Protein Therapy Can Reverse Alzheimer’s In Mice

Credit: Wikipedia

Injecting a protein called interleukin 33 staves rescues Alzheimer’s pathology in mice and staves off decline

65 million people are predicted to develop Alzheimer’s disease by 2033 but current therapies are woefully inadequate and the search is on for a game changing treatment. A new study by scientists from Glasgow and Hong Kong has revealed that protein therapy could be an effective weapon against the condition. 

“The relevance of this finding to human Alzheimer’s is at present unclear. But there are encouraging hints. For example, previous genetic studies have shown an association between IL-33 mutations and Alzheimer’s disease in European and Chinese populations. Furthermore, the brain of patients with Alzheimer’s disease contains less IL-33 than the brain from non-Alzheimer’s patients” 

Recruiting the immune system

Interleukin 33 (IL-33) is a cytokine protein produced across the body. Cytokines are small proteins involved in cell signalling. Il-33 helps to stimulate immune activity and is particularly concentrated witin the central nervous system. After noticing that levels of Il-33 appear to drop in the brains of older patients with Alzheimer’s, researchers questioned whether this could play a role in disease development – allowing harmful plaques to build. 

“IL-33 is a protein produced by various cell types in the body and is particularly abundant in the central nervous system (brain and spinal cord). We found that injection of IL-33 into aged APP/PS1 mice rapidly improved their memory and cognitive function to that of the age-matched normal mice within a week”

Credit: National Institute on Aging, National Institutes of Health

Clearing out and reducing inflammation

There has already been plenty of research demonstrating that inflammation in the brain helps drive Alzheimer’s, and inflammation is essentially harmful immune activity. Curiously, when Il-33 was injected into the brains of mice with a model of Alzheimer’s it both stimulated immune activity and reduced inflammation. Il-33 seems to recruit an enzyme called neprilysin, which can digest soluble amyloid. Following Il-33 injection plaque number and size were noticeably reduced. Inflammation has been shown to enable disease progression in previous research, and in this study Il-33 appeared to reduce inflammation and help prevent any further tangles developing. 

“Exciting as it is, there is some distance between laboratory findings and clinical applications. There have been enough false ‘breakthroughs’ in the medical field to caution us not to hold our breath until rigorous clinical trials have been done. We are just about entering Phase I clinical trial to test the toxicity of IL-33 at the doses used. Nevertheless, this is a good start”

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