An interesting paper published in Alzheimer’s research and therapy 9th June 2021 reviewed this issue.
The authors, Zhou and others suggest that dementia like cognitive impairment is an increasingly reported complication of SARS-CoV-2 infection.
However, the underlying mechanism responsible for this complication remains unclear.
They argue that a better understanding of the causative processes by which COVID-19 may lead to cognitive impairment is essential to developing preventative and therapeutic interventions.
They conducted a network based multimodal omics comparison of COVID-19 and neurological complications.
They also compared the transcriptomic profiles of Alzheimer’s disease marker genes from patients infected with COVID-19 as well as the prevalence of SARS-CoV-2 entry factors in the brains of Alzheimer’s disease patients not infected with SARS-CoV-2 virus.
They found significant network based relationships between COVID-19 and neuro inflammation and brain microvascular injury pathways and processes which are implicated in Alzheimer’s disease.
They also detected aberrant expression of Alzheimer’s disease biomarkers in the cerebrospinal fluid and blood of patients with COVID-19.
Whilst the analyses showed relatively low expression of SARS-CoV-2 entry factors in human brain, neuro inflammatory changes were pronounced.
They also found that the expression of SARS-CoV-2 host factors and antiviral defence genes were elevated in brain endothelial cells of Alzheimer’s disease patients.
Healthy controls relative to neurons and other cell types suggesting the possible role for brain microvascular injury and COVID-19 mediated cognitive impairment.
Overall, individuals with various Alzheimer’s disease risk alleles displayed reduced expression of antiviral dispense genes compared to other individuals.
Their results suggested significant mechanistic overlap between Alzheimer’s disease and COVID-19.
This was centred on neuro inflammation and microvascular injury.
They suggested that the negative effects of COVID-19 on the central nervous system may have a long term impact that could possibly increase the likelihood of developing Alzheimer’s disease like dementia.
They found a strong network based relationship between SARS-CoV-2 host factors and disease associated genes/proteins of dementia-like cognitive impairment.
Their research showed that it was unlikely for SARS-CoV-2 to directly target neurons.
However, they were unable to rule out the possibility of the SARS-CoV-2 may enter the brain through cerebral endothelium using receptors.
Due to the shared pathways and network based relationships between COVID-19 and other diseases such as Alzheimer’s disease, repurposing, COVID-19 treatments may help individuals with other diseases including Alzheimer’s. For example, they recently identified melatonin as a re-purposable drug for COVID-19.
Multiple preclinical studies showed that melatonin was a potential treatment for Alzheimer’s disease as well.
They argue that their findings could lay the foundation for future research that ultimately leads to testable and measurable serum biomarkers that could identify patients at the highest risk of neurological complications with COVID-19.
The London General Practice, the leading London doctors’ clinic, supports patients with all aspects of COVID-19 disease including diagnosis, support and long term complications.
It provides a full diagnostic service including:
- COVID PCR testing
- Lateral flow testing
- Rapid antigen testing required by regulation for travel.
It also provides a COVID assist service for those suffering with COVID symptoms and has brought together a multidisciplinary team to support those patients who have Long COVID or post-acute COVID.
Dr Paul Ettlinger
BM, DRCOG, FRCGP, FRIPH, DOccMed