Passive Immunization Reduces Behavioral and Neuropathological Deficits in an Alpha-Synuclein Transgenic Model of Lewy Body Disease
2011

Passive Immunization Reduces Behavioral and Neuropathological Deficits in an Alpha-Synuclein Transgenic Model of Lewy Body Disease

Sample size: 40 publication 10 minutes Evidence: high

Author Information

Author(s): Masliah Eliezer, Rockenstein Edward, Mante Michael, Crews Leslie, Spencer Brian, Adame Anthony, Patrick Christina, Trejo Margarita, Ubhi Kiren, Rohn Troy T., Mueller-Steiner Sarah, Seubert Peter, Barbour Robin, McConlogue Lisa, Buttini Manuel, Games Dora, Schenk Dale

Primary Institution: Department of Neurosciences, University of California San Diego

Hypothesis

Can passive immunization with a monoclonal α-synuclein antibody reduce deficits associated with α-synuclein accumulation in a transgenic mouse model?

Conclusion

The study found that passive immunization with the 9E4 antibody effectively reduced behavioral deficits and neuropathological alterations in α-synuclein transgenic mice.

Supporting Evidence

  • The 9E4 antibody reduced behavioral deficits in the water maze.
  • Immunization with 9E4 decreased accumulation of calpain-cleaved α-synuclein.
  • In vivo studies showed that 9E4 traffics into the CNS and promotes α-syn clearance.
  • Passive immunization may be therapeutically relevant for patients with Parkinson's Disease and Lewy Body Dementia.

Takeaway

Researchers gave special antibodies to mice with a brain problem to see if it would help them think and move better, and it worked!

Methodology

Transgenic mice over-expressing α-synuclein were treated with the 9E4 antibody and assessed for behavioral and neuropathological changes.

Limitations

The study was conducted in a mouse model, which may not fully replicate human conditions.

Participant Demographics

Transgenic mice expressing human α-synuclein under the PDGF-β promoter.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0019338

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