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Related Concept Videos

Neural Regulation01:37

Neural Regulation

Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.

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α -Synuclein Modification in an ALS Animal Model.

Eun Jin Yang1, Sun-Mi Choi

  • 1Department of Medical Research, Korea Institute of Oriental Medicine, 483 Expo-ro, Yuseong-gu, Daejeon 305-811, Republic of Korea.

Evidence-Based Complementary and Alternative Medicine : Ecam
|June 14, 2013
PubMed
Summary

Bee venom (BV) treatment reduced misfolded alpha-synuclein aggregates and improved proteasomal activity in a mouse model of Amyotrophic Lateral Sclerosis (ALS). This suggests BV may help slow motor neuron loss in ALS patients.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease characterized by progressive paralysis, often linked to mutations in Cu/Zn-superoxide dismutase 1 (SOD1).
  • Overexpression of mutant SOD1 in transgenic mice leads to paralysis and protein aggregate accumulation in the central nervous system.
  • Bee venom (BV), derived from honeybees, is traditionally used for inflammatory conditions.

Purpose of the Study:

  • To investigate the effects of bee venom (BV) on misfolded protein aggregates, specifically alpha-synuclein.
  • To assess the impact of BV on ubiquitin-proteasomal activity in a mouse model of ALS (hSOD1(G93A)).

Main Methods:

  • Bee venom (BV) was administered to 98-day-old hSOD1(G93A) transgenic mice.
  • Levels of detergent-insoluble polymerization and phosphorylation of alpha-synuclein were analyzed.
  • Proteasomal activity in the brainstems of treated mice was evaluated.

Main Results:

  • BV treatment significantly reduced detergent-insoluble polymerization and phosphorylation of alpha-synuclein in hSOD1(G93A) mice.
  • Phosphorylated and nitrated alpha-synuclein levels were notably decreased in the spinal cords and brainstems of BV-treated mice.
  • Reduced proteasomal activity was observed in the brainstems of BV-treated symptomatic hSOD1(G93A) mice.

Conclusions:

  • Bee venom (BV) treatment appears to attenuate the dysfunction of the ubiquitin-proteasomal system in a symptomatic hSOD1(G93A) ALS mouse model.
  • These findings suggest that BV may offer a therapeutic strategy to slow motor neuron loss associated with misfolded protein aggregates in ALS.