The interference between SARS-COV-2 and Alzheimer's disease: Potential immunological and neurobiological crosstalk from a kinase perspective reveals a delayed pandemic.

Coronavirus disease 2019 (COVID-19) has infected over 700 million people, with up to 30% developing neurological manifestations, including dementias. However, there is a lack of understanding of common molecular brain markers causing Alzheimer's disease (AD). COVID-19 has etiological cofactors with AD, making patients with AD a vulnerable population at high risk of experiencing more severe symptoms and worse consequences. Both AD and COVID-19 have upregulated several shared kinases, leading to the repositioning of kinase inhibitors (KIs) for the treatment of both diseases. This review provides an overview of the interactions between the immune system and the nervous system in relation to receptor tyrosine kinases, including epidermal growth factor receptors, vascular growth factor receptors, and non-receptor tyrosine kinases such as Bruton tyrosine kinase, spleen tyrosine kinase, c-ABL, and JAK/STAT. We will discuss the promising results of kinase inhibitors in pre-clinical and clinical studies for both COVID-19 and Alzheimer's disease (AD), as well as the challenges in repositioning KIs for these diseases. Understanding the shared kinases between AD and COVID-19 could help in developing therapeutic approaches for both.