Alzheimer’s disease is a progressive neurodegenerative disease that affects an individual’s behavior, memory, and mental capabilities. Alzheimer’s allows for the build-up of proteins in the brain, which lead to brain dysfunction. Unfortunately, it is the most common cause of dementia, which progressively leads to brain damage.
Some of the key features or symptoms of Alzheimer’s disease includes memory loss, inability to think or reason, change in mood, personality and behavior, and a general cognitive decline. Many things can increase an individual’s risk including age, genetics, and/or lifestyle factors. Specifically, older individuals with a family history of Alzheimer’s have increased risk. Other research suggests diabetes, heart disease, and obesity also increase risk. For diagnosis, various cognitive evaluation exams are conducted with full medical history intake and imaging. Unfortunately, there is no cure for Alzheimer’s disease, but currently some medications and therapies can help reduce symptoms and slow progression.
Scientists are working to develop more effective therapies to improve Alzheimer’s disease treatment and cure patients. A recent paper, published in the journal Alzheimer’ & Dementia, outlines how the deletion of an intracellular pathway can protect against proteins that induced Alzheimer’s disease. The study was led by Dr. John R. Lukens, who is a Professor in the Department of Neuroscience and the Center for Brain Immunology and Glia at the University of Virginia. His work primarily focuses on the investigation of various treatments for central nervous system (CNS) diseases, including infections, amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease), and Alzheimer’s Disease.
The group found that a molecule called STING within the cells helps generate harmful plaque and protein, which builds up to generate Alzheimer’s disease. Through the use of mice as science models to mimic human disease, the team blocked STING in mice with Alzheimer’s. As a result, the mice treated with the STING inhibitor had reduced cognitive decline compared to the mice without treatment. This experiment, among others to confirm findings, demonstrated that STING directly correlates with the progression of Alzheimer’s disease.
Further biological analysis showed that by blocking STING, brain cell activity that drives Alzheimer’s was dampened. Treatment also protected healthy neurons, and improved memory function. Interestingly, while STING can help immune cell function under healthy conditions, a chronic upregulation of the pathway can lead to hyperactivity and generate deleterious effects.
Scientists also believe that STING may contribute to Parkinson’s disease, Lou Gehrig’s disease, dementia, and other memory-loss disorders. Therefore, therapeutic benefits of blocking STING in Alzheimer’s may also extend to similar diseases. Further investigates indicates that DNA damage as we age activates STING-related inflammation in the brain. This novel discovery helps explain why aging increases risk of Alzheimer’s disease.
This discovery by Lukens and others identifies a cellular pathway partially responsible for the establishment of Alzheimer’s disease. Additionally, STING is present throughout most stages of Alzheimer’s disease. Consequently, STING can be used as a target for treatment to improve cognitive function. Scientists are only beginning to understand the complex disease but hope this advancement can pave the way for more effective treatments and develop a cure for patients with Alzheimer’s disease.
Paper, Alzheimer’ & Dementia, John R. Lukens, University of Virginia
