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New Findings: β-Amyloid Improves Paralysis in a Mouse Model of Multiple Sclerosis

The identifying hallmark of Alzheimer’s disease is the presence of β-amyloid plaques in the brains of patients.  β-amyloid (Aβ) plaques arise from the aggregation of dense deposits of Aβ peptide and cellular material surrounding neurons.  Because of this unmistakable association of β-amyloid plaques with Alzheimer’s disease, Aβ has quite a bad reputation in the world of neurodegenerative disorders.

However, a study published on August 1 offers some evidence that thickens the plot of the Aβ story.  The laboratory of Dr. Lawrence Steinman, senior author of the article, studies a mouse model of experimentally-induced multiple sclerosis known as experimental autoimmune encephalomyelitis (EAE).   Multiple sclerosis is an inflammatory autoimmune disorder that disrupts neuronal signaling throughout the central nervous system.  The hallmark feature of multiple sclerosis is the presence of lesions.  Rather than being an aggregate of peptides, these lesions are formed by destruction of the myelin sheath surrounding neurons.  The myelin sheath is essential for efficient propagation of neuronal signals.

In an effort to characterize the immunomodulatory potential of Aβ in this model, Grant et al. injected Aβ into the peripheral circulation of mice with EAE.  The researchers had expected that the addition of Aβ would worsen EAE disease progression due to the putative pro-inflammatory effects of Aβ.  However, they were in for a surprise.  Instead of exacerbating symptoms in EAE mice, the injection of Aβ actually improved paralysis symptoms.  Further, when Aβ was injected prior to MS-like clinical disease onset, paralysis was prevented.

These interesting results will undoubtedly open up an array of new questions pertaining to Aβ and its complex effects on the nervous system.  While Aβ is expressed in the normal nervous system, its function under healthy circumstances remains to be defined.  While the Aβ plaques of Alzheimer’s disease express numerous inflammatory mediators, the presence of Aβ in the periphery may actually suppress the secretion of inflammatory mediators by lymphocytes, actually making it immunosuppressive.

The story of Aβ is complex, but hopefully these new findings will open doors to new therapies for Multiple Sclerosis, and maybe even Alzheimer’s disease, in the future.

What do you think?

How do you think Aβ might relate to the improvement of MS-like symptoms in mice?  Is there any relation between the development of Alzheimer’s disease and Multiple Sclerosis?

Further Reading:

Grant JL, Ghosn EE, Axtell RC, Herges K, Kuipers HF, Woodling NS, Andreasson K, Herzenberg LA, Herzenberg LA, Steinman L.  (2012).  Reversal of Paralysis and Reduced Inflammation from Peripheral Administration of β-Amyloid in TH1 and TH17 Versions of Experimental Autoimmune Encephalomyelitis. Sci Transl Med. Aug 1;4(145):145ra105.


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