Alzheimer's protein helps with multiple sclerosis

Triggers of Alzheimer's plaques relieve MS symptoms

08/02/2012

Alzheimer's beta-amyloid, according to a US research team, could help treat multiple sclerosis (MS) patients. In experiments on mice, the protein has helped alleviate the typical symptoms of MS, say the scientists to Jacqueline Grant of the Institute of Neurology and Neuroscience at Stanford University in the journal "Science Translational Medicine".

The peptides amyloid beta 40 (Aβ40) and amyloid beta 42 (Aβ42) are essential components of the so-called "senile plaque deposits in Alzheimer's disease," write Grant and colleagues. In animal studies, injection of the peptides in mice with a MS-like disease unexpectedly contributed to alleviating the symptoms and in some cases even delaying the onset of the disease. It may be possible to use this effect for new approaches to MS therapy in the future, according to the hope of the US scientists.

Surprising effect of Alzheimer's proteins
As the levels of beta-amyloid in MS brain lesions and injured axons are elevated in MS patients, US neurologists suspected a link between the peptides known as Alzheimer's plaques and multiple sclerosis. They tested this hypothesis by experimenting with mice that had MS-like disease (Experimental Autoimmune Encephalomyelitis, EAE) and injected the beta-amyloid protein fragment into the abdomen. If the researchers actually expected a worsening of the symptoms, then a clearly positive effect was shown instead. "Treatment with Aß42 or Aβ40 caused a reduction in brain motor paralysis and brain inflammation in four different models of experimental autoimmune encephalomyelitis," said the researchers.

Beta-amyloid relieves MS symptoms
According to Jacqueline Grant and colleagues, the injected beta-amyloid in the mice resulted in "attenuation of motor paralysis, reduction of inflammatory lesions in the central nervous system (CNS), and suppression of lymphocyte activation." Effects that may be useful in the future for the treatment of MS patients. Damage to the brain due to the deposition of beta-amyloid was not observed in the mice. According to the researchers, the peptides have left no traces in the brain of the animals. Overall, the result of the treatment was consistently positive and in some rodents even the onset of EAE could be delayed, write the US scientists.

Effect of Alzheimer's Peptides on the Immune System
Presumably, the injection of beta-amyloid has little to do with the processes in the brain of MS patients, but their positive effect on the effect on the immune system, so the assessment of Jacqueline Grant and colleagues. According to the experts, the immune cells responsible for the onset of the autoimmune disease MS are activated in the body, not in the brain. Only then they start their attack on the central nervous system. The circulating in the blood after the injection of beta-amyloid apparently inhibits the production of immune cells, so that the MS-typical negative effects in the brain are less strong, the US researchers report. The beta-amyloid thus act similar to modern MS drugs, which also block the white blood cells outside the brain. Also the count test with mice, which could produce no beta amyloid, confirmed the results, so Grant and colleagues further. These animals became significantly faster or more severe in EAE.

Therapeutic implementation of the results uncertain
Although the US scientists were quite confident in the future to use the Alzheimer's peptide for the treatment of MS patients, but still remain to answer some questions. Because before beta-amyloid or a similar peptide can be used as a drug, it should also be clarified whether not possibly an increase in the risk of Alzheimer's threatens. Because amyloid beta 40 and amyloid beta 42 are considered as the main trigger of Alzheimer's. They are an essential component of the so-called plaques, which are deposited in Alzheimer's patients in the brain and, according to current knowledge, the death of the nerve cells result. If it is increasingly deposited in the brain after an infection, this could favor the onset of the neurodegenerative disease. (Fp)

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