Active immunization with amyloid-beta 1-42 impairs memory performance through TLR2/4-dependent activation of the innate immune system.

Active immunization with amyloid-β (Aβ) peptide 1-42 reverses amyloid plaque deposition in the CNS of patients with Alzheimer's disease and in amyloid precursor protein transgenic mice. However, this treatment may also cause severe, life-threatening meningoencephalitis. Physiological responses to immunization with Aβ(1-42) are poorly understood.

A case of Rasmussen encephalitis treated with rituximab.

Background: A 20-year-old woman was referred to our intensive care unit with a high frequency (every 1-2 min) of focal motor seizures. She had been diagnosed as having biopsy-proven Rasmussen encephalitis (RE) of the right hemisphere 7 years previously, since when she had been treated with numerous antiepileptic drugs, as well as with continuous immunotherapies, such as tacrolimus, corticosteroids, mycophenolate mofetil, intravenous immunoglobulin and immunoadsorption. Although hemispherectomy had been avoided due to slow progression of RE, she had not been seizure-free for more than 7 weeks since diagnosis.