Measurement of serum GH and IGF-1 levels.
  • Assessment of liver gene expression for GH and IGF-1 receptors.

Main Results:

  • Hypothalamic gene expression for Ghrh and Sst remained unchanged, while Npy and Agrp were altered.
  • Pituitary Gh, Ghrhr, and Ghr gene expression were upregulated; somatotropic cell volume was unchanged.
  • Elevated serum GH with low IGF-1 and downregulated liver Ghr/Igf1r expression indicated GH resistance.

Conclusions:

  • Acute EAE is characterized by a state of GH resistance, possibly linked to reduced nutrient intake during peak CNS inflammation.
  • The GH/IGF-1 axis is significantly involved in MS/EAE pathogenesis and warrants further investigation for therapeutic potential.