Mice have reduced motor paralysis and brain inflammation following treatment with β-amyloid
THURSDAY, Aug. 2 (HealthDay News) -- Peptides that play a key role in the pathology of Alzheimer's disease have been found to reduce motor paralysis and brain inflammation in mouse models of multiple sclerosis (MS), according to an experimental study published in the Aug. 1 issue of Science Translational Medicine.
Building on previous results showing that β-amyloid (Aβ)-42 protein is present in MS lesions and damaged axons, Jacqueline L. Grant, Ph.D., from Stanford University in California, and colleagues injected mice with experimental autoimmune encephalomyelitis, a model of MS, with Aβ42 or Aβ40 peptides outside the brain.
The researchers found that both peptides reduced motor paralysis and brain inflammation and could reduce ongoing paralysis induced by autoreactive T cells. Lymphocytes from mice treated with Aβ42 could also reduce MS symptoms when transferred to wild-type mice. Mice deficient in amyloid precursor protein had worse disease. Mice treated with either peptide had changes in their peripheral lymphoid and myeloid subsets, and Aβ treatment reduced proinflammatory cytokines and chemokines in the blood. No Aβ was detected in the brain in treated mice.
"Because Aβ42 and Aβ40 ameliorate experimental autoimmune inflammation targeting the central nervous system, we might now consider its potential anti-inflammatory role in other neuropathological conditions," Grant and colleagues conclude. "The anti-inflammatory role of Aβ described here contrasts with the presumed role of Aβ in Alzheimer's disease, where great attention has focused on the pathogenicity of Aβ as a central target for experimental therapy."
Two authors have applied for a provisional patent pertaining to the study.
Abstract (http://stm.sciencemag.org/content/4/145/145ra105 )Full Text (subscription or payment may be required) (http://stm.sciencemag.org/content/4/145/145ra105.full )