Many aging minds harbor a common fear: that thoughts, once reliably efficient, will become slow and scattered. Where the elderly could once quickly traverse the brain’s complex passageways, they now risk losing their way. 

Out of many neurodegenerative diseases, Alzheimer’s sticks out, afflicting an estimated 6 million people aged 65 and older. Fortunately, new scientific discoveries have shed light on these broken pathways, with a common protein providing potential prevention of the disease. 

The National Institutes of Health defines Alzheimer’s as a neurodegenerative disease, characterized by amyloid-beta (Aβ) “plaque” buildup in spaces between neurons and neurofibrillary tangles. Over time, these proteins disrupt communication between nerve cells, phenotypically presenting as a loss of memory and general cognitive failure. Interestingly, there tends to be a 15 to 20-year lag between the initial detection of the Aβ plaque and obvious cognitive decline. For this reason, preventative methods could be instrumental in keeping symptoms at bay. 

With this intention, researchers at St. Jude Children’s Research Hospital published a study this past August, highlighting the role of midkine in stopping amyloid-beta from forming harmful clumps associated with Alzheimer’s. The lab analyzed the properties of midkine, a promising deterrent of Aβ clumps. Midkine is a small growth factor protein found in regular cell function, particularly during embryonic growth. Its role in cell growth makes it susceptible to overexpression in certain cancers, providing a useful biomarker for tracking tumor progression. 

Using a number of tools —  including fluorescence assays, circular dichroism, electron microscopy, and nuclear magnetic resonance — on similar disease models, the research team found a protein-level pattern similarity between midkine and Aβ. Using a fluorescent marker for Aβ assemblies, researchers observed Aβ dispersion in the presence of midkine. Following this finding with a mouse study, they observed higher accumulation of amyloid-beta when the midkine gene was removed and unexpressed. 

Having established midkine’s role in mitigating amyloid pathology, the researchers’ next step involves observing midkine’s binding structure.

If successful, this could have major therapeutic implications, as they would be able to design small molecules to function similarly. 

That said, researchers agree there is more to Alzheimer’s than just amyloid occlusion, which has held the research spotlight for nearly 30 years. New studies explore other entities implicated in pathogenesis, including microglia, astrocytes, apolipoprotein E, and several others. Nevertheless, amyloid-reducing drugs remain undoubtedly implicated in the disease and are anticipated to work in tandem with other Alzheimer’s preventative methods. Paired with positive exercise, diet, and mental stimuli, midkine’s discovery ushers in renewed hope for current and future patients, offering them a chance toward peace of mind.