Thanks to noteworthy research by the Cleveland Clinic we now know there is a link between COVID and Alzheimer’s Disease. What does this recent pioneering research mean to the public?
According to WHO (World Health Organization), around 50 million people have dementia, and there are nearly 10 million new cases every year. Dementia refers to deterioration in memory, thinking, behaviour and the ability to perform daily activities.
Even though dementia is associated with older adults, many young people suffer from this syndrome. Alzheimer's disease is the most common form of dementia. Alzheimer's disease covers at least 60% of dementia cases.
Dementia impacts several aspects of our lives, including physical, psychological, social, and economic. It not only impacts patients with dementia but also their families and carers. As we know, Alzheimer's disease currently affects 6.2 million Americans.
I keep asking myself and reflecting on my posts how we can conquer causes of Alzheimer's and other dementia types using new technology opportunities. We need more collaborative research to deal with this debilitating disease.
Whenever I hear about a research study related to cognitive health, I’m all ears. Many human beings are suffering from conditions of cognitive decline. It is inevitable as we age. However, experiencing the decline in younger ages is not desirable. Now, COVID-19 is making this disease worse.
I recently posted two articles to News Break related to dementia. In the first article, I touched on a few culprits for dementia, introduced the concepts of cognitive reserves, and how I took preventative measures considering the previously elevated cortisol as a symptom of my chronic stress.
In the second article, I introduced a drug named aducanumab branded as Aduhelm by Biogen in the United States. I provided perspectives covering a broad range of thoughts and sentiments by professionals and the public as reflected in traditional and social media. Media sentiments demonstrate both celebration and apprehension for approval of this promising drug by the FDA.
Like many aspects of life, Covid-19 affected our mental health as well. Since the emergence of the virus, COVID-19 patients experienced symptoms of neurological problems. These problems were mentioned in the press, including many local and global news outlets. However, there was not a single study to point the underlying mechanism and relationships.
In this article, I want to introduce a recent study from the Cleveland Clinic published June 9, 2021, that gave us an informed indication. The research paper, authored by 11 scientists, was published on BMC, which is part of Springer Nature's Alzheimer's Research & Therapy.
BMC put the paper in the open-access section of the site so that it can be read free by Internet users.
The paper informs that "dementia-like cognitive impairment is an increasingly reported complication of SARS-CoV-2 infection. However, the underlying mechanisms responsible for this complication remain unclear. A better understanding of causative processes by which COVID-19 may lead to cognitive impairment is essential for developing preventive and therapeutic interventions".
Implications of study
Let me introduce this study, its implications, and plans.
Researchers found significant network-based relationships between COVID-19, neuroinflammation and brain microvascular injury pathways and processes. These pathways and processors are implicated in Alzheimer's disease.
From my understanding, the critical hallmarks of Alzheimer's disease are neuroinflammation and microvascular brain injury.
The research team detected abnormal expression of Alzheimer's disease biomarkers in the cerebrospinal fluid and blood of patients with COVID-19.
Even though analyses of research showed relatively low expression of SARS-CoV-2 entry factors in the human brain, neuro-inflammatory changes were noticeable.
They identified the expression of SARS-CoV-2 host factors (such as BSG and FURIN) and antiviral defence genes called LY6E, IFITM2, and IFITM. Furthermore, single-nucleus analyses showed elevated Interferon Alpha And Beta Receptor Subunit 1 (IFNAR1) genes in brain endothelial cells of Alzheimer's disease patients. You can learn more about these genes from GeneCards human gene database.
Thus, the elevation of IFNAR1 suggests a possible role for microvascular brain injury in COVID-19-mediated cognitive impairment.
From genetics observations, patients with the Alzheimer's disease risk having APOE E4/E4 displayed reduced antiviral defence genes expression compared to APOE E3/E3 individuals.
What does the research result mean to the public?
This research shows a significant mechanistic overlap between Alzheimer's disease and COVID-19, centered on neuro-inflammation and microvascular injury.
These findings can help scientists improve their understanding of COVID-19-associated neurological manifestations and guide them to develop preventive and treatment intermediations.
Researchers pointed out that causal relationships and mechanistic pathways between COVID-19 and AD need future investigations.
Wearing my technology hat, for me, one interesting aspect of the study was the use of artificial intelligence. The study method leveraged artificial intelligence to compare existing datasets between patients with COVID-19 and Alzheimer's.
My understanding and conclusion of this research are that the COVID-19 virus may impact two critical factors in our brain. The first factor is mentioned in the study is. The second factor is how it affects pathways involved in neuroinflammation and brain microvascular injury. These genes and pathways could lead to cognitive impairment related to Alzheimer's disease.
Humanity has already faced a massive challenge concerning this debilitating disease (Alzheimer's). Now, we know that the COVID-19 virus is another contributor to the growth of this disease.
This finding indicates that while scientists are working hard to find solutions for Alzheimer's disease, we also need to be mindful of further implications of COVID-19 on dementia, particularly in our aging population.
Thank you for reading my perspectives.